Introduction to GI Flashcards

1
Q

How is unidirectional flow between different sections of the GI tract controlled?

A

A series of muscular sphincters control the flow via inherent myogenic mechanisms.

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2
Q

Which sphincter maintains the highest resting pressure? What is its function? What kind of muscle is it and what controls it?

A

The upper esophageal sphincter. Its job is to prevent air from entering the esophagus. It consists of striated muscle and is under control of the swallowing center in the medulla and relaxes during swallowing to permit food to enter the esophagus.

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3
Q

What is the function of the lower esophageal sphincter? What kind of muscle is it and what controls it?

A

It separates the esophagus and the stomach. It is composed of smooth muscle that relaxes during swallowing. It functions to coordinate the passage of food into the stomach after swallowing/ deglutination and to prevent reflux of gastric contents.

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4
Q

What does an incompetent LES result in?

A

GERD

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5
Q

What is the function of the pyloric sphincter? What kind of muscle is it and what controls it?

A

It separates the stomach from the duodenum, and its resting pressure contributes to regulation of gastric emptying and prevention of duodenal-gastric reflux. The pyloric sphincter will only open if the duodenum can handle the contents in the stomach, it is very selective.

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6
Q

What does reflux of the pyloric sphincter lead to?

A

Reflux of bile acids and digestive enzymes can lead to gastritis, ulcer formation, and risk of perforation

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7
Q

About how much do we ingest each day in fluid and food?

A

2 liters

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8
Q

How much fluid does the GI tract add to what we ingest each day? What does the fluid do?

A

8-9 liters to facilitate digestion and absorption of the nutrients

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9
Q

Where is most of the fluid secreted by the GI tract absorbed? How much fluid do we excrete each day?

A

The small intestine. 100 - 200 mL

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10
Q

What are the primary nerve nets of the ENS named?

A

The myenteric plexus (Auerbach’s) and the submucosal plexus (Meissner’s)

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11
Q

Where is the myenteric plexus (Auerbach’s) located? What does stimulation cause?

A

The myenteric plexus (Auerbach’s) is between the longitudinal and circular muscle layers of the GI tract, and extends from the proximal end of the esophagus to the rectum. Stimulation primarily increases tonic contraction or ‘tone’ of the gut, the intensity of rhythmic /phasic contractions, and velocity of conduction of excitatory waves thus enhancing peristalsis.

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12
Q

Where is the submucosal plexus (Meissner’s) located? What does stimulation cause?

A

The submucosal plexus (Meissner’s) is between the circular muscle and submucosa in the small and large intestines. It’s primarily involved with controlling local intestinal secretions, absorption, and contraction of the submucosal muscle which affects local infolding of the GI mucosa.

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13
Q

Order the following from the side that faces the blood to the side that faces the digested contents: Serosa, Epithelium, lamina propria, myenteric plexus, submucosal plexus, muscularis mucosae, circular muscle, longitudinal muscle, submucosa:

A

Serosa, longitudinal muscle, myenteric plexus, circular muscle, submucosal plexus, submucosa, muscularis mucosae, lamina propria, epithelium

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14
Q

Whic ENS plexus is involved with secretions? Which with motility/ tone?

A

Submucosal plexus does secretions.

Myenteric plexus does tone and contractions.

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15
Q

“The GI tract has an intrinsic ENS,” what does this mean? How can it achieve this?

A

The ENS is able to function independently responding to input from the local environment through mechanoreceptors, chemoreceptors, and osmoreceptors in the epithelial lumen even in the absence of extrinsic innervation. It has different programmed responses to different stimuli.

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16
Q

Where do the extrinsic signals to the ENS come from?

A

The PNS and SNS.

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17
Q

What do mechanoreceptors in the ENS do?

A

Mechanoreceptors sense stretch of the smooth muscle, and the generated signal is transduced through the myenteric plexus, stimulating contractions.

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18
Q

What do chemoreceptors in the ENS do?

A

Chemoreceptors sense the chemical composition of the chyme and regulate motility and secretion of buffers to control luminal pH during the influx of acidic chyme into the duodenum.

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19
Q

What do osmoreceptors in the ENS do?

A

Osmoreceptors sense the osmolarity of the chyme in the small intestine. This is important, because there is only a one-cell barrier between the chyme in the lumen of the small intestine and the capillaries, and hypertonic chyme can exert an osmotic force, pulling fluid out of the cells (and ultimately the plasma). Thus, the osmoreceptors control the amount of chyme entering the small intestine, as well as the amount of secretions necessary to buffer the chyme.

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20
Q

What does PNS activity do to the gut?

A

PNS activation leads to increased motility in the wall of the gut, relaxation of sphincters, and enhanced secretions (e.g. mucus, hormones, acid, buffers).

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21
Q

What are vagovagal reflexes?

A

These are long reflexes in which both afferent and efferent impulses are carried by neurons in the ‘mixed’ vagus nerve. They are prominent in coordinating GI function.

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22
Q

How do the PNS and SNS affect GI motility and secretions?

A

PNS activation promotes digestion and absorption by: increasing salivary, pancreatic and gastric acid secretions; increasing contraction of smooth muscle wall; and relaxing sphincters. SNS activation inhibits digestion and absorption by relaxing the gut wall, reducing secretions, contracting sphincters, and diverting blood flow from the GI tract by contracting the vasculature.

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23
Q

A hierarchy of five levels of neural organization determines the moment-to-moment motor behavior of the digestive tract: what are each of the levels and how do they work?

A

Level 1, the ENS, behaves like an independent integrative nervous system. Level 2 is the prevertebral ganglia of the SNS. Levels 3-5 are within the CNS and the are; 3 Central sympathetic centers, 4 central parasympathetic centers, 5 higher brain centers.

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24
Q

What are the interstitial cells of Cajal?

A

They are the pacemakers in the GI tract (abundant in the myenteric plexus) that generate electrical slow waves

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25
Q

When does contraction of GI muscle wall occur?

A

Only when action potentials are generated at the peaks of these slow waves.

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26
Q

What are slow waves? Do they result in muscle contraction or action potentials?

A

slow waves - These are slow undulating changes in the resting membrane potential. There is no action potentials/no muscle contractions

27
Q

What are spike potentials?

A

These action potentials are produced when threshold is reached during the plateau phase of the slow wave, triggering phasic contractions. In GI muscle, the action potentials last 10-40 times longer than the nerve action potential, and are produced largely by Ca2+ entry through L-type VSCCs (plus some Na+ influx). Thus, disordered GI motility may be a side effect of treating cardiovascular disease with L-type VSCC blockers.

28
Q

What are excitatory motor neurons in the ENS?

A

ACh and Substance P are excitatory motor neurons.

29
Q

What are inhibitory motor neurons in the ENS?

A

VIP (vasoactive intestinal peptide) inhibitory motor neurons

30
Q

How do the slow waves cause the circular muscles of the GI tract to contract?

A

Gap junctions connect the ICCs to the circular muscle. Ionic current flows across the gap junctions to depolarize the membrane potential of the circular muscles to threshold for the discharge of action potentials.

31
Q

How are slow wave motor patterns influenced?

A

By hormones, paracrine factors, the ANS and drugs.

32
Q

Where is slow wave frequency highest? Where is it lowest?

A

Slow wave frequency is highest in the small intestine, intermediate in the colon and lowest in the stomach (e.g., up to ~12/min in small intestine during extreme activation vs ~3/min in stomach).

33
Q

What is true about the maximal contractile frequency when compared to slow waves? What is responsible for slow wave production?

A

The maximal contractile frequency in the muscle does not exceed the frequency of slow waves. However, it may be less if the slow wave does not produce a spike/action potential. Neural and hormonal input modulate the production of action potentials and thus the strength of muscle contractions. ICCs are responsible for the frequency of slow waves.

34
Q

What effect does stretch, ACh, and PNS have on slow waves? What about Norepinephrine and SNS?

A

They depolarize leading to spikes. They hyperpolarize decreasing the chance of a spike.

35
Q

What controls peristalsis and segmentation?

A

Motility in the small intestine is primarily under local control of the myenteric plexus and consists of both peristalsis and segmentation. Segmentation forms pockets of chyme and serves to mix and propel the chyme, although normally peristalsis creates aboral movement (away from mouth).

36
Q

When can peristaltic rushes occur?

A

Irritation of the intestinal mucosa by infectious agents, for example, causes a peristaltic rush/diarrhea that serves to clear the intestine of the irritant.

37
Q

What is the myenteric reflex? Explain it in terms of contraction of smooth circular muscle:

A

It is peristalsis, or also called “the law of the gut.” A contractile ring forms on the orad side of the distended segment moving towards the distended segment and pushing contents towards the anus. Receptive relaxation occurs downstream and aids this unidirectional movement.

38
Q

Describe the pattern of contraction in the circular muscle layer and the longitudinal muscle during peristalsis:

A

The circular muscle layer behind the bolus contracts, whereas the longitudinal layer relaxes, resulting in a propulsive segment, which propels the bolus into the receiving segment. The simultaneous shortening of the longitudinal layer and relaxation of the circular layer results in expansion of the lumen, which prepares the receiving segment for the bolus.

39
Q

How is local control of motility achieved?

A

In response to the presence of chyme in the lumen of the small intestine, mechanoreceptors and chemoreceptors transduce signals to ascending and descending neurons. The ascending pathway leads to excitatory motor neurons (ACh, substance P) behind the bolus of chyme, stimulating depolarization of the slow waves, generation of an action potential, and contraction. At the same time, the descending pathway ends in inhibitory motor neurons (VIP, NO), which hyperpolarize the slow waves in the muscle, causing relaxation in front of the bolus. The overall result is a peristaltic contraction, moving the bolus toward the anus.

40
Q

What is physiological ileus?

A

It is the absence of motility in the small & large intestine. It is the output of a specific motor program stored in the ENS. It is a normal state and remains in effect for varying periods of time in different intestinal regions. A subset of inhibitory neurons are active and suppress the response of the circular muscle to the electrical slow waves.

41
Q

What is pathological ileus (paralytic ileus)?

A

It is a state when the normal periods of quiescence are much longer. In this case, the inhibitory neurons are abnormally active and continuously suppress myogenic activity. Passage of stool and gas are impaired, and individuals experience cramping pain, nausea and vomiting. As examples, altered motility and delayed transit is common after abdominal surgery (postoperative ileus), anticholinergic or opiate drug treatment.

42
Q

What is contractile activity in the GI tract like during fasting or interdigestive state?

A

It is characterized by long periods of quiescence in conjunction with short rhythmic waves of strong propulsive contractions that pass down the distal stomach and small intestine. The contractions are known as the Migrating Motor Complex.

43
Q

What does the Migrating motor complex function to do?

A

Functions to ‘sweep’ the stomach and small intestine of residue including undigested food/fiber, bacteria (may prevent overgrowth), desquamated cells. Note during this phase, the pyloric sphincter is inhibited and particles larger than 2 mm can pass into the duodenum.

44
Q

When does the migrating motor complex occur?

A

About 3 hours after a meal, and at cyclic intervals of 90 minutes.

45
Q

What causes the migrating motor complex to occur?

A

Motilin, synthesized in the duodenal Mo cells, is released into the circulation and stimulates the contractions (5-10 min) seen during the active phase. Motilin acts through the ENS and ANS to stimulate contractions.

46
Q

What happens in the absence of the MMC? Why?

A

In the absence of the migrating motor complex, indigestible material called “bezoars” accumulate and can obstruct the lumen of the stomach in particular. The pyloric sphincter typically maintains a strong tone preventing food larger than 2mm from leaving the stomach.

47
Q

When are the involuntary events of swallowing initiated?

A

When food enters the pharynx.

48
Q

What is the pharyngeal phase of swallowing?

A

Food in the pharynx activates sensory neurons that project via the vagus and glossopharyngeal
nerves to the swallowing center in the medulla. Efferent impulses are sent back to the pharynx, esophagus, esophageal sphincters and stomach
causing: the soft palate to pull upward preventing food reflux into the nasopharynx, movement of epiglottis and pharynx to prevent food from entering trachea, and relaxation of the UES.

49
Q

What is the esophageal phase of swallowing?

A

The swallowing reflex also initiates a primary peristaltic wave that propels food through the open UES, followed by closure of the UES, and continued peristalsis that traverses the length of the esophagus, terminating in opening of the LES, and receptive relaxation of the stomach. If the primary wave fails to move all food into the stomach, a secondary peristaltic wave results from distension of the esophagus.

50
Q

Disorders of swallowing resulting in partial or total paralysis of the swallowing mechanisms can occur with damage to what structures?

A

Damage to CN V, IX, or X; patients under deep anesthesia; paralysis of swallowing muscles as in muscular dystrophy and myasthenia gravis;

51
Q

What is receptive relaxation?

A

Receptive relaxation in the lower esophageal sphincter and fundus is primarily regulated by a vagovagal reflex after swallowing. The transmitter released by the postganglionic vagal fibers is vasoactive intestinal polypeptide (VIP).

52
Q

What results from receptive relaxation in the stomach?

A

In the stomach, receptive relaxation results in an increase in intragastric volume but not intragastric pressure.

53
Q

What is accommodation in the stomach?

A

As food accumulates in the stomach there is a gradual relaxation of the entire stomach, called accommodation, which allows storage of food without an increase in intragastric pressure. This process is also mediated by a vagovagal reflex

54
Q

How is gastric emptying effected by the contents of the meal? How is it regulated?

A

It is slower after ingestion of a high-fat meal, and rapid after ingestion of liquid saline. Receptors in the small intestine sense the contents of the chyme and regulate emptying to optimize absorption.

55
Q

What happens to gastric accommodation after a vagotomy?

A

Accommodation is reduced because the vagovagal response is needed.

56
Q

What is achalasia?

A

Achalasia is the failure of the LES to relax during swalling.

57
Q

What causes GERD?

A

When LES tone is not properly maintained. LES resting tone is typically high.

58
Q

How is the stomach divided functionally?

A

It is divided into a proximal gastric reservoir (fundus and 1/3 of body) and distal antral pump (caudal 2/3 of body, antrum, pyloris)

59
Q

What is the gastric reservoir important for?

A

Muscles in the gastric reservoir portions of the stomach are adapted for maintaining continuous contractile tone. They do not contract phasically. This area functions to accommodate arrival of a meal without a significant increase in intragastric pressure. A second function is to maintain constant compressive forces on the contents of the reservoir which push the contents into the antral pump region

60
Q

What is the antral pump important for?

A

Muscles of the antral pump contract phasically, which propels chyme towards the gastroduodenal junction. These are strong propulsive waves that are generated at a frequency of ~3/min (set by the ICC pacemaker potential). Propulsive and retropulsive forces serve to grind/triturate the stomach contents, reducing the particle size.

61
Q

What is propulsion in the stomach?

A

Movement of solid particles toward the antrum involves interaction of propulsive gastric contractions and occlusion of the pylorus, termed propulsion

62
Q

What is grinding in the stomach?

A

Once a bolus of material is trapped near the antrum, it is churned to help reduce the size of the particles, called grinding

63
Q

What is retropulsion in the stomach?

A

Only a small portion of gastric material-that containing particles smaller than ~2 mm-is propelled through the pylorus to the duodenum. Thus, most gastric contents are returned to the body of the stomach for pulverization and shearing of solid particles, a process known as retropulsion

64
Q

What happens to particles larger than 2mm after propulsion, grinding, and retropulsion has occurred?

A

Particles larger than 2 mm are initially retained in the stomach but are eventually emptied into the duodenum by MMCs during the interdigestive period.