PHGY 210 Lecture Notes - Sodium-Potassium Alloy, Microvillus, Nonsteroidal Anti-Inflammatory Drug

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Published on 11 Sep 2014
School
McGill University
Department
Physiology
Course
PHGY 210
Professor
Stomach ( 3 functions)
1) Temporary storage 1-2 L, only in proximal stomach ( thin wall)
2) Physical disruption & mixing of contents ( bolus  semi-liquid Chyme), distal
3) Propulsion into duodenum ( small amounts at time), distal only ( thick wall)
Empty stomach-50 ml, full up to 1500 ml.
Increasing in size, but no increasing pressure – called Receptive relaxation! – only for proximal part, and physical
presence of food isn’t required, because it is part of deglutition reflex.
ANS fibers activate inhibitory ENS neurons (proximal region) they release NANC NTs onto smooth muscle. Once
bolus in stomach , physical distention sustains RR by local enteric reflexes and Vago Vagal reflexes.
If Vagus is cut - no RR possible ( very limited), pt suffers from increased pressure in stomach (can only eat small meals).
So Deglutition reflexes has Oral, Pharyngeal, Esophageal and Gastric phases.
1) Generate pressure to transport pharynx
2) Reflex protecting airways
3) Relax UES
4) Contract pharyngeal constrictors
5) Primary peristalsis propagated along esophagus
6) Relax LES
7) Accommodate through gastric receptive relaxation
Proximal stomach – NO PERISTALSIS
Distal – yes, Peristalsis (weak moderate, intense towards duodenum, antral systole )
GI peristalsis – propagated contraction results from a series of local enteric reflexes in response to local distention.
Amplitude of contraction depends on magnitude of stimulus ( the greater the distention greater the amplitude of
contraction – depends on neural and hormonal factors).
Frequency, Direction and Velocity depends on electrical characteristics of smooth muscle.
Electrical activity of stomach
Proximal stomach – steady resting potential ( -60 mV), no BER, no ERA.
Distal stomach – resting potential is unsteady with rhythmic depolarize. waves (10-15 mV) at regular intervals with
uniform time course - called BER or ECA
They exist continuously( property of muscle cells) independent of innervation. They are synchronous circumferentially,
but migrate along longitude axis. They are no contractions, only waves. Frequency is constant for given region.
Occasionally spikes occur at peak of BERs – this is contraction –called ERA (electrical response activity), also
synchronous and migrate
ECA (BER) – constantly present, not initiative of contraction
-propagated from cell to cell ( to adjacent cells) – myogenic ability
-f constant for given region
-detectable in both circular and longitudinal muscles
--origin – interstitial cells of Cajal ( non neuronal non muscle cells)
ERA ( Spikes) – intermittent
- phase locedto BER ( ECA)
- stimulus  Ach or Stretch
- Ca dependent
- in longitudinal and circular fibers
- cell to cell propagation – myogenic
- number of spikes proportional to magnitude of stimulus ( incr # spikes incr strength of contract)
Contractions – associated with spikes ( ERA)
-amplitude of contractions proportional to number of spikes
-MAXIMAL frequency of contractions is limited by frequency of BER
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Frequency determined by BER, Amplitude by magnitude of stimulus
Propagation of stimulus require intact ENS !!!
Pyloric Sphincter: - anatomically well developed, functionally insignificant
-open at rest, closes by antral peristalsis
-very narrow lumen, acts as filter.
Since lumen is narrow, only small portion goes tru, the rest is bounced back to stomach. Retropulsive turbulent flow allows
for effective mixing in stomach and chime formation.
Emptying of liquids -proportional to pressure gradient between prox and dist stomach.
Liquids doesn’t require peristalsis! Pyloric sphincter is open in absence f peristalsis, liquids empty easily.
1) normally, there is RR, so delta P is small.
2) If Vagus to prox stomach is cut delta P is large, No RR, liquids propagated too fast.
3) If Vagus to distal stomach is cut – then delta P is very small, propagation is slow. Which affect solids more than
liquids.
Emptying of solids
1) Fundic reservoir ( prox st)
2) Antral pump (distal st) depends on: a) frequency of contractions, b) fluidity of chime.
c) amplitude of contraction (local Ach release and stretch-distention)- More stretch – more amplitude of contraction.
Stretching activates local ENS reflexes and vago-vagal reflexes. If we cut vagal to distal is major problem – will be
no stimulation to increase amplitude of contraction  sluggish emptying.
Enterogastric reflex in pyloric receptors to detect:
1) Distention ( too much distention inhibit emptying)
2) ph<3.5 (content that ph < 3.5 inhibit emptying to prevent damage of small intest mucosa)
3) Osmolarity ( hypertonic meals require more time)
4) Chemical composition : Fat>>Proteins>Carbs ( fats longer time to process, and so on)
ALL this inhibition happens by neural and hormonal pathways:
NEURAL ONES - Local reflexes carry info from duodenum to stomach to slow down
- Vago-vagal reflexes carry info to CNS to  efferent ANS that goes back to ENS in stomach
- Sympathetic NS innervate ENS neurons in distal stomach. YOU NEED to INHIBIT EXCITATORY ENS neurons
and ACTIVATE INHIBITORY ENS neurons
HORMONAL: Secretin, CCk, GIP, VIP, and neurotensin – released in duodenum, to portal vein, to act pn distal stomach.
In general: Gastric factors increase motility, Duodenal factors decrease motility. There is a balance!
Vomiting is passive, due to reverse pressure gradient ( abdo muscle contract, diapgragm decrease, content move up due to
increase in intraabdominal pressure)
Vomiting centers in medulla are activated by afferent sources of diff types ( pharyng stim, smell, cardiac icschemia,), 
activates Nausea center somewhere in medulla Widespread autonomic discharge ( imbalance b/w sym and parasymp
activity) presents as salivation, dilated pupils, sweating, constriction of blood vessels, shallow breathing) Retching – abrupt,
uncoordinated resp mvts with glottis closed-incomplete attempt to vomit  Emesis (vomiting) – actual expulsion of contents
of upper GIT: individual takes deep breath, relaxation of upper GI tract+ spasm of puloric antrum and duodenum, closes
glottis, contracts abdominal muscles, the diaphragm is displaced upwards pressing on gastric contents.
Drug often to do not act directly on Vomiting Center ( because of blood brain barrier)
But they act on CTZ (chemoreceptor trigger zone) that is outside of BBB. Impulses are then send from CTZ to Vomiting
center.
If you destroy CTZ – you cannot vomit in response to drugs, but you can still vomit due to physical stimul or phych
If you destroy vomiting center – No vomiting possible!
SMALL UPPER INTESINE (Segmentation and peristalsis)
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