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GIGU Exam 1 > Lecture 5: Motility of GI System > Flashcards

Lecture 5: Motility of GI System Flashcards

1
Q

What does motility involve?

A

Contraction and relaxation of the walls and sphincters of the GI tract

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2
Q

What are the layers of the GI tract, inside to outside?

A

1. Mucosa Layer

  • Epithelium
  • Lamina propria (connective tissue)
  • Muscularis mucosae (Changes shape & SA of epithelium)

2. Submucosa Layer

  • Submucosal/Meissner Plexus——

3. Muscular Layer

  • Circular Muscle
  • Myenteric Plexus
  • Longitudinal Muscle

4. Serosa

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3
Q

What is the muscularis mucosae?

A

Smooth muscle that controls the shape and surface area of the epithelium

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4
Q

What occurs with contraction of the circular muscle

A

contraction decreases the diameter of segment

circular = contracts

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5
Q

During contractions, what does the longitudinal muscle do?

A

Lengthen segment

longitudinal = lengthen

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6
Q

Describe slow waves.

A

Depolarization and repolarization of the membrane potential to allow action potentials to occur more easily.

When membrane potential crosses threshold, AP can occur.

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7
Q

What are phasic contractions?

A

Periodic contractions followed by relaxation

  • Esophagus*
  • Antrum of stomach*
  • SI*
  • GI tissues involved in mixing and propulsion*
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8
Q

Which organs utilize phasic contractions?

A

Esophagus

Antrum of stomach

Small intestine

Tissues involved in mixing and propulsion

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9
Q

What are tonic contractions?

A

Constant level of contraction w/o regular periods of relaxation

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10
Q

Which organs utilize tonic contractions?

A

Orad of stomach

Lower esophagus

Ileocecal junction

Internal anal sphincters

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11
Q

What NT increases the amplitude of slow waves and action potential?

A

Acetylcholine

Think parasympathetic = rest & digest. AcH is NT released by postsynaptic neuron in PNS

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12
Q

What NT decreases the amplitude of slow waves and action potential?

A

Norepinephrine

Think sympathetic = fight or flight = don’t want to be pooping. NE is NT released by postsynaptic neuron in Sympathetic system

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13
Q

What is the Enteric NS

A

Branch of ANS that consists of the Submucosal plexus (Meissner’s) & Myenteric plexus (Auerbach’s) that control the GI system

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14
Q

What does the Submucosal plexus control

A

GI secretions and local blood flow. Senses the lumen environment.

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15
Q

What does the Myenteric (Auerbach’s) Plexus control?

A

GI movement. Relaxation and contraction of the intestinal wall.

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16
Q

What cells are considered the pacemaker cells of the GI system - generate and propagate slow waves?

A

Interstitial cells of Cajal (ICC)

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17
Q

What is the relationship between interstitial cells of Cahal (ICCs) and GI motility

A

ICCs generate and propagate slow waves to smooth muscles (circular & longitudinal) via gap junctions. If slow waves reache threashold, an AP is generated which leads to contraction of the smooth muscles

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18
Q

What are the swallowing phases & are they voluntary or involuntary?

A

Oral phase - voluntary

Pharyngeal phase - involuntary

Esophageal phase - involuntary

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19
Q

List the steps of the pharyngeal phase

A
  1. Soft palate is pulled upward
  2. Epiglottis moves to cover larynx
  3. UES relaxes
  4. Peristalic wave of contraction is initiiated in pharynx
  5. Food is propelled through open UES
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20
Q

Describe the swallowing reflex

A
  1. Somatosensory receptors detect food in pharynx
  2. Afferent sensory information is sent through the Vagus N. & Glossopharyngeal N.toswallowing center in the medulla.
  3. Swallowing center sends efferent motor info to muscles of pharynx and upper esophagus causing the UES to relax
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21
Q

What is the primary peristalsic wave

A

First part of esophgeal swallowing that is controlled by the medulla (swallowing reflex)

CANNOT OCCUR AFTER VAGOTOMY

22
Q

What causes the LES to relax

A

Nitric Oxide & Vasoactive intestinal peptide (VIP)

23
Q

What is secondary peristalsic wave & what controls it

A

Occurs if primary wave fails to empty the esophagus or if gastric contents reflux into the esophagus. Controlled by ENS & medulla.

CAN OCCUR W/O ORAL & PHARYNGEAL PHASE & EVEN AFTER VAGOTOMY

24
Q

What is achalasia

A

Impaired peristalsis due to incomplete relaxation of LES during swallowing resulting in the back up of food and elevation of LES resting pressure

25
What causes achalasia
- Decreased numbers of ganglion cells in myenteric plexus - Degeneration of inhibitory neurons producing NO/Vasoactive intestinal peptide that produce relaxation - Damage to nerves in the esophagus, preventing it from squeezing food into the stomach
26
What are symptoms of achalasia
Backflow of food in the throat (regurgitation) Difficulty swallowing both liquids and solids (dysphagia) heartburn chest pain
27
What is Gastroesophageal reflux disease (GERD)
Abnormal relaxing/weakening of LES resulting in reflux of stomach contents into the esophagus leading to inflammation
28
What causes GERD
Motor abnormalities that result in abnormally low pressures in the LES.
29
What are symptoms of GERD
Heartburn and acid regurgitation gastrointestinal bleeding irritation of esophageal lining scar tissue in esiphagus Barrett's esophagus
30
What is receptive relaxation
Relaxation of the LES & orad region of stomach in preparation to receive food. Controlled by the vagalvagal reflex
31
What occurs in the orad and caudad region of the stomach
Orad: Receiving food Caudad: Mixing and digestion
32
What substance decreases contractions and increase gastric distensibility
CCK
33
Distinguish segmentation vs persitaltic contractions
Segmentation: mixing not moving Peristaltic: circular and longitudinal muscles work in opposition to complement each other's actions which leads to movement of food.
34
What increases APs & force of gastric contractions
Parasympathetic stimulation gastrin motilin
35
What decreases APs and force of gastric contractions
Sympathetic stimulation secretin GIP
36
What increases the rate of gastric emptying
1. Decreased distensibility of the orad stomach 2. Increased force of peristaltic contractions of the caudad stomach 3. Decreased tone of pylurus (relaxes) 3. Increased diameter and inhibition of segmenting contractions of the proximal duodenum
37
What factors inhibit gastric emptying
1. Relaxation of orad (increase in distensibility) 2. Decreased force of peristaltic contractions 3. ncreased tone of pylroic sphincter 4. Segmentation contractions in intestine 5. Entero-gastric reflex
38
What is entero-gastric reflec
Negative feedback from duodenum that will slow down the rate of gastric emptying
39
What are the mechanisms of the entero-gastric reflex
1. Presence of acid in the duodenum stimultaes secretin release which inhibits stomach motility via gastrin inhibition. 2. Fats in duodenum stimulutae CCK and GIP release which inhibit stomach motility 3. Hypertonicity in the duodenum inhibit gastric emptying
40
What is gastroparesis
Slow emptying of the stomach/paralysis of the stomach in the absecnce of mechanical obstruction
41
What are causes of gastroparesis
Diabetes mellitus (Type 1) Injury to Vagus nerve
42
What are symptoms of gastroparesis
Nausea, vomiting, early feeling of fullness when eating, weight loss, abdominal bloating, abdominal discomfort
43
How are large particles of undigested residue remaining in the stomach emptied? When does it occur?
Migrating myolectric complex/migrating motor complex 90 minute intervaks during fasting (inhibited during feeding)
44
Migrating motor complexes are important for preventing what
Small Intestinal bacteral overgrowth (SIBO)
45
What substances stimulate contraction in the intestine
Serotonin Certain prostaglandins Gatrin, CCK, motilin and insulin
46
What substances inhibit contraction in the intestine
Norepinephrine Secretin Glucagon
47
What is the rectosphincter reflex
As the rectum fills with feces, the smooth muscle wall of the rectum contract and the internal anal sphincter relaxes. Why don't you poop yourself? The external anal sphincter is tonically closed (under voluntary control)
48
How is sensation of rectal distension and voluntary control of the external anal sphinceter mediated
They are mediated by pathways within the spinal cord that leas to the cerebral cortex. Destruction of these pathways causes a loss of voluntary control of defecation
49
What is Hirschsprung disease
Low levels of VIP leads to smooth muscle constriction and loss of coordinates movement in the LI. This causes colon contents to accumulate *colon equivalent of achalasia*
50
What are symptoms of Hirschsprung disease
Failure to pass stool. Poor feeding, vomitting, constipation, swollen belly, malnutrition. **Present at birth**

GIGU Exam 1 (25 decks)

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