GI Motility Flashcards

1
Q

How can a fever contribute to diarrhea?

A

A fever increases the body’s metabolism. An increase in metabolism causes the Pacemaker cells of the Interstitial Cells (Cells of Cajal) to speed up the rate of the Slow Waves (Basic Electrical Rhythm) which increases the rate of motility through the GI tract

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2
Q

How do the Vagal Nerves affect motility in the GI tract?

A
  1. Causes Primary Peristalsis propelling a Bolus of food via contraction of muscles behind the Bolus while relaxing muscle around the Bolus
  2. Causes Gastric Accommodation which relaxes the Stomach
  3. Causes Depolarization of GI Interstitial Cells (Cells of Cajal) for Contraction
  4. Relaxation of Taneia Coli in the Lower GI Tract allowing Haustrae (pockets) to be smoothed out and Feces to move forward
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3
Q

Why can you get the urge to defecate soon after eating?

A

Mass Movements fill the Descending Colon and Rectum with Feces activating the Defecation (Rectosphincteric) Reflex:

  1. You begin to eat so food is now present in the Upper GI Tract
  2. Gastrin and the Vagus Nerve cause the relaxation of the Colon’s Taneia Coli meaning the Haustrae (pockets) get smoothed out
  3. Feces is forced forward into the Descending Colon and Rectum
  4. Defecation (Rectosphincteric) Reflex is stimulated giving you the urge to shit and relaxing the Internal Anal Sphincter
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4
Q

What is the Migrating Myoelectric Complex (MMC)?

A

The special type of motility that takes place during the interdigestive state

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5
Q

Describe the process of the Migrating Myoelectric Complex (MMC):

A
  1. “Housekeeping movement” to sweep undigested material and bacteria into the Colon
  2. Starts 3-4 hours after eating in the mid-stomach and goes through the Terminal Ileum
  3. Each cycle has 4 phases and lasts 75-120 mins
  4. Phase 3 lasts 10 mins and is stimulated by Motilin to have a series of contractions to sweep material to the lower GI tract
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6
Q

Where does Motilin come from? What does it stimulate?

A
  1. M cells in the GI Tract
  2. For about 10 mins during Phase 3 of MMC, Motilin stimulates unique rhythmic peristaltic contractions to move undigested materials and bacteria into the Colon
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7
Q

Is Swallowing:

A. Voluntary (Skeletal)
B. Involuntary (Smooth)
C. Both
D. Neither

A

C. Both

Swallowing begins as voluntary with skeletal upper esophagus and Pharynx and becomes involuntary as ENS and AND take over

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8
Q

What is Primary Peristalsis?

A

A PNS action (Vagus Nerve) that propels a Bolus of food via contraction of muscles behind the Bolus while relaxing muscle around the Bolus

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9
Q

What is Secondary Peristalsis?

A

Contractions that happen via the ENS during a situation where you ingest something dry that is stuck in the . Esophagus:

  1. Submucosal Plexus submits mucous
  2. Myenteric Plexus produces contractions
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10
Q

What is the point of the Lower Esophageal Sphincter?

A
  1. Relaxes to allow Bolus of food to enter the Stomach
  2. If Floppy you get GERD
  3. Achalasia is a Smooth Muscle disorder where ENS is absent in the LES and it CANNOT RELAX so food CANNOT ENTER
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11
Q

What is Achalasia? How can it be treated?

A
  1. mooth Muscle disorder where ENS is absent in the LES and it CANNOT RELAX so food CANNOT ENTER
  2. Cut small holes in the LES and Administer Proton Pump Inhibitor
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12
Q

What is Gastric Accommodation?

A

Vagal Nerve (PNS) mediated receptive relaxation of the Stomach

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13
Q

What is the principle of Bariatric Surgery?

A

Reducing the ability of the stomach to accommodate food

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14
Q

List how fast meals digest from fastest to slowest from those mentioned below:

Fat/Lipids (Oleate Meal)
Carbohydrates (Saline Meal)
Proteins (Acid Meal)

A

Fastest to Slowest:

  1. Carbohydrates (Saline Meal)
  2. Proteins (Acid Meal)
  3. Fat/Lipids (Oleate Meal)

Fats/Lipids MAKE YOU FEEL FULL LONGEST

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15
Q

Why do Lipids take so long to digest even though they are metabolized easily?

A

They are not absorbed readily by Enterocytes of the Small Intestine because they are Hydrophobic

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16
Q

What is the Resting Membrane Potential of the GI Tract and what makes it unique?

A

The GI tract’s Resting Membrane Potential is NOT a flat line like it is in other systems. GI’s RMP has SLOW WAVES that are always present and reflect slight variations throughout the tract. Because these slight changes are always present, Slow Waves are referred to as the “BASIC ELECTRONIC RHYTHM”.

NOTE: BER is NOT Action Potential!!!

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17
Q

What causes contractions of the GI tract?

A

Contractions of the GI Tract are caused by ACTION POTENTIALS that SPIKE the PEAKS of the Slow Waves when the interstitial cells (Cells of Cajal) are DEPOLARIZED ABOVE -40mV

NOTE: THE GREATER THE DEPOLARIZATION ABOVE -40mV, THE STRONGER THE CONTRACTIONS

18
Q

Match the the below terms into 2 groups of 4:

Parasympathetic Stimulation
Sympathetic Stimulation

Hyperpolarizes
Depolarizes

Stimulates Action (Spike) Potential
Stops Action (Spike) Potential

Starts GI Contractions
Stops GI Contractions

A

Parasympathetic Stimulations DEPOLARIZES GI cells (Cells of Cajal) which STIMULATES Action (Spike) Potential and STARTS GI Contractions.

Sympathetic Stimulations HYPERPOLARIZE GI cells (Cells of Cajal) STOPPING Action (Spike) Potential and STOPPING GI Contractions.

19
Q

What sets the Maximal Possible Rate of Propulsion through the GI Tract?

A

The Basic Electrical Rhythm AKA the “Slow Waves” set the Maximal Possible Rate of Propulsion through the GI Tract

20
Q

Where is the only place that Slow Waves cause SOME contraction?

A

Stomach, normally Slow Waves cause NO Contraction

21
Q

What is the normal Slow wave rate in the Stomach?

A

3 Waves/min

1 Wave/20 seconds

22
Q

What is the normal Slow wave rate in the Small Intestine?

A

10-12 Waves/min

1 wave/5-6 seconds

23
Q

What sets the speed/pace of the Slow Waves along the GI Tract?

A

Pacemaker Cells in the Interstitial Cells (Cells of Cajal)

24
Q

What result would increasing your metabolism have on the Slow Waves?

A

It would cause the Pacemaker cells of the Interstitial Cells to speed up the rate of the Slow Waves and increase the rate of motility through the GI tract

25
Q

Depolarization leading to an Action (Spike) Potential in Interstitial Cells (Cells of Cajal) causes what to occur?

A

CONTRACTION OF SMOOTH MUSCLE

Increase in the Influx of Ca into Smooth Muscle cells which binds to Calmodulin, forming cross bridges and causing contraction

26
Q

What can cause Depolarization of Interstitial Cells ultimately leading to an Action (Spike) Potential and GI Contractions?

A
  1. Stretch (acting on ENS)
  2. Gastrin
  3. Vagal Nerve Stimulation (PNS)
  4. Serotonin
27
Q

What can cause Hyperpolarization of Interstitial Cells ultimately stopping an Action (Spike) Potential and stopping GI Contractions?

A
  1. Norepinephrine
  2. Sympathetic Nervous System
  3. Nitric Oxide
28
Q

What are the types of Motility in the Small Intestine?

A
  1. Peristalsis

2. Segmentation (MORE COMMON)

29
Q

How does Peristalsis function?

A

Vagal Control (Extrinsic to GI) leads to:

  1. Chyme is present in the intestine
  2. Circular Muscle that is Proximal to the Chyme (behind it) becomes DEPOLARIZED and CONTRACTS
  3. Circular Muscle that is Distal to the Chyme (ahead of it) becomes HYPERPOLARIZED and RELAXES
  4. Chyme moves Distal (ahead) down the GI Tract
30
Q

How does Segmentation function?

A

ENS Control (Intrinsic to GI) leads to:

  1. Chyme is present in the Intestine
  2. Circular Muscle on either side of the Chyme is contracted forming “Pockets”
  3. Results in Mixing and Propulsion
31
Q

What type of Motility in the Small Intestine is most common?

A

Segmentation

32
Q

What hormone is instrumental to the emulsification and digestion of fats in the Duodenum?

A

CCK

33
Q

What is the function of CCK in the Small Intestine?

A

works in conjunction with the Vagus Nerve’s anticipatory actions

  1. Stimulates contractions in the Gallbladder to release Bile into the Bile Duct
  2. Relaxes the Sphincter of Oddi allowing Bile to flow from the Bile Duct into the Duodenum
  3. Bile in the Duodenum can now emulsify and “taxi” fats to the Enterocytes for absorption
34
Q

What are the types of Motility in the Colon?

A
  1. Segmental Propulsion (SLOW and COMMON)

2. Mass Movements

35
Q

What is the major type of Motility in the Colon? How does it work?

A

Segmental Propulsion:

The Taneia Coli (3 Longitudinal Bands that run through the Colon) contract to make sacs called HAUSTRAE where Chyme is STORED and DEHYDRATED to make Feces

36
Q

What are Mass Movements?

A

Peristaltic Contractions giving you the urge to SHIT that are stimulated by GI hormones (GASTRIN) and the Vagus Nerve WHEN YOU START EATING and Chyme is present in upper GI Tract!

37
Q

What is the process of Mass Movement?

A
  1. You begin to eat so food is now present in the Upper GI Tract
  2. Gastrin and the Vagus Nerve cause the relaxation of the Colon’s Taneia Coli meaning the Haustrae (pockets) get smoothed out
  3. Feces is forced forward into the Descending Colon and Rectum
  4. Defecation (Rectosphincteric) Reflex is stimulated giving you the urge to shit and relaxing the Internal Anal Sphincter
38
Q

What are the two important Reflexes we NEED TO KNOW?

A
  1. Defecation (Rectosphincteric) Reflex- urge to defecate and relaxation of the Internal Anal Sphincter
  2. Gastrocolic Reflex- food in the stomach stimulates Colonic Mass Movements (really active in babies)
39
Q

What is the cause of Runner’s Shits?

A
  1. Blood flow is relaxed from the GI tract and flows towards muscles so the Taneia Coli relax and the Haustrae are smoothed out
  2. Pressures are created by the body movement so Feces moves towards the Descending Colon and Rectum STIMULATING the DEFECATION (RECTOSPHINCTERIC) REFLEX
40
Q

Constipation does what?

A

Slows GI Motility so Bacteria can act more on the waste and cause inflammation and possibly cancerous polyps

41
Q

What is Hirschsprung’s Disease?

A

Smooth Muscle Disorder of the Lower GI Tract due to LACK of ENS so Internal Anal Sphincter CANNOT RELAX meaning Feces will back up and result in Megacolon

42
Q

How can Hirschsprung’s Disease be treated?

A

Cutting out the part of the Colon that lacks ENS innervation