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13 Cards in this Set

  • Front
  • Back
GI structure

GI structure

From the oesophagus to the anal canal, it has a similar basic structure


- Primed by pacemaker cells (interstitial cells of Cajal) = initiate a spreading basal electrical rhythm (BER)


- Spike potentials occur when the threshold is crossed. Causes muscle contraction


Sensitive to stretch = stimulation of gut activity directly or via local neural reflexes. Co-ordination by the myenteric plexus

Chyme activates mechanoreceptors → engage with myenteric plexus


- Upstream = contraction of muscle


- Downstream, release of vasoactive intestinal polypeptide (VIP) = relaxation of muscle


Direction of propulsive movements downstream

Gut activity


- Modified by extrinsic autonomic nerves


- Also modified by locally produced chemicals & hormones

Modified by extrinsic autonomic nerves


- PNS- ↑ motility via ACh on mAChR's, or indirectly by modifying activity of interstitial cells of Cajal


- SNS- ↓ motility:


- Directly via NA on β-adrenoceptors


- Indirectly via NA on α₂-adrenoceptors, presynaptically on parasympathetic nerve terminals = ↓ ACh release from parasympathetic nerves



Stages of GI motility

1. Mastication


2. Deglutition- 2 stages of swalling, oropharyngeal & oesophageal




The oesophagus is a hollow tube separated at each end by sphincters


- Zone of elevated pressure prevents transit from 1 region to another & separates oesophagus from stomach


Swallowed food is pushed one 1 end by peristalsis (wave-like contraction)

Oesophageal peristalsis



Mechanoreceptors in pharynx detect bolus, initiate 1⁰ peristaltic wave


- Controlled by vagal nerve, speed is 5cm/s, lats 7-10s, gravity assisted, rate of movement is proportional to viscosity of bolus




If food is not projected to stomach, a 2nd wave is initiated by local vago-vagal reflexes




Empty oesophagus- small intermittent waves, salivary swallowing (7-70/hr)

Gastric motility

Primed by pacemaker cells, initiate BER (every 3-5min)


- Not always associated with peristaltic wave, just when underlying tissue is at its more excitable


Smooth muscle excitability is controlled by:


- Myogenic properties of sm cells - Intrinsic & extrinsic nerve activity


- Hormones or locally produced chemicals



Gastric motility

Empty stomach = feeble contractions


Full stomach= 1st hr peristaltic waves weak as pyloric sphincter is closed, later waves more powerful


- Associated with mixing of gastric content & emptying into duodenum

Control of gastric motility

Neural control- vagal relaxatory fibres = relaxation in corpus & fundus, mediated by VIP. Stimulated by oesophageal & gastric distention


- SNS via NA inhibitis, via inhibition of PNS ganglionic transmission. Stimulated via distention of small intestines


Vagal fibres release ACh to stimulate gastric motility


Hormones:


- Stimulatory- gastrin (antrum), motillin (from small intestine)


- Inhibitory- gastrin (proximal stomach), secretin, CCK

Rate of movement of contents


- Meal composition

Rate at which gastric contents pass into duodenum depends on motility & meal composition


- Standard meal is fastest, protein is medium, lipids are slow


- Volume- greater the volume of contents, the faster the rate of emptying


- Fragment size- solid fragments <1mm only pass into duodenum suspended in liquid phase


- Osmolarity- osmolarities > & <200mOsm slow emptying


- Acid- excess acid in small intestine slows gastric emptying


- Fat- fat in upper small intestine slows gastrin emptying



Small intestine motility

In the small intestine, intestinal contents are mixed with secretions of mucosal cells & with pancreatic juice & bile


2 types of muscular contraction:


- Segementing - mixing. Occurs in circular muscle, moves chyme to & fro, increases exposure to mucosal surface. BER duodenum 12/min, terminal ileum 9/min = allows movement down the tract


- Peristaltic- more longitudinal over short distance. After a meal, occasional long distance wave (migrating motility complex)

Control of small muscle motility

1. Myogenic mechanisms- stretch


2. Myenteric plexus (local regulation). Stimulatory = ACh, gastrin, CCK. Inhibitory = VIP, opiods, NO


3. Extrinsic nerves- some vagus, sympathetic (presynaptic inhibition), direct


4. Local chemicals- fat slows transit time

Large intestinal motility

Food takes ∼12 hours to reach terminal ileum


- Ileal-caecal sphincter prevents retrograde movement of bacteria from colon


Large intestine reabsorbs water & stores faeces. Movement slow & non-propulsive. Haustral contractions kneads content. 2/hr


- 3-4 per day powerful contractions drive contents to distal large intestine prior to defecation, initiated by food in stomach (gastro-colic reflex)

Defecation

Rectum is usually empty


- Arrival of faecal material = desire to defecate via sensory nerves = peristaltic wave in colon & internal anal sphincter relaxes




Anus- tonically contracted ring of smooth muscle with voluntary control of external anal sphincter




Defecation reflex: Myenteric plexus is weak, PS spinal reflex present, voluntary effect