Digestive system lecture 4 Flashcards
What is main form of contractile activity in the distal stomach?
What is there none of in the proximal stomach
-peristalsis, there is no peristalsis in the proximal stomach
What is gastrointestinal peristalsis, resultin from what, in response to what?
-propagated wave of contraction results from local enteric reflexes in response to local distension
WHat does the magnitude of stimulus and interaction of neural and hormonal factors influence?
What does electrical characterisitcs (in proximal somtach) of smooth muscle affect?
-amplitude of contraction
-affects the frequncy, direction and velocity of peristalsis
What is the electrophsiology of the upper and lower stomach?
UPPER STOMACH=No peristalsis, bc of steady resting potential
LOWER STOMACH=Rhythmic waves of partial depolarization, Does not cause muscle contraction
What is the electrophysiolgy values of the lower stomach?
How long does it last, what about in the stomach?
What is a slow wave?
+10 to 15 mv, lasting from 1-4 seconds recurring at regular intervals
-in stomach it is every 20 seconds (3/min)
-SLOW WAVES = Basic Electrical Rhythm (BER) Electrical Control Activity
What are the myogenic properties of the distal stomach, how do the first rhytmic waves occur/where?
How do the second propgations occur?
-Occur synchronously in the circumference of the stomach
-occur with delay, more distally in the stomach
What is BER syncrhronus in what direction, and where does it migrate?
What does it not cause
BER is synchronous circumferentially but migrates down the longitudinal axis
-Does not cause muscle contraction
What are the 2nd electrical signals at the peak of BER depolarization associated with?
the second electrical signal (ERA) (the spikes) are associated with contraction
How does contraction occur in the other waves of depolarization?
-occur slighly later each time (giving us a peristaltic wave
What do the spikes also lead to?
What happens when we have more Ach?
spikes lead to muscle tension
-more Ach=more depolarization=more spikes=higher muscle contraction
When do ERA spikes occur, what does the magnitude determine?
-“the spikes” only occur at the peak of depolarization
-The magnitude of the stimulus determines the number of spikes
-The number of spikes determines the amplitude of the muscle contraction
What happens if spikes occur at all peaks of BER?
-BER will be operating at a higher frequency and contraction will also occur in the stomach 3x per min
When is BER present?
Where is it propagated from?
-What is the frequency
in what muscle types is it detectable
-constantly present – DO NOT cause contractions
- propagated from cell to cell
- Frequency constant for a given region (3x/minute - max)
- detectable in both longitudinal and circular muscle
What are the interstial cells of Cajal (ICC), where are they located?
In what directions does it extend, and act as?
network of non-neuronal, non-muscular cells, located between the smooth muscle layers and the enteric
plexuses, extending in circumferential and longitudinal directions, may act as an intermediary between the neurons and the smooth muscle.
What doe ICC (Interstitial cells of cajal) function as?
- Function as the pacemakers for the spontaneous Basic Electrical Rhythm seen in the gastrointestinal tract.
What do ICC pacemaker cells play a role in, the 3 things?
a) origin and propagation of BER
b) communication between nerves and muscle
c) coordinating groups of muscle cells
What are the properties of the ERA (spikes)?
What are they phase locked to, what is their stimulus?
-intermittent
- phase-locked to BER
- stimulus–> ACh and stretch
What are the ERA spikes dependent on?
Where are they found?
What is the cell propagation via?
Ca++
-found in longitudinal and circular fibers
-cell to cell propagation via gap junctions (myogenic)
What do number of spikes/burst determine?
What are the contractions associated with?
WHat is the amplitude of contraction associated with?
What is the maximal frequency of contraction limited to?
spikes/burst–> magnitude of stimulus
-associated with Spikes (ERA)
- MAXIMAL f of contractions is LIMITED by f of BER
- amplitude of contractions –># spikes/burs
What happens to band on contractions in gastric peristalsis?
What does the entire portion of the stomach do?
The band of contraction becomes wider and the contractions stronger and
more rapid as they approaches the pyloric sphincter.
-The entire terminal portion of the stomach – the antrum and the pyloric
sphincter – contract synchronously to CLOSE THE PYLORIC SPHINCTOR
What is the pyloric sphincter?
When is it open/closed?
What is the size of the lumen and what does it act as?
-thick ring of circular muscle that is well developed anatomically but functinally insignificant
-open at rest, closed by antral peristalsis
-very narrow lumen (1-2mm in diameter): behaves as filter
What is the distal stomach responsible for?
-distal stomach is responsible for mixing and propulsion
What happens when the pyloric spincter closes?
What is this called
-a little bit of the bolus squeezes through but the rest bounces back to get mixed up, it is called retropulsive flow
How does gastric emptying of liquids occur?
What is the pressure difference?
Emptying due to △P between Proximal stomach and Duodenum
-pressure in proximal stomach (P1) is greater than pressure in duodenum (P2)
What do we normally have in gastric emptying of liquids?
What happens when we have a vagatomy (cut of vagus nerve) to proximal stomach?
-normally have RR (receptive relaxation) therefore the change in P is small, so there is slow flow
-change in P is large
What does gastric emptying of solids depend on?
Where is it stored?
What does distal stomach function as in this case?
-depends on peristaltic contractions in distal stomach
-Stored in the FUNDIC RESERVOIR (proximal stomach)
2.Distal stomach functions as an ANTRAL PUMP
What are the 3 main factors in distension?
-strech of muscle
-local ENS reflex–> Ach gets released onto musculature causing contraction
-vago-vagal reflex (amplifies AcH release)
What happens when you cut vagi to distal stomach, why does this happen?
What do factors in the duodenum control?
-sluggish emptying bc there is no feedback proecess that increases peristaltic contractions
-Factors in the duodenum also control the rate of gastric emptying/ antral peristalsis
What can cells detect to slow down release?
-How does distension help slow down?
pH<3, high osmolarity, and chemical compsotion of food as fat»protein»carbs (longest to shortest to breakdown)
-distension also leads to vagal vagal inputs which lead to sympathetic action to slow down
What are some enterogastron hormones that can control antral peristalsis
-secretin
-CCK
-GIP
-VIP
-Neurotensin
How do gastric vs duodenal factors affect the stomach what do they increase/decrease?
-gastric factor lead to increased motility
-duodenal factors lead to decreased motility
