Lecture 16 - GI Physiology (through slide 44) Flashcards

1
Q

Layers of the Gut Tract Wall

A

Outer to inner: 1.Serosa 2.Longitudinal smooth muscle layer 3.Myentericplexus (of Auerbach) 4.Circular smooth muscle layer 5.Meissner’s plexus (submucosal plexus) 6.Submucosa 7.Mucosa

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2
Q

Serosa:

A
  • Outer layer of connective tissue and simple squamous epithelium
  • Continuous with mesentery
  • Pathway for blood vessels to gut tube
  • Missing in some parts (i.e., esophagus):
  • Replaced with adventitia connecting to abdominal wall
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3
Q

Submucosa:

A

Incorporates blood vessels and submucosal plexus

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4
Q

Mucosa:

A
  • Forms a continuous sheet lining entire G.I. tract.
  • Loose CT with sensory nerves, blood vessels and some glands
  • Includes muscularis mucosa:
  • Thin layer of smooth muscle
  • Creates mucosal ridges and folds
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5
Q

Propulsive movements:

A
  • Stimulation at any point in the gut can cause a contractile ring to occur.
  • Contractile ring moves forward after it appears.
  • Usual stimulus is distension.
  • May also occur due to chemical or physical irritation or strong parasympathetic signals.
  • Requires presence of functional myenteric plexus.
  • Can occur in any direction but usually dies out when traveling in an oral direction.
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6
Q

Mixing movements:

A
  • May be caused by peristaltic contractions themselves.

* At other times local intermittent constrictive contractions occur every few centimeters in the gut wall.

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7
Q

Slow Waves

A

Complex interactions among the smooth muscle cells and the interstitial cells of Cajal(smooth muscle cell electrical pacemakers).
•Cells of Cajal undergo cyclic changes that periodically open and produce inward (pacemaker) currents that may generate slow wave activity.

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8
Q

•Slow waves set baseline for ___. •Slow waves are NOT action potentials. •Slow waves are slow, oscillating potentials inherent to the smooth muscle itself in some parts of the digestive tract and spread through ___.

A

intermittent spike potentials

gap junctions

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9
Q

•Slow waves occur ___. •Slow waves originate in ___ (pacemakers). •Intensity varies between ___ mv. •Frequency ranges from 3 to 12 per minute (increases from stomach to duodenum). •Slow waves set the ___ of contraction for each part of the GI tract.

A

spontaneously

interstitial cells of Cajal

5-15

maximum frequency

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10
Q

Spike Potentials

A
  • Action potentials.
  • Spike potentials excite muscle contraction.
  • Occur automatically when resting membrane potential of GI smooth muscle becomes more positive than -40 mv.
  • The higher the slow wave potential, the greater the frequency of the spike potentials.
  • Last 10-40 times as long as a typical action potential in a large nerve fiber (10-20 ms).
  • Spike potentials are responsible for opening calcium-sodium channels in GI smooth muscle cells.
  • Channels open and close slowly.
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11
Q

Factors that Cause Depolarization

A
  • Stretching of muscle
  • Stimulation by acetylcholine (parasympathetic)
  • Lack of sympathetic stimulation
  • Stimulation by specific GI hormones
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12
Q

Factors that Cause Hyperpolarization

A

Norepinephrine and epinephrine (sympathetic)

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13
Q

Causes of Tonic Contractions

A
  • Continuous repetitive spike potentials
  • Hormones
  • Continuous entry of calcium ions
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14
Q

Pattern of Motility

A
  • Local stimulus like stretch from bolus
  • Opens sodium channels
  • Slow waves pass locally through gap junctions
  • Spikes occur causing action potentials
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15
Q

Types of gastrointestinal reflexes

A
  • Reflexes that are integrated entirely within the gut wall enteric nervous system
  • Reflexes from the gut to the prevertebral sympathetic ganglia and then back to the GI tract
  • Reflexes from the gut to the spinal cord or brain stem and then back to the GI tract
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16
Q

Reflexes that are integrated entirely within the gut wall enteric nervous system control:

A
  • Much of the GI secretion
  • Peristalsis
  • Mixing contractions
  • Local inhibitory effects
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17
Q

Reflexes from the gut to the prevertebral sympathetic ganglia and then back to the GI tract:

A
  • Transmit signals long distance to other areas of the gut tract
  • Cause evacuation of the colon (gastrocolicreflex)
  • Inhibit stomach motility and secretion (enterogastricreflex)
  • Empty ileal contents into the colon (colonoileal reflex)
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18
Q

Four official GI hormones

A
  • Gastrin
  • CCK (cholecystokinin)
  • Secretin
  • Gastric Inhibitory Peptide (GIP)
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19
Q

“candidate” hormone

A

motilin

20
Q

slides 17-21

A

details on hormones

21
Q

Receptive relaxation:

A
  • Initiated by stomach distension
  • Proximal region of stomach relaxes to accommodate ingested meal.
  • CCK increases distensibility of proximal end of stomach.
22
Q

Mixing and digestion: Stomach

A
  • Distal end of stomach contacts to mix food with gastric secretions.
  • Wave of contraction closes distal end of stomach and propels food back into stomach for mixing.
  • Stimulation by vagus nerve increases gastric contractions.
  • Sympathetic stimulation decreases gastric contractions.
23
Q

Motor functions of stomach:

A
  • Storage of large quantities of food
  • Mixing of food with gastric secretions
  • Slow emptying of chime into the small intestine
24
Q

Gastric Emptying

A
  • Distal end of stomach contracts to propel food into duodenum.
  • Gastric emptying is fastest when contents are isotonic.
  • Fat stimulates release of CCK and slows emptying.
  • Acid in duodenum inhibits gastric emptying by interneurons in the GI plexuses.
25
Q

Gastroileal reflex:

A

Presence of food in stomach triggers peristalsis in ileum.

26
Q

Two types of movement in the intestine

A

•Mixing and propulsive contractions

27
Q

Localized contractions

A

cause segmentation: •“Chop” the chyme2 to 3 times per minute •Mix the food with secretions

28
Q

Peristaltic contractions

A

can occur in any part of the small intestine and move toward the anus (0.5 to 2.0 cm/sec): •Travel only 3 to 5 cm before dissipating •Therefore, three to five hours are required for passage of chime through the small intestine.

29
Q

Mixing and digestion: Small Intestine

A
  • Stimulation by vagus nerve increases intestinal contractions.
  • Sympathetic stimulation decreases intestinal contractions.
30
Q

Segmentation (mixing) contractions: Small Intestine

A

Mix intestinal contents by sending chime in both directions without a net forward movement.

31
Q

Peristaltic contractions:

A
  • Highly coordinated by enteric nervous system
  • Propel chime toward large intestine
  • Occurs after digestion and absorption have taken place
  • Enterochromaffin cells in intestine sense food and release serotonin.
  • Serotonin binds to receptors on primary efferent neurons, initiating peristaltic reflex.
32
Q

Proximal colon:

A
  • Distension of proximal colon with fecal material causes ileocecal sphincter to close to prevent reflex of fecal into small intestine.
  • Segmentation contractions in proximal colon create haustra.
  • Mass movements occur 1-3 times/day and move colonic contents long distance toward the sigmoid colon.
  • Most colonic water absorption occurs in proximal colon.
33
Q

Distal colon:

A
  • Fecal material becomes semisolid and moves slowly.

* Mass movements propel fecal material into rectum.

34
Q

Defecation:

A
  • Internal anal sphincter relaxes as fecal material moves into rectum.
  • Urge to defecate occurs when rectum is 25% filled.
  • Defecation is prevented because external anal sphincter is closed.
  • Defecation occurs when external anal sphincter is voluntarily relaxed.
  • Valsalva maneuver results in increased abdominal pressure.
35
Q

Gastrocolic reflex:

A
  • Food in stomach increases frequency of mass movements.
  • When stomach is stretched with food, there is a rapid parasympathetic component.
  • A slower CCK and gastrin component is also involved
36
Q

Principal functions of the colon:

A
  • Absorption of water and electrolytes from fecal matter

* Storage of fecal matter until it can be expelled

37
Q

Haustrations:

A

•Produced by large circular constrictions plus contractions of the teniaecoli

38
Q

Functions of mucous:

A
  • Adheres to food and other particles
  • Spreads thin film over surfaces
  • Coats wall of gut, preventing actual contact of food
  • Causes fecal particles to adhere to one another
  • Resistant to digestion by GI enzymes
  • Has amphoteric properties making it useful for buffering small amounts of acids and bases
39
Q

Functions of saliva:

A
  • Initial starch digestion (α-amylase) and initial triglyceride digestion (lingual lipase)
  • Lubrication of food and protection of mouth and esophagus
40
Q

Composition of saliva:

A
  • High potassium ion and bicarbonate concentrations
  • Low sodium and chloride ion concentrations
  • Hypotonicity
  • Contains α-amylase, lingual lipase, and kallikrein
41
Q

Saliva production is controlled mostly by ___, but also by ____ –both result in increase in saliva production.

A

parasympathetic system
•Muscarinic cholinergic receptors on both acini and ducts
•Second messenger is inositol 1,4,5-triphosphate (IP3) and increased [Ca2+]
sympathetic system
•Β-adrenergic receptors
•Second messenger is cAMP

42
Q

Cranial Nerves VII and IX, aka ____ control saliva production.

A

facial

glossopharyngeal

43
Q

Factors that increase saliva production

A
  • Food in mouth (via parasympathetic activation)
  • Smells
  • Conditioned reflexes
  • Nausea
44
Q

Factors that decrease saliva production

A
Via inhibition of parasympathetic system: 
•Sleep 
•Dehydration 
•Fear 
•Anticholinergic drugs
45
Q

Secretory cell types in gastric glands:

A
  • Mucous neck cells
  • Chief (peptic) cells
  • Parietal (oxyntic) cells
46
Q

Gastric Secretions: Chief Cells

A

Secrete pepsinogen (inactive pepsin):
•Proteolytic enzyme
•pH range of activity = 1.8 to 3.5 Release is stimulated by:
•Ach from vagus nerves or gastric enteric nervous plexus
•Response to acid in stomach

47
Q

Gastric Secretions: Parietal Cells

A

Secretory product is HCl
- Dissociation of water inside the cell into H+ and OH─ (when OH meets co2, HCO3 forms─increases blood pH and will eventually be secreted by pancreas to neutralize H+ in duodenum)