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104-theme 1- the alimentary system > motility of the GI tract > Flashcards

motility of the GI tract Flashcards

1
Q

what is the role of the GI tract?

A

to extract chemical energy, vitamins, minerals and water from ingested products

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2
Q

what is the basic four layer structure of the GI tract? 4

A
  • mucosa (epithelium, lamina propria, muscularis mucosae)
  • submucosa ( artery, vein, submucosal nerve plexus)
  • muscularis externa (circular muscle, myenteric nerve plexus, longitudinal muscle)
  • serosa
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3
Q

what are the functions of the:

oesophagus 1
stomach 4
small intestine 4
large intestine 3

A

Oesophagus:

  • Transport

Stomach:

  • Storage
  • Secretion
  • Mixing
  • Digestion

Small intestine:

  • Secretion
  • Mixing
  • Majority of digestion
  • Absorption

Large intestine:

  • Limited absorption
  • Faeces formation
  • Gut microbiota
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4
Q

what is motility governed by? 4

A
  • involuntary contraction of smooth muscle with pacemaker interstitial cells of Cajal (ICC)
  • except upper oesophagus and external anal sphincter (striated skeletal muscle/ voluntary)
  • smooth muscle is a single unit- gap junctions allow electrical coupling and contraction as a functional syncytium
  • smooth muscle is organised into connected bundles of outer longitudinal and inner circular smooth muscle in the muscularis layer
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5
Q

how does motility occur? 4

A
  • autonomously with external regulation
  • the intrinsic nervous system (ENS) controls GI motility and secretion independently
  • there are 2 interconnected plexuses in the gut wall, myenteric plexus and submucosal plexus
  • extrinsic autonomic sympathetic and parasympathetic innervation allows central modification
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6
Q

what is the intrinsic enteric nervous system? 3

A
  • reflex contraction in response to local stimuli (stretch, nutrients, irritation, hormones)
  • myenteric plexus (Auerbach’s) in muscularis layer for motility
  • submucosal plexus (Meissner’s) in submucosal layer for secretion and local blood flow
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7
Q

what is the extrinsic autonomic nervous system (ANS)? 3

A
  • ANS modifies basal activity of the ENS
  • parasympathetic innervation= excitatory to motility and secretion (via vagus and pelvic splanchnic nerves)
  • sympathetic innervation= inhibitory to motility and secretion (via thoraco-lumbar innervation)
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8
Q

how can hormonal secretion affect GI motility?

name 2 hormones?

A
  • endocrine hormones are secreted by the entero-endocrine cells in the epithelial layer of the GI mucosa and enter the portal blood circulation
  • cholecystokinin (CCK)
  • motilin
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9
Q

cholecystokinin (CCK)

  • stimulus for secretion 3
  • site of secretion
  • actions 3
A
  • protein
  • fat
  • acid

-I cells of the small intestine

  • stimulates pancreatic secretions
  • gallbladder contraction and growth of exocrine pancreas
  • inhibits gastric emptying
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10
Q

motilin

  • stimulus for secretion 3
  • site of secretion
  • actions 2
A
  • fat
  • acid
  • nerve

-M cells of the duodenum and jejunum

  • stimulate gastric motility
  • stimulates intestinal motility
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11
Q

what mechanisms can cause contraction in the GI tract? 4

A
  • Like all excitable cells, smooth muscle cells have a fluctuating negative electrical potential difference across the membrane
  • Results in two types of electrical activity:
  • Slow waves= cyclical oscillations of membrane potential spontaneously initiated by pacemaker ICCs
  • Spike potentials= generated once threshold is reached resulting in Ca2+ influx and smooth muscle contraction
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12
Q

describe the stimulation of smooth muscle contraction in the GI tract? 4

A
  • Slow waves provide a basic electrical rhythm
  • Spike potential causes contraction by further depolarisation to threshold levels
  • Depolarisation stimulated by stretch, hormones, excitatory neurotransmitter acetylcholine release from the ENS excitatory motor neurons or P/S
  • Inhibition by hyperpolarisation caused by inhibitory ENS, sympathetic NT norepinephrine or hormones
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13
Q

what are the two types of contraction that occur in the GI tract?

A
  • segmentation for mixing

- peristalsis for propulsion

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14
Q

describe segmentation for mixing? 2

A
  • bursts of circular muscle contraction and relaxation

- back and forth pendular movements also occur

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15
Q

describe peristalsis for propulsion? 4

A
  • Local distention triggers contraction behind bolus and relaxation in front
  • Wave of contraction
  • Requires functional myenteric plexus
  • Law of intestines= movement aborally
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16
Q

describe an end innervation dysfunction? 3

A
  • Hirschsprung’s disease:
  • A rare congenital absence of the myenteric plexus, usually involving a portion of the distal colon
  • The pathological aganglionic section of colon lacks peristalsis and undergoes continuous spasm, leading to functional obstruction and sever constipation
17
Q

what are the three stages of swallowing? 3

A
  • oral
  • pharyngeal
  • oesophageal
18
Q

describe the oral stage of swallowing? 4

A
  • Under voluntary control
  • Tongue pushes up against hard palate and contracts to force lubricated bolus into the pharynx
  • The pharynx consists of the oropharynx, nasopharynx and laryngopharynx
  • Bolus enters the oropharynx initiating the pharyngeal stage through stimulation of sensory receptors
19
Q

describe the pharyngeal phase of swallowing? 7

A
  • Swallowing centre in the medulla oblongata and pons in the brain stem (reflex)
  • Motor efferents in trigeminal, glossopharyngeal and vagal nerves cause series of muscle contractions moving bolus through oropharynx into laryngopharynx and into oesophagus
  • Soft palate elevates over posterior nares to close nasal pharynx
  • Epiglottis closes larynx
  • Respiration is inhibited
  • Upper oesophageal sphincter relaxes
  • Pharyngeal muscle contraction propels bolus into oesophagus
20
Q

describe the oesophageal phase of swallowing? 6

A
  • Primary peristalsis moves bolus downwards
  • Circular muscle contracts behind bolus, longitudinal muscle contracts in front to shorten fibres and push wall outward
  • Mucus lubricates and reduces friction
  • Relaxation of lower oesophagus and lower oesophageal sphincter (LOW) occurs
  • Secondary peristalsis stimulated by stretch
  • Coordination is via intrinsic myenteric and extrinsic vagal innervation
21
Q

name some oesophageal motility dysfunctions? 2

A
  • achalasia

- gastro-oesophageal reflux

22
Q

describe achalasia? 3

A
  • LOS fails to relax causing food to remain in the oesophagus
  • Cause may be vagal or myenteric defect
  • Distension, inflammation, infection, ulceration
23
Q

describe gastro-oesophageal reflux? 3

A
  • LOS tone lost leading to flow of acidic gastric contents into oesophagus
  • Inflammation, ulceration
  • May be linked to hiatus hernia where portion of stomach protrudes through diaphragm into thorax causing gastric reflux
24
Q

what are the 3 primary motor functions of the stomach?

A
  • Storage= the vasovagal reflex mediates receptive relaxation reducing muscle tone and allowing reservoir function
  • Mixing= fragmentation of food and mixing with secreted gastric juice for digestion
  • Emptying contents into the duodenum at a controlled rate
25
Q

how does the mixing stage of the stomach happen? 3

A
  • slow peristaltic wave are initiated in the body of the stomach moving stomach contents towards the pyloric antrum
  • food is forced back for further mixing and digestion
  • this process of propulsion and retropropulsion occurs in cycles to produce chyme
26
Q

describe the emptying stage of the stomach? 2

describe the regulation of this? 2

A
  • highly regulated with primary inhibitory feedback signals from the small intestine
  • more powerful peristaltic contractions build to force chyme into the duodenum
  • excitatory= ENS/ANS neuronal stimulation and hormones (motilin)
  • inhibitory= ANS regulation, duodenal enterogastric reflexes and hormones (CCK, secretin)
27
Q

how can we slow gastric emptying? 2

why do we do this?

A
  • ANS/ENS reduction
  • hormonal reduction
  • to slow the presence of chyme in the duodenum and give enough time for digestion to occur
28
Q

name 2 gastric motility dysfunctions?

A
  • dumping syndrome

- gastroparesis

29
Q

describe dumping syndrome? 4

A
  • Rapid emptying of gastric contents into the small intestine
  • Occurs following ingestion of a large meal after gastrectomy
  • Characterised by nausea, pallor, sweating, cramps, vertigo and sometimes fainting within minutes
  • May be cause by hypertonic duodenal contents causing rapid entrance of fluid
30
Q

describe gastroparesis? 5

A
  • Stomach fails to empty
  • Prevents proper digestion
  • Causes bloating and nausea
  • May be cause by gastric cancer or peptic ulcers
  • Occasionally observed through impaired vagal stimulation to the stomach in severely diabetic patients who develop autonomic neuropathy
31
Q

describe motility in the small intestine? 3

A
  • Motility patterns allow the majority of digestion and absorption of nutrients here over 3-5 hours
  • Large surface area for absorption provided by circular folds (plicae circulares), villi projections of the mucosa and ‘brush border’ microvilli on the epithelial cell apical surface
  • Two types of motility= mixing and circulation for maximum exposure to absorptive epithelium, propulsion of chyme aborally
32
Q

how is motility in the small intestine controlled? 4

A
  • Motility controlled by intrinsic motor patterns modified by hormonal and ANS neural stimuli
  • Segmentation for mixing= stretch receptors trigger myenteric stimulation of muscle contraction
  • No net movement
  • Propulsive peristalsis= stretch, hormones= excitation= gastrin, CCK, insulin, motilin, serotonin, inhibition=secretin and glucagon
33
Q

describe propulsive peristaltic reflexes? 6

A
  • Gastroenteric reflex= gastric distention activates myenteric plexus to promote SI peristalsis
  • Gastroileal reflex= gastric distention promotes peristalsis in the ileum to force chyme through ileocaecal valve into the caecum
  • Migrating motor complex (MMC):
  • Series of peristaltic contractions, between meals, every 90 mins sweeps contents into colon
  • Intrinsic enteric control, hormone motilin
  • Absence can lead to bacterial overgrowth
34
Q

describe disruption to peristalsis in the small intestine? 3

A
  • Peristaltic rusk= mucosal irritation, ENS and ANS neural reflexes rapidly sweep contents of SI into colon
  • Paralytic ileus= loss of peristalsis following mechanical trauma
  • Vomiting= reverse peristalsis initiated in distal small intestine to expel intestinal and gastric contents
35
Q

describe motility in the small intestine? 3

A
  • Motility is more sluggish to allow optimal absorption of water and electrolytes (proximal), formation and storage of faeces (distal)
  • commensal microbiome aids, digestion, synthesises B and K vitamins
  • Longitudinal muscle in muscularis thickened to form three bands, taniae coli, which tonically contract to form haustral bulges
36
Q

how is motility in the small intestine controlled? 5

A
  • Via mixing and propulsion under intrinsic enteric control modified by neural and hormonal stimuli
  • Mixing contractions via haustral churning
  • Peristalsis:
  • Mass movements occur 2-3x a day= forceful peristaltic contractions force contents into sigmoid colon and rectum
  • Gastro-colic and duodeno-colic reflexes= mass movements occur after meals on stretching via ANS
37
Q

describe the defecation reflex? 5

A
  • Initiate’s defecation to expel faeces containing residues of digestion, bacteria, bile pigment, mucosal debris
  • Mass movements push faecal matter into normally empty rectum
  • Stretch receptors in are stimulated and activate the ENS and parasympathetic ANS
  • Involuntary contraction of longitudinal muscle in the rectum opens the internal anal sphincter
  • the constricted external anal sphincter is voluntarily relaxed to allow defecation

104-theme 1- the alimentary system (17 decks)

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