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58 Cards in this Set
- Front
- Back
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How would you define motility?
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Motility is the process that 1)mixes GI contents and
2) propels them along the tract |
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How would you define secretion?
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Secretion is the process by which GI glands release water/substances
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How would you define digestion?
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Process by which food is broken down into smaller absorbable molecules
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How would you define absorption?
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Process by which nutrients are absorbed by cells lining the GI tract.
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What are the two arrangements of muscle in the GI tract? Which is closer to the lumen?
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There is longitudinal muscle and circular muscle. Circular muscle is closer to the lumen.
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How does the GI system act like a syncitium?
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The muscle fibers are electrically connected to one another via gap junctions. This allows waves of depolarization via ion flow to spread.
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Can electrical connections spread between cross layers(longitudinal and circular layers of SM)
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Yes, can cross layers or excite within the layer.
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What does the distance travelled of depolarization in smooth muscle depend on?
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The distance travelled of depolarization depends on f (Excitability) of muscle.
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Are slow waves action potentials? What generates them?
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Slow waves are not action potentials- but rather slow undulating changes in RMP if 5 to 15 mV.
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What kinds of frequency of undulating slow waves do we see in the stomach, duodenum, and illeum?
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3/min in the stomach
12/min in duodenum 8/min in illeum |
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What kinds of cells are responsible for creating the slow waves?
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Interstitial cells of cajal
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Do slow waves typically cause contraction of muscle?
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No, except in the stomach.
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What sorts of factors control the resting membrane potential of GI cells?
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-Depolarizing stimuli = stretch, ACh, gastrin, motillin
-Hyperpolarizing stimuli- norepinephrine, epinephrine, SNS, secretin, CCK. |
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What are some unique characteristics of GI action potentials - what causes them, how long do they last?
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GI action potentials are unique in that they occur on top of the slow waves whenever RMP > -40mV. They are slower than in skeletal muscle or nerve, lasting 20 ms. They are due to influx of Calcium (some Na), and the influx of Ca++ impacts contractile force.
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What is another name for Meissner's plexus?
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Meissner's plexus is also called the submucosal plexus.
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What is another name for Auerbach's plexus?
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Auberbach's plexus is also called the Myenteric plexus.
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What is another name for the submucosal plexus?
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The submucosal plexus is also called Meissner's plexus.
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What is another name for myenteric plexus?
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Myenteric plexus is also called Auberbach's plexus.
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What constitutes the enteric nervous system?
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The combination of Meissners and Auerbachs plexuses.
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What is the function of ENS? How does the ENS function with lesions to PNS/CNS?
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The ENS integrates motor and secretory activities of the GI system. If SNS/PNS nerves are lesioned, many processes will continue almost normally as they are controlled by the ENS.
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How does the myenteric plexus control motor activity in the gut?
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Can Increase
1) Tonic contractions (increased tone of the gut wall) 2) Intensity of contractions 3) rate of contractions 4) conduction velocity (more rapid peristalsis) Remember there are some inhibitory neurons in myenteric - secrete vasoactive intestinal polypeptide (VIP) that inhibits sphincter tone of pylorric and ileocecal valve. |
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Where is the myenteric plexus located in the gut?
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The myenteric plexus lies between the longitudinal and circular layers.
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What does the submucosal plexus in the gut do?
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Submucosal plexus is more LOCAL than the myenteric plexus- it receives sensory signals from epithelium and uses that to control local intestinal secretion, local absorption, and local contraction of the submucosal muscle.
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What are the 3 main inhibitory substances? How do they work?
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VIP -> works by upregulating cAMP, increasing SM relaxation.
NO -> works by upregulating cGMP, increasing SM relaxation Sympathetic stimulation -> works by hyperpolarization, increasing smooth muscle relaxation. |
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What are the 3 parasympathetic systems in GI tract control?
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1) Cranial division- vagus nerves to esoph, stomach, pancreas, and less to SI
2) Sacral division-2nd-4th sacral segments of SC to distal large intestine (defecation reflex) at sigmoidal, rectal, and anal regions 3) Postganglionic division - in myenteric and submucosal plexuses- increases activity of ENS, increases activity of most GI functions. |
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What is the organization of the sympathetic innervation in the GI tract
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Originates from T5 to L2 and consists of preganglionic fibes. From the SC, these fibers enter sympathetic chains to postganglionic neurons in the celiac and mesenteric ganglia. These fibers innervate all the GI tract (rather than the parasymp which is concentrated at oral and anal regions).
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How does sympathetic innervation inhibit the GI tract?
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1) Direct effects on SM (norepinephrine on the muscle)
2) **Inhibitory effects on NE on neurons of the ENS. |
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How are afferent sensory nerve fibers stimulated?
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Afferent sensory nerve fibers are stimulated by
1) mucosal irritation 2) gut distention 3) chemical substances This can then cause excitation or inhibiton of motility/secretion. |
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Describe how some afferent sensory nerve fibers leave the ENS?
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Some of the sensory fibers have neurons in the enteric nervous system, and their axons terminate in the prevertebral sympathetic ganglia.
Others have their cell bodies in the DRG or CN ganglia, which means they transmit gut signals back to the SC or medulla via the vagus. |
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What are gastrointestinal reflexes that are integrated entirely within the ENS gut wall used for?
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These are for basic reflexes controlling secretion, peristalsis, mixing contractions, etc.
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What are GI reflexes that go from the gut to prevertebral sympathetic ganglia and back to the GI tract used for.
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These are for transmitting signals from one region of the GI tract to another- Gastrocolic, enterogastric, colonoileal reflexes.
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What are GI reflexes from the gut to the SC/BS back to GI tract used for?
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1)To control gastric motility/secretion (from stomach/duodenum to BS and back to stomach)
2) Pain reflexes-inhibit GI tract 3) Defecation reflexes- colon and rectum to SC and back. |
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What is the vagovagal reflex?
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Vagal sensory nerves relay stretch info to brainstem, causing vagal efferents to parietal and G cells in the stomach (allows stomach to hold more food).
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What is the enterogastric reflex?
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Inhibition of stomach motility/secretion due to intestinal filling.
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What is the intestinointestinal reflex?
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Distention of one portion of intestine leads to decreased contractions caudad of the bolus.
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What is the gastroileal reflex?
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Stomach activity leads to ileocecal relaxation- empty small intestine to process next meal.
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What is the gastrocolic reflex?
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Filling of stomach leads to mass movement in colon
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Are hormones more important in controlling secretion or motility?
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Secretion.
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What kind of cells make CCK? How does it affect motility?
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I cells secrete CCK in duod/jej in response to fats.
Increases Gall bladder motility (releases fats), Inhibits stomach motility |
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What kind of cells make secretin? How does it affect motility?
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S cells of duodenum secrete in response to acid. Inhibits GI motility.
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When is GIP secreted? How does it affect motility?
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GIP secreted by mucosa of upper small intestine in response to FA, AA, CHO.
Decreases stomach motility. |
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What are the 2 basic movements of the GI tract?
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Propulsive
and mixing |
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How do propulsive movements work?
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These movements involve forward movement of a contractile ring around the gut wall. Any material in front of the ring is moved forward.
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What are typical stimuli for peristalsis?
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Distension of the gut or chemical/physical irritation.
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What smooth muscle tubes have peristalsis in our body?
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gI tract
ureter bile duct |
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What is necessary for propulsive movements to occur?
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Intact, active myenteric plexus.
Responses in the retrograde direction die out very quickly also. |
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What is the Peristaltic reflex and the law of the gut?
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The peristaltic reflex says that the gut relaxes downstream to allow movement towards the anus (recetive relaxation), which may explain why food only moves in retrograde direction. This relaxation reflex occuring in the anal direction is the Law of the gut.
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T/F Mixing movements are homogenous throughout the GI tract?
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False, they are heterogeneous.
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What are the two major kinds of mixing movements?
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1) Peristaltic movements against a sphincter
2) Local intermittent constrictive contractions along the gut wall for a few seconds- then repeat at other locations- chopping and shearing contents. |
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What is the splanchnic circulation?
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This means all blood passing through the gut, liver and spleen then immediately drains into the liver via the portal vein, passes through sinusoids, and then leaves via hepatic vein to vena cava
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What kind of cells live in sinusoids in the liver?
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Reticuloendothelial cells that clean blood -removing bacteria and particulate matter.
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Where do fat based and non fat based absorbed nutrients in the gut travel?
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Non fat based travel in the portal vein to liver where the hepatic and reticuloendothelial cells temporarily store 75% of nutrients. Fat based nutrients are not carried in portal circulation- they are absorbed in lymphatics and are taken to blood via the thoracic duct.
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What is the blood supply of gut?
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Celiac trunk - stomach
SMA - SI and LI IMA - LI |
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What is important to know about the microvasculature of the vilus?
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Countercurrent flow- 80% of its O2 diffuses from artery to vein. The villus is ischemia vulnerable since 80% of oxygen diffuses from arteries to veins (ischemia in pathological conditons, normally this 80% is okay)
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Is Adenosine a vasodilator?
Is Ang II? Is endothelin? Is bradykinin? Is NE? Is Vasopressin? Is ACh? Is PGF2Alpha? Histamine? Is Beta agonist? Is NO? VIP? |
Vasoconstrictors - endothelin, NE, vasopressin, ang2, pgf2alpha,
Vasodilators- histamine, NO, Beta agonist, adenosine (ADilator ADenosine), VIP, bradykinin |
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What is postprandial hyperemia?
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Blood flow increases in response to a meal- blood flow proportional to local metabolic activity- increased flow to villi during absorption and increased motor activity. Flow returns to normal during resting state.
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Through what mechanisms does postprandial hyperemia occur?
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1) Dilator release (CCK, VIP, gastrin secretin)
2) GI glands secrete kinins 3) Decreased oxygen, increased adenosine |
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What is autoregulatory escape?
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Normally, SNS stimulation causes intense vasoconstriction to the GI system. But after a while, vasodilators build up, and blood flow resumes to prevent ischemia.
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