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Control of motility and secretion in the upper GI Flashcards

1
Q

Components of the ENS

A 
myenteric plexus (between two external muscle coats)
submucosal plexus (submucosa, small and large intestine only)
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2
Q

Outputs of ENS & ANS

A

muscularis externa
muscularis mucosae
exocrine/endocrine cells

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3
Q

Muscularis externa

A

By myenteric plexus

Controls motility: tonic contraction, rhythmic segmentation, oscillatory movements, peristalsis

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4
Q

Muscularis mucosae

A 
By submucosal plexus
further mixing (movement of the villi)
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5
Q

Role of hormones in GI motility

A

Modulate responses to ICCs and their impact on the intracellular calcium concentration during initiation of a slow wave
Influence resting contractility of muscle in the upper GI

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6
Q

Secretory components of the stomach

A

gastrin (endocrine)
histamine (endocrine)
ACh (ENS)

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7
Q

Enterochromaffin-like cell

A

Modulated by gastrin and ACh of ENS to produce histamine to trigger the release of acid, in addition to their own effects on parietal cells

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8
Q

Enteric intrinsic interneurons

A

influence acid secretion by parietal cells directly
secretion of gastrin through GRP (would also increase acid secretion by parietal cells)
in the cepahlic, gastric, and intestinal phases of stimulation of gastric secretion

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9
Q

Enterogastric reflex

A

certain substances are sensed in the duodenum, then enterogastrones (hormones) are released as a reflex that travels through the celiac ganglions to the effectors in the stomach

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10
Q

Myenteric (Auerbach’s) plexus

A

within muscularis externa, between two layers of muscle
Sensory: receptors in gut wall that senses mechanical, chemical or thermal stimuli, then relates signal to interneurons within ganglia

Interneurons receive from sensory then transmits to motor neurons, which innervate the smooth muscle, exocrine and endocrine/parietal cells

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11
Q

Submucosal (Meissner’s) plexus

A

located in the submucosa
Similar reflex as myenteric (sensory –> motor), except only a small number of innervates the smooth muscle layer (muscularis mucosae)

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12
Q

NTs in longitudinal layers of the muscularis externa

A

Excitatory: ACh
Inhibitory: NO, vasoactive intestinal peptide, purines (ATP, beta-NAD)

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13
Q

NTs in circular layers of the muscularis externa

A

Excitatory: ACh, substance P, serotoninin (5-HT)
Inhibitory: NO, vasoactive intestinal peptide, purines (ATP, beta-NAD)

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14
Q

Submucosal plexus NT

A

Stimulatory: ACh (motility), VIP (glandular/exocrine)
Regulates secretion
Regulates motility of the muscularis mucosae

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15
Q

Co-localization

A

neurons that contain more than one type of NT

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16
Q

Secretomotor neuron

A

neuron that is able to induce a gland to secrete a substance

17
Q

Slow wave

A

Spontaneous rhythmic fluctuations in the RMP intrinsic to the GI tract
1-5 s/oscillation
frequency (region-specific): distal stomach - 3 cycles/min, duodenum - 12 cycles/min
Determine the fq of phasic smooth muscle contractile events

18
Q

Tonic contraction (tone)

A

muscularis externa circular muscle contractions that functionally separate different areas of the GI tract
allows for unidirectional movement

19
Q

Sphincter

A

site of prolonged tonic contraction

ensures unidirectional movement

20
Q

RMP in the GI tract

A

-40 to -80 mV

Determined by: Na and K channels, Na/K ATPase

21
Q

Phases of a slow wave

A

Rising phase: entry of Ca through CaV channels and others, and release from intracellular storage

Repolarization: activation of Ca-dependent K channels, concominant reduction in cytosolic Ca

Plateau: due to inward Ca current and outward K fluxes

22
Q

Spike potentials

A

contraction begins when electrical threshold is reached for opening of CaV channels

In some regions: spike action potentials are also generated, results in larger Ca influxes through CaV –> greater contractions

23
Q

Interstitial Cells of Cajal (ICC)

A

Pacemaker cells
concentrated in myenteric plexus (ICCMY) and muscle (ICCMI)
ICCMY responsible for generating and propagating slow waves (Ca oscillations)

Gap junctions allow for electrical coupling

24
Q

Factors that contribute to Ca influx in GI tract (6)

A
  1. CaV (L-type) - predominant
  2. Store-operated Ca channels (SOCs) - open in response to depletion of intracellular Ca
  3. Stretch-activated Ca channels
  4. NTs and hormones acting on receptors coupled to activation of phospholipase C and release of IP3, resulting in release of intracellular Ca (ACh, substance P)
  5. Receptor-operated Ca channels (ROCC)
  6. Ca ATPases, Na/Ca exchangers: extrude Ca following contractions, also reuptake into intracellular storage
25
Q

Peristaltic reflex arc

A 
Intrinsic/local reflex involving aborally propagated circular muscle contractions behind the bolus, initiated by intraluminal distention coupled to a wave of relaxation (reflex relaxation) in the distal part of the GI tract
NT: 5HT/serotonin secreted by epithelial enteroendocrine cells to stimulate sensory neurons
Rhythmic segmentation (circular)
Oscillatory movements (Longitudinal)
26
Q

Functions of the esophagus

A

Deglutition (movement of food from pharynx to stomach)
prevention of air entry into the stomach/reflux of gastric contents
Eructation (belching)
Vomiting

27
Q

Resting pressure of the pharynx

28
Q

Resting pressure of the esophagus

A

UES: 25-60
Body: approximates intrathoracic pressure (-5 to -15 inspiration, -2 to +5 expiration), flaccid
LES: 10-40

29
Q

Pressure during swallowing

A

Pharynx: >100 (bolus moves from pharynx –> body)
UES: 0-60 reflex relaxation in response to food in pharynx, then closes
Body: 90-100 - high pressure peristaltic movements moves food in 9-10 seconds
LES: 0-40 - bolus moves from high-P body into lower-P stomach (5-10), then closes

30
Q

Pathway in pharyngeal peristalsis

A
  1. Bolus of food –> tactile receptors –> sensory info sent to swallowing centre (brainstem), received by afferent reception neurons. Reflex relaxation of UES occurs.
  2. Afferent info sent to cortex and central pattern generator of the swallowing centre
  3. Efferent info –> coordinated contraction of pharyngeal muscles, peristalsis to propel food into UE
  4. Reflex relaxation of the LES occurs with swallowing or distention of esophagus/stomach. Myenteric cholinergic neurons activate VIP, NO, purine (ATP, beta-NAD)-containing inhibitory neurons to mediate relaxation
31
Q

Pathway in primary peristalsis

A

Continuation of the pharyngeal peristalsis, transverses esophagus in 9-10 seconds
Does not require sensory input from the esophagus

  1. Swallowing centre coordinates the action of efferent vagal somatic nerves firing from the Nucleus Ambiguus –> sequential activation of striated muscles in the esophagus
  2. Vagal PS input from the dorsal motor nucleus of the vagus –> initiates peristaltic wave in smooth muscle; control of the wave progression by myenteric plexus (vagal initiation, intrinsic regulation)
32
Q

Pathway in secondary peristalsis

A

If primary peristalsis is insufficient in clearing the food from the esophagus, distention initiates secondary peristalsis
Similar to primary wave except that it can occur in the absence of pharyngeal swallowing

  1. Local distention in the esophagus sends sensory info to the swallowing centre
  2. Involves extrinsic innervations via the dorsal motor nucleus of vagus for initiation in UE
  3. involves both the vagus and myenteric plexus in the smooth muscle
  4. Clears food remnants and refluexed gastric juice following primary wave
33
Q

Reflex relaxation of the ES’s

A

UES: neurally mediated in response to food bolus in the pharynx
LES: neurally mediated in response to swallowing or distention of the esophagus/stomach, both vagal and efferent fibres and intrinsic neurons are involved. Myenteric cholinergic neurons activate VIP, NO, and/or purine-containing inhibitory neurons

34
Q

Spontaneous transient LES relaxation (TLESR)

A

Occurs 20-30x/day, lasting 10-60 seconds
Pathological conditions: more frequent and prolonged - excessive reflux/extended contact time of gastric contents with the mucosa, can result in heartburn and damage

35
Q

Extrinsic modification of ENS

A
  1. ANS
    - PS motor from brainstem via vagus to the pharynx to first 2/3 of colon
    - sacral spinal cord/pelvic nerves to distal
    - sym motor from thoracic/lumbar SC
    - sensory neurons from ENS –> ANS
  2. Higher CNS brain centres
    - hormonal factors in GI and external senses (smell, sight) - influence ANS
  3. immune system
    - locally acting paracrine factors that can stimulate immune cells (e.g. mast cells) to produce their own factors (i.e. histamine) - can directly influence GI motility and secretion
36
Q

Myenteric plexus innervation

A

esophagus to rectum

37
Q

Submucosal plexus innervation

A

small and large intestines only

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