GI Motility Flashcards
What are the layers of the walls of GI (superficial to deep)? (4)
→ Serosa
→ Muscularis externa
(longitudinal then circular muscle)
→ Submucosa
→ Mucosa
(muscularis mucosa, lamina propria, then mucous membrane)
Where is the Enteric NS found in the layers of GI? (2)
Myenteric plexus
→ in between outer longitudinal and inner circular muscle layers (muscularis externa)
Submucosal plexus
→ in submucosa
What is the structure of smooth muscle? (6)
→ non-striated
→ dense bodies (serving as attachment points for cytoskeletal proteins through cell membrane)
→ intermediate filaments such as desmin (scaffoliding structure)
→ no T-tubules
→ no SR
→ specialised for long-term contraction with limited ATP
Features of unitary smooth muscle
- form a sheet or bundles of tissue
- connected by gap junctions
- contract as single unit
- coordinated contractions
uterus, bladder, GI tract, small blood vessels
Features of multi-unit smooth muscle
- discrete, individual fibres
- stimulated independently
- fine contractions
iris, ciliary body, pilorecetor muscles, large airways, large arteries
What is the Smooth muscle contraction process? (6)
1) Ca2+ enters cell causing increase intracellular [Ca2+]
2) leading to Ca2+ binding to calmodulin (calcium binding messenger protein)
3) Ca2+-calmodulin complexes activate MLCK
4) MLCK phosphorylate myosin heads
- increasing myosin ATPase activity
5) Phosphorylated myosin binds with Actin forming cross-bridges
6) causing actin to slide along myosin
- causing contraction
What is the smooth muscle relaxation process? (4)
1) Calcium pumped out or moves into SR
2) which decreases MLCK activity
3) causing de-phosphorylation of myosin heads via myosin phosphatase
4) no cross-bridges formed, so muscle relaxation
Enteric nervous system on the GI tract
PARASYMPATHETIC
- promotes motility/ secretion
SYMPATHETIC
- inhibits motility/ secretion
- contracts sphincters
MYENTERIC PLEXUS
- controls GI motility
SUBMUSCOSAL PLEXUS
- controls both GI motility and secretion
How is the Enteric NS controlled?
Parasympathetic and sensory will activate submucosal and myenteric plexus
- promoting secretions and motility
Sympathetic will inhibit submucosal myenteric plexus
- inhibiting secretions and motility
How do reflexes control GI motility (5)
Gastroileal reflex
→ stomach activity promotes ileocaecal sphincter openening
Colonileal reflex
→ inhibits ileal emptying when colon stretched
Gastrocolic/dudenocolic reflex
→ food entering stomach or duodenum promotores motility of colon
Enterogastric reflex
→ distended small and large intestines inhibtis stomach motility and secretion
Intestinointestinal reflex
→ overdistention in one part of intestine leads to relaxation in another part
Oral phase of deglutition (swallowing)?
VOLUNTARY
1) food chewed and lubricated with saliva to form a bolus
2) tongue propels it to back of mouth triggering somatosensory recpetors
3) somatosensory receptors send info to medullary swallowing centre to close upper oesophageal sphincter
Pharyngeal phase of deglutition (swallowing)? (4)
INVOLUNTARY
1) food propelled from pharynx to oesophagus
2) soft palate raised to prevent it entering nasopharynx
3) Epiglottis contracts to block larynx to prevent aspiration
4) Upper oesaphageal sphincter opens to allow food to enter
Oesophageal phase of deglutition (swallowing)? (4)
INVOLUNTARY
1) Bolus is propelled from the pharynx into the oesophagus
2) Upper oesophageal sphincter contracts to prevent reflux
3) Primary peristaltic wave propels the food bolus from the oesophagus into the stomach
4) Second peristaltic wave can be initiated to clear food
How does peristalsis occur?
Behind bolus:
→ Longitudinal muscle relaxation by VIP and NO
→ Circular muscle contraction by ACh and substance P
At bolus:
→ Longitudinal muscle contraction by ACh and substance P
→ Circular muscle relaxation by VIP and NO
What causes wave of peristalsis in pharynx and upper third of oesophagus? (2)
→ Striated muscle cells
→ controlled by Glossopharyngeal and Vagus
What causes wave of peristalsis in second and third of oesophagus?
→ Smooth muscles
→ controlled by Myenteric Vagus N
How do muscles contract during peristalsis? (and relax)
Contraction
→ circular muscles contract
→ longitudinal muscles relax
Relaxation
→ circular muscle relax
→ longitudinal muscles contract
What is Hirschsprung’s disease?
- severe constipation is seen in congenital megacolon
- characterised by absence of ENS in distal colon
- no migration of neurones of the myenteric plexus into rectum
Involved segments
- increased tone
- very narrow lumen
- devoid of propulsive activity
Treatment
- removal of diseased segment
What are slow waves? (3)
these are basal contracations (partial depolarisation)
that co-ordinate and synchronise GI muscle contraction throughout GI tract (by controlling the appearance of spike potentials)
generated by interstitial cells of Cajal (myenteric plexus)
What is the resting membrane potential of smooth muscle cells?
Between -50 and -60 mV
- has spontaneous fluctuations
How do co-ordinated muscle contraction cause contraction? (5)
1) bolus distends gut stretching the wall
2) which stimulate GIT wall nerves
3) activating ENS to release Ach to SMC at distended site
4) increasing membrane potential in distended site
5) Slow waves pass over this area to form spike potentials - causing contraction
What inhibits slow waves?
Noradrenaline and SNS, will decrease membrane potential
Process of smooth muscle migrating motor complexes
ENS signals initiate onset of MMC
- Quiescence
- GIT has minimal or no contractile activity
- allows for resting period before MMC cycle
- Initiation
- activation of ENS leads to onset of irregular low-amplitude contractions
- X/A cell -> ghrelin -> brain-> vagus nerve
- contractions granulated increase in frequency and amplitude, preparing for the next phase
- Active phase
- intense coordinated contractions
- rapid contractions propel luminal contents forward, clearing out residual natural
- M cell -> motilin-> blood vessel
What is achalasia? (5)
Failure of oesophageal peristalsis and relaxation of the lower sphincter
→ caused by loss of vasoactive intestinal peptide (VIP) and NO releasing inhibitory neurones in myenteric plexus
→ meaning only excitatory neurones dominate preventing relaxation
→ Autoimmune cytotoxic T cell infiltration and antibodies to myenteric neurones
→ treated with Botulimin toxin (acetylcholine release inhibitor and a neuromuscular junction blocking agent)
Process of the Gastric accommodation reflex? (6)
- Food enters the stomach
- Sensory receptors detect distension and stretching of the stomach walls
- Volume and pressure information sent to medulla via vagus nerve (vagovagal reflex)
- Efferent Vagal nerve signals to fungus and proximal stomach
- Activation of inhibitory motor neurones and release of VIP and NO
- Relaxation of smooth muscle cells in stomach
(mediated by vagovagal reflex pathway)
4 Functions of the gastric accommodation reflex
1) Prevents pressure rising in the stomach
2) Provides time to allow efficient mixing and breakdown of doos
3) Control release of chyme into the duodenum
4) Allow stomach to be temp food store
What are the churning actions of stomach? (7)
1) slow waves causes peristalsis starting in corpus (body) to antrum
2) Slow wave causes pyloric sphincter contraction
3) and a stronger wave follows to grind up food into smaller pieces
4) causing increased pressure which causes retropulsion (back to corpus)
5) Grinding motion breaks food down further, creating liquid chyme
6) liquid chyme is released slowly into duodenum between contractions
7) Remaining particles cleared via migrating motor complexes
What is Gastroparesis? (4)
→ delayed gastric emptying due to vagal injury
→ meaning weaker stomach contractions
→ and failure of pyloric sphincter to relax
→ Common in diabetes as hyperglycaemia damages vagus N (preventing vagovagal reflex) and interstial cells of Cajal.
Where is the vomiting centre and how is it activated?
Medulla oblongata
- receives signals from other centres (chemoreceptor trigger zone) and coordinates output
Process of Emesis
PHASE 1
- Giant retrograde peristaltic contraction
- relaxation of proximal segments
- closed lower oesophageal sphincter
PHASE 2
- increased intraabdominal pressure due to muscle contractions
- dec thoracic pressure
- closed lower oesophageal sphincter
PHASE 3
- abdominal wall contraction
- pyloric contraction
- open lower oesophageal sphincter
How does Emesis (vomiting) occur?
Range of different triggers cause activation of vomiting (Emetic) centre in medulla:
- activating vagus N and ENS
Therefore causing:
- gastric relaxation
- decrease pyloric tone
- retrograde duodenal peristalsis
- downward diaphram contraction
- abdominal muscle contraction
- chest wall muscle contraction
Hence increasing intra-gastric pressure.
Accompnied with upper and lower eosophageal relaxation and glottis closure, causing vomitting
How does segmentation in small intestine help with digestion?
- slow waves cause phasic contractions and pinching at regular intervals of different regions of circular muscles in small intestine
- to promote mixing of chyme and digestive secretions and brings it in closer contact with mucosa
Describe colonic motility
poor motility in colon to allow greater water and electrolyte reabsorbtion
Haustration (mixing):
contractions of larger segemention areas of circular muscles to create pockets (haustra)
Mass Movement (propulsive)
triggered by gastrocolic and dodenocolic reflexes to enhance rate of peristalsis in descending and sigmoid colon
Features of small intestine motility
- segmentation
- different regions of circular muscle contract to pinch off lengths of gut content
- as one set of contractions end another begins
- helps mixing with digestive secretions and bring them into close contact with mucosa
- elicited by slow waves
