Motility of GI Tract Flashcards

1
Q

Where is the submucosal plexus located?

A

Between the circular muscle and the submucosa

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2
Q

What is the function of the circular and longitudinal muscles?

A
  • Circular muscle contraction decreases the diameter of the tube
  • Longitudinal muslce contraction decreases the length of the tube
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3
Q

What do slow waves do within GI tract?

A
  • Slow waves are depolarization and repolarization of the membrane and it doesn’t always end up in an AP
  • They set the frequency of depolarization
  • Appearance of an AP determines if there will be a contraction
  • Slow waves aren’t APs!
  • Neural activity and hormonal activity modulate APs and strength of contraction
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4
Q

What are phasic contractions?

A
  • Periodic contractions followed by relaxation for the mixing and propulsion of food through the GI tract
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5
Q

What are tonic contractions?

A
  • Sustained contractions without regular periods of relaxation, seen in sphincters
    • These only need to be opened at certain times, so there is constant contraction closing the valve until something needs to pass
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6
Q

How do slow waves AP and contractions relate in the smooth muscle?

A
  • The greater number of AP’s on top of slow waves results in a larger contraction
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7
Q

How does Ach affect slow waves?

A

It increasese the amplitude of slow waves and the number of AP’s

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8
Q

How does NE affect slow waves?

A

Decreases amplitude of slwo waves

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9
Q

What three things cause increase in amplitude of slow waves?

A
  • Stretch
  • Ach
  • Parasympathetics
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10
Q

What two things cause hyperpolarization decreasing amplitude of slow waves?

A
  • Sympathetics
  • NE
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11
Q

What does the submucosal (Meissner’s) plexus control?

A

GI secretions and local blood flow

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12
Q

What does the myenteric (Auerbach’s) plexus control?

A

GI movements

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13
Q

What are Interstitial cells of Cajal?

A
  • Pacemaker for GI smooth muscle
  • They generate and propagate slow waves, and these occur spontaneously and spread via gap jxn
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14
Q

Describe how swallowing works.

A
  1. Oral phase is voluntary and initates the swallowing process
  2. Pharyngeal phase is involuntary. The soft palate is pulled up moving the epiglottis relaxing the upper esophageal sphincter, peristaltic waves are initiated in the pharynx and food is propelled through the sphincter
  3. Esophageal phase is involuntary and is controlled by swallowing reflex and ENS
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15
Q

What controls the involuntary swallowing reflex?

A

Medulla:

  • the food moves in the pharynx and afferent sensory input occurs via CN9 and 10 to the swallowing center in the medulla, which sends info to the brainstem nuclei giving efferent input to the pharynx
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16
Q

What are the two types of peristaltic waves? (describe them)

A
  1. Primary: continuation of pharyngeal peristalsis controlled by the medulla.
    1. cant occur with a vagotomy
  2. Seconday: only occcurs if primary wave fails to empty the esophagus or if gastric contents reflux into esophagus. The medulla and ENS help. This can occur in absence of oral and pharyngeal phases and can occur after a vagotomy
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17
Q

40 min slide 204

A

m

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18
Q

What are two challenges of the intrathoracic esophagus and how are they solved?

A
  • Keeping air out of the esophagus at the upper end and keeping acidic gastric contents out of lower end
  • UES and LES are closed except when food is passing
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19
Q

How does achalasia affect the esophagus, what causes it, what can it result in clinically?

A
  • It impairs peristalsis, the LES relaxation during swallowing is incomplete resulting in a backup of food and increase in LES resting pressure
  • Decreased numbers of ganglion cells in myenteric plexus and degeneration involves neurons producing NO/VIP. This results in damage to nerves in esophagus preventing it from passing food into stomach
  • Results in regurgitation dysphagia, heart burn and chest pain
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20
Q

What is GERD, what causes it, what happens in GERD, what are the complications?

A
  • Changes the barrier btw the esophagus and stomach because the LES relaxes abnormally or is weak.
  • Occurs due to motor abnormalities that result in low pressures in the LES seen if the intragastric pressure increases
  • Constant reflux and inflammation leads to GERD resulting in:
    • acid, pepsin and bile flowing back up esophagus
    • heartburn and acid regurgitation
  • Complications:
    • GI bleeding, Irritation of esophagus lining, scar tissue, Barrett’s esophagus
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21
Q

43 yr old male with htn and 5 yr history of dyshpagia. Food and occasionally liquids get stuck at upper sternum with every meal. He can get food down with repeated swallowss or drinking water. He has spontaneous regurgitation of clear foamy liquid and undigested food in his mouth especially when bending over. He has lost 8 lbs. He denies heartburn or odynophagia and admits he can’t belch. PMH is unremarkable other than 20 PPY. What is going on? What test would be helpful?

A
  • Achalasia, the lower esophageal sphincter is not opening properly. The food never reaches the stomach which is why he has undigested food regurgitation. There is nerve damage to fibers that produce VIP and NO which cause vasodilation and the nerurons that release Ach are spared.
  • Barium swalllow and esophgeal motility study would be helpful
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22
Q

Describe receptive relaxation in the orad region of stomach.

A
  • Decrease in pressure of the stomach and increase in volume of the orad region mediated vagovagal reflex
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23
Q

How does CCK affect the stomach?

A

It decreases contraction and increases gastric distensibilty

24
Q

Describe contractions of the stomach.

A
  • Little contraction occurs in the orad
  • Peristaltic contraction is the primary contraction type and it starts in the mid stomach and increases in force and velocity as they move towards the pylorus
  • As the velocity and force increases it pushes the bolus against the closed sphincter resulting in retropulsion
25
Q

How are gastric contractions regulated?

A
  • Parasympathetic stimulation, gastrin and motilin increase the AP and force of contractions
  • Sympathetic stimulation through secretin and GIP decreases AP and force of contractions
26
Q

What causes the rate of gastric emptying to increase?

A
  • Decreased distensibility of orad
  • Increase in the force of peristaltic contractions of the caudad stomach
  • decrease tone of pylorus
  • Increase in diameter and inhibition of segmenting contractions of prox duodenum
27
Q

What inhibitis gastric emptying?

A
  • Relaxation of orad increasing distensibility
  • Decrease peristaltic contractions
  • Increase tone of the pyloric spihincter
  • Segmentation contractions in the intestine
  • Entero-gastric reflex: negative feedback from duodenum slowing down gastric emptying
28
Q

How long does gastric emptying take?

A

~3 hours

29
Q

What is the enterogastric reflex?

A
  • NFB from duodenum to slow down the rate of gastric emptying
    • Acid in the duodenum stimulates secretin which inhibits stomach motility via gastrin inhibition
    • Fats in the duodenum stimulate CCK and GIP which inhibit stomach mobility
    • Hypertonicity in the duodenum inhibits emptying
30
Q

What stimulates the release of CCK

A

Fats in duodenum

31
Q

What stimulates Secretin release?

A

Acid in the duodenum

32
Q

Desccribe symptoms causes and treatement for slow gastric emptying.

A
  • Fullness, loss appetite, N/V
  • Gastric ulcer scar tissue, cancer, eating disorders, vagotomy
  • Pyloroplasty, balloon dilation
33
Q

What is Gastroparesis?

A
  • Slow emptying of stomach/paralysis of stomach in absense of mechanical obstruction
  • can be caused by DM- 20% of T1DM patients have this
  • could also be caused by vagus nerve injury
  • Sx:
    • N/V
    • early fullness
    • weight loss
    • bloating and ab discomfort
34
Q

What are MCC’s?

A
  • Periodic bursting peristaltic contractions occuring at 90 min intervals and during fasting. Motilin mediates this and it is inhibited during feeding
  • Purpose is to empty undigested residue and control the numbers of bacteria in the stomach
35
Q

what are segmentation contractions?

A
  • Generatess back and forth movements for mixing of chyme with enzymes and absorption
  • produces no forward propulsive movements along the small intestine
36
Q

What are peristaltic contractions in the SI?

A

Circular and longitudinal muslces work to complement each other moving the chyme from orad to caudad region

  • reciprocal innervation
37
Q

Compare and contrast slow waves in the SI to stomach

A
  • Slow waves are always persent whether there are contractions or not
  • Different from the stomach, slow waves in SI don’t initiate contractions
    • slow wave frequency sets max requency of contractions
38
Q

What initiates the peristaltic reflex in the SI?

A
  • Serotonin released by enterochromaffin cells binding IPAN
39
Q

What is the hormonal control for intestine contractions?

A
  • Serotonin stimulating contractions
  • Prostaglandins can stimulate contractions
  • Gastrin, CCK, motilin and insulin stimulate contractions
  • Secretin and glucagon inhibit
  • Epi inhibits contractions
40
Q

Vomiting reflex?

A
  • Controlled by medulla, nerve impulses travel via vagus and symp afferents
  • Reverse peristalsis in SI
  • Stomach and pylorus relaxes
  • Forced inspiration to increase abdominal pressure
  • Movements of larynx
  • LES relaxation
  • Glottis closes
  • Forced expulsion
41
Q

what occurs to allow flow of contents from ileum to cecum?

A
  • Distension of ileum causes relaxation of sphincter
42
Q

What prevents passage of contents from colon to ileum?

A

Distension of the colon causes contration of the sphincter to prevent backflow

43
Q

What are the muscle layers of the LI?

A
  • Longitudinal muscle contains Taeniae coli- 3 flat bands of longitudinal fibers running from cecum to rectum
  • circular muscle which is continuous from cecum to anal canal
44
Q

What kind of muslce makes up the internal anal sphincter?

A

Smooth

45
Q

What kind of muscle makes up the external anal sphincter?

A

Skeletal

46
Q

What innervates internal anal sphincter

A

Pelvic sphlanic nerve

47
Q

What innervates external anal sphincter?

A

Somatic ns via pudendal

48
Q

What two nerves are part of the PSNS for the large intestine?

A
  • Vagus nerve to cecum, ascending and transverse colon
  • Pelvic nerves from sacral part of spinal cord S2-4 to the descending and sigmoid colon and rectum
49
Q

In the LI, what does the superior mesenteric ganglion supply?

A

Proximal region

50
Q

In the LI, what does the inferior mesenteric ganglion supply?

A

Distal region

51
Q

Ini LI what does the Hypogastric plexus supply?

A

Distal rectum and anal canal

52
Q

In the LI, what happens if there is poor motility?

A
  • Constipation can occur because poor motility results in greater absorption of water and vitamins resulting in hard feces in the transverse colon
53
Q

In the LI, what happens if there is excess motility?

A
  • Less absorption causing diarrhea or looses feces
54
Q

Describe the rectosphincteric reflex

A
  • As the rectum fills with feces the smooth muscle wall contracts and the internal anal sphincter will relax allowing feces to move
  • Under control of ENS and neurons within the spinal cord
55
Q

In general describe the path for sensation of rectal distension and voluntary control of external anal sphincter, what happens if it is damaged?

A
  • Mediated by paths in the spinal cord that ultimately lead to cerebral cotex
  • If this path is damaged there is a loss of voluntary control of defication
56
Q

What is hirschprungs disesase, what causes it and what is treatment?

A
  • absent ganglion cells from parts of the colon resulting in low VIP levels resulting in SM constriction and loss of coordinated movement
  • Colon contents can’t move and accumulate
  • Present at birth causing constipation
    • newborns fail to pass meconium, poor feeding, jaundice,vomiting
    • older kids constipation,swollen belly, malnutrition
  • Treat with surgical resection of colon lacking innervation