8. Gastrointestinal Motility Flashcards Preview

Year 1 - Term 2: Digestion, Metabolism and Growth > 8. Gastrointestinal Motility > Flashcards

Flashcards in 8. Gastrointestinal Motility Deck (19)
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1
Q

Describe the extrinsic innervation of the gut.

What comprises the enteric NS in the gut?

A

Autonomic NS. Vagal and pelvic outflows, generally excitatory (ACh). Spinal afferents (e.g. hypogastric and greater splanchnic nerves), generally inhibitory (NA).

NB: colonic movements influenced by stress

Myenteric plexus in muscularis propria/externa between circ and long muscles, primary motility controller. Submucosal plexus in submucosa, primary fluid exchange controller. Sensory and motor nerve endings in mucosa. Interacts with gut endocrine and immune systems.

2
Q

Where are enteric motor neurons found?

Where are enteric sensory neurons found?

What do the excitatory and inhibitory motor neurons release?

A

Circular muscle

Mucosa

ACh and NO (so contracts and relaxes in oral -> anal direction = peristalsis)

3
Q

What are the interstitial cells of Cajal (ICCs)?

How can the wave spread over many centimeters?

A

Around myenteric plexus within muscle (in stomach, colon), and around the submucosal plexus (in colon). Create rhythm of electical slow waves causing phasic muscle contractions (myogenic) by spontaneous depolarisation

Gap junctions allow communication - muscle arranged as a functional syncytium

NB: ICC generates current and connected to SM cell too.

4
Q

What is the dominant nervous control system responsible for the following areas A-E?

A

A: CNS (vagus)

B: ENS, myogenic and CNS (vagal)

C: ENS

D: ENS and myogenic

E: ENS and CNS (spinal)

5
Q

What is the migrating motor complex?

Where can it originate?

What are it’s 3 functions?

A

Occurs during hunger, 3 phases every 90-120 minutes and ends in high amplitude propagating contractions.

Stomach (vagus-dependant) or small intestine (vagus-independant)

Clear undigested material, prevent bacteria overgrowth, hunger sensations (esp at stage 3)

6
Q

Describe the 3 phases of food intake and the triggers for each.

A

1. Coeliac phase: senses detect food, MMC’s abolished, prepares GI tract: saliva, gastric acid, pancreatic secretion, gastrin, ghrelin

2. Gastric phase: satiation, early digestion, gastric emptying. Triggered by mechanical effect

3. Intestinal phase: feedback and satiation. Triggered by chemoreceptor activation in small bowel

7
Q

Describe CNS (vagal) control of peristalsis in the oesophagus.

What happens when the bolus reaches the stomach?

What 2 things allow consumption of big meals?

A

10 peristaltic wave upon swallowing (striated muscle). Stretch receptors stimulated and local reflex causes 20 peristaltic wave (smooth muscle) forcing bolus into stomach as LOS relaxes.

Fundus: receptive relaxation (vago-vagal reflex releases CCK). Then adaptive relaxation takes over (enteric reflex, releases NO from ENS).

Relaxation. Release gas to reduce pressure on stomach (Transient LOS Relaxation allows gas escape).

8
Q

What are the functions of the distal stomach?

Describe the gradients of slow wave activity in the stomach.

What happens if the food is not digested properly but has reached the pyloric sphincter?

A

Propulsion with grinding and mixing (acid and peptidases), pushing towards pyloric sphincter

ICCs generate slow waves which propagate from dominant pacemaker in corpus (body) around and down to pylorus. Higher frequency near greater curvature. Sets of rings of contraction moving down stomach.

It is sent back up the stomach for more churning.

9
Q

Describe the 3 phases of the sieving function.

What happens after phase 3?

A

Mid corpus contraction mixes and breaks down food, together with gastric acid + peptidases. Then 3 phases:

1) propulsion: rapid flow of liquids with suspended small particles, and delayed flow of large particles towards pylorus

2) emptying: of liquids with small particles. Large ones retained in bulge of terminal antrum

3) retropulsion: of large particles and clearing of terminal antrum.

Antrum movement enables powerful contractions to futher break down food particles.

10
Q

What 4 things regulate the rate of expulsion from the stomach?

What does the gastric emptying curve look like for liquids and solids?

A

1) physical properties (lq vs s; particle size)
2) neuronal and hormonal feedbacks (sense physical properties)
3) nutritional value/content (maintains constant flow of nutrients to intestine via feedback, to slow gastric emptying, promote satiety and regulate insulin secretion. Via nerves and hormones)
4) volume (large vol empties faster than small)

Liquids: exponential = fast emptying. Solids: lag phase (20-30mins) = slow emptying, then the viscous chyme is emptied in a mainly linear fashion

11
Q

How does signalling from the upper GI tract differ during and after food intake?

What is the primary soure of feedback signalling for pysiological regulation in the GI tract?

A

During and initially after: gastric distention and accomodation = major determinants of nutrient intake. Beginning of feedback control back to brain via vagus nerve.

After: nutrient intake influenced by signalling from intestine after exposure to nutrients. Vagus nerge controls TLOSR.

Enteroendocrine cells

12
Q

Describe the 2 feeback regulations of gastric emptying.

A

1) Duodenal and jejunal brakes: vagal afferents to BS via CCK production (can activate radial fibres to BS) to regulate stomach movement. E.g. if too much fat exiting, liberate CCK and tell stomach to slow down a bit (and person to slow the eating): contraction reduction, enhance relaxation and storage, and reduce opening of pyloric sphincter
2) Ileal brake: fats are usually digested and absorbed in duodenum, fats reach ileum, feedback slows gastric emptying and induces satiety. Mediated by hormones released from endocrine cells.

13
Q

What are 2 roles of the lower oesophageal sphincter?

What causes the following (in GI terms):

a) gastro-oesophageal reflux
b) early satiety/nausea
c) neuropathy
d) dysrhythmia
e) obesity

A

Prevent reflux, TLOSRs

a) failure to clear acid/dysfunctional LOS
b) incomplete gastric accomodation
c) e.g. diabetes
d) nausea (gastroparesis)
e) poor feedback control

14
Q

Describe how hormones create peristalsis.

What do enteric sensory nerurons detect and initiate in response?

A

Contraction at front via excitatory ACh release from enteric sensory nerve. Relaxation at back via inhibitory NO release to move bolus along. Continual stop-start process.

Detect: intraluminal stimuli e.g. chemical (nutrients, low pH), and mechanical (stretch). Initiate: peristalsis, increased secretion and vascular flow

  • Can ‘talk’ to multiple neurones because of multiple dendritic projections. Info transmitted via interneurons to motor neurons.*
  • = COVERS peristalsis in oesophagus ans SI but a bit diff in LI*
15
Q

Describe what happens and transit speed in the different parts of the colon.

Describe the shape of the colon.

A

Ascending: Mixing, absorption, fermentation. Slow transit. Transverse: absorption. Relatively fast transit. Descending: storage. Slow, partly voluntary transit.

Taenia coli: outer 3 seperate bands of longitudinal smooth muscle - project lengthways = diff to SI and oesophagus. Circular muscle present. In absence of continuous band of longituinal muscle, can bulge out to form haustra, which gives more space of nutrient breakdown and bacteria to work.

16
Q

Describe the ascending colon.

What controls movement of ascending colon?

What 2 things modulate the enteric NS?

A

Rich in living bacteria. Site of fermentation and absorption of H2O/ions/nutrients. Haustra increase SA. Retropulsion/segmentation churns and slows transit.

Propulsion, retropulsion, segmentation, ICCs generate slow waves of electrical activity propagating short distances in oral/anal directions, release of local mediators (e.g. 5-HT from endocrine cells - 5-HT3 receptor antagonists can cause constipation). Also influenced by local environment!

Local and circulating hormones. Central/spinal NS.

17
Q

Describe the kind of movement that facilitates content movement from ascending to descending colon.

How does the conscious recognition for the need to poo arise?

What kind of nerve facilitates this?

A

Mass movement: contents enter AC = haustra, constrictive ring occurs (giant migrating contraction) and haustra disappear from a portion of AC. About 20cm of colon distal to constrictive ring lose their haustra and contract as unit, propelling faecal material to transverse colon. Haustra return.

Mass movements usually persist for 10-30 minutes.

Mass movement into rectum - pressure rises and internal anal sphincter starts to relax and external anal sphincter starts to contract.

Spinal efferent to bowel to talk to enteric NS and drive process.

18
Q

What 2 things normally prevent defecation?

What 2 things happen when defecation is initiated?

What happens in defecation?

A

Tone of internal anal sphincter and puborectalis. Mechanical effects of acute anorectal angle.

Puborectalis muscle and external anal sphincter relax. Intraabdominal pressure increased

External sphincter relaxation and rectal propulsive contractions. (If hold it in then keep sphincter contracted)

19
Q

How do we distinguish between a poo and a fart?

What conditions may affect the colon?

A

We have a sensitive mechanism to distinguish between mechanical and chemical (gas e.g. methane, hydrogen sulphide) forces.

Pseudo-obstruction, diarrhoea, slow transit constipation, chronic constipation (e.g. parkinsons, MS - spinal damage = no longer have gut -> brain control), megacolon/impaction/faecal incontinence (elderly)