Gi1. Neural/hormonal Control And Splanchnic Circulation

Front 1

Motility

Back 1

The movements that mix and circulate GI contents and propel them along the length of the tract.

Front 2

Secretion

Back 2

Release of water and substances into GI tract from glands associated with it.

Front 3

Digestion

Back 3

breaking down food/large molecules to smaller absorbable molecules.

Front 4

Absorption

Back 4

Entry of nutrient molecules into the cells lining the GI tract; subsequently enter bloodstream.

Front 5

5 layers of the GI wall (ext to lumenal)

Back 5

1. Serosa
2. Longitudinal muscle
3. Circular muscle
4. Submucosa
5. Mucosa

Front 6

What overlies the serosa?

Back 6

The mesentary (dorsal) that keeps the GI tract attached to the body wall.

Front 7

Function of longitudinal muscle:

Back 7

Allows the GI tract to bulge and increase its volume

Front 8

Function of circular muscle:

Back 8

Contraction to narrow the lumen diameter

Front 9

What structure lies between the longitudinal and circular muscle layers?

Back 9

Myenteric nerve plexus!

Front 10

What structure lies beneath the circular muscle layer? What is it important for?

Back 10

Submucosal/Meissner's nerve plexus; senses the contents of the GI tract.

Front 11

What is directly underneath Meissner's nerve plexus?

Back 11

Submucosa

Front 12

What is just under submucosa?

Back 12

Mucosal muscle

Front 13

What's under the mucosal muscle?

Back 13

Mucosal glands and mucosal layer

Front 14

What structures are found within the folds of the submucosa?

Back 14

-Submucosal glands
-Mucosal glands

Front 15

What is at the very innermost layer of the GI wall?

Back 15

Epithelial cells

Front 16

How does GI muscle function and what enables it?

Back 16

As a syncytium - due to gap junctions between adjacent cells.

Front 17

Function of gap junctions:

Back 17

-Fast spread of ionic flow between adjacent muscle cells
-Moreso longitudinal than sideways

Front 18

Normal resting membrane potential of gut smooth muscle:

Back 18

-50 -> -60 mV

Front 19

What is GI muscle contraction like?

Back 19

Continual, slow, and Spontaneous - intrinsicly stimulated

Front 20

What are the 2 types of electrical waves in GI sm muscle?

Back 20

1. Slow oscillations
2. Spike potentials

Front 21

Function of slow waves:

Back 21

Controls the rythmic contractions of the gut

Front 22

What are slow waves like?
(ie what do they not do, and what is their amplitude)

Back 22

-NOT action potentials
-Range from 5-15 mV in intensity

Front 23

What generates slow waves?

Back 23

Interstital cells of Cajal - act as electrical pacemakers for smooth muscle cells.

Front 24

Where are interstial cells located?

Back 24

Between the circular and longitudinal muscle layers (Myenteric nerve plexus)

Front 25

How are interstitial cells connected to the muscle cells?

Back 25

By gap junctions

Front 26

How fast are the oscillations of interstitial cell generated contractions in the:
-stomach
-duodenum
-ileum

Back 26

Stomach = 3/min
Duodenum = 12/min
Ileum = 8/min

Front 27

What causes the periodic changes in membrane potential of slow waves?

Back 27

Periodic changes in Na/K ATPase activity - Na influx when membrane depolarizes changes intracellular ion concentration.

Front 28

What is NOT caused by slow waves?

Back 28

-NO calcium entry
-NO action potentials
-NO muscle contraction

Front 29

What IS caused by slow waves?

Back 29

Resting membrane slow depolarizations to generate spike potentials

Front 30

At what potential are spike potentials generated?

Back 30

-40 mV

Front 31

How do spike potentials compare to skeletal muscle potentials?

Back 31

Much slower (5x); take ~20mSec

Front 32

What is the primary cause of Spike potentials?

Back 32

Influx of calcium via Ca/Na channels

Front 33

What is the nature of Ca/Na channels that cause spike pots?

Back 33

-Slow to open
-Slow to close
-Primarily allow Calcium influx into muscle cells

Front 34

What is the effect of the calcium influx during spike potentials?

Back 34

Causes smooth muscle contraction!

Front 35

What are 4 things that stimulate spike potentials / membrane depolarization?

Back 35

1. Stretch
2. Acetylcholine
3. PNS
4. Specific hormones

Front 36

What are 2 things that stimulate membrane hyperpolarization?

Back 36

1. Norepi/Epi
2. SNS

Front 37

What causes smooth muscle contraction?

Back 37

Calcium - Ca/Calmodulin activates MLCK - activates myosin allowing for powerstroke.

Front 38

What are the 2 layers that make up the Enteric Nervous System?

Back 38

-Myenteric nerve plexus
-Submucosal/Meissner's plexus

Front 39

Another name for Myenteric plexus:

Back 39

Auerbach's

Front 40

Function of the ENS:

Back 40

Independent and autonomous Integration of motor and sensory activities of the GI system

Front 41

What does the ENS also have input from?

Back 41

PNS/SNS

Front 42

How far does the ENS extend?

Back 42

From esophagus to anus

Front 43

Function of Myenteric plexus:

Back 43

Control of GI movements

Front 44

Function of Meissner's plexus:

Back 44

Control of GI bloodflow and secretions

Front 45

What type of autonomic nerves input into the ENS?

Back 45

SNS - mainly postganglionics
PNS - mainly preganglionics

Front 46

Where do visceral afferents from the GI tract extend?

Back 46

-Prevertebral SNS ganglia
-Spinal cord
-Vagal nerves in the brainstem

Front 47

What is the structure of the myenteric nerve plexus like?

Back 47

-A linear chain of many interconnecting neurons
-Extends entire length of GI tract between musc layers

Front 48

Myenteric plexus is important for controlling:

Back 48

Motor activity in the gut

Front 49

4 things increased by myenteric plexus stimulation:

Back 49

1. Tonic contraction of gut
2. Intensity of rythmic contractions
3. Rate of Rythmic contraction
4. Velocity of excitatory wave conduction along the gut wall

Front 50

General consequence of myenteric plexus stimulation:

Back 50

More Rapid Peristalsis

Front 51

Are all nerves in the myenteric plexus excitatory?

Back 51

No; some are inhibitory

Front 52

What NT do inhibitory neurons of the myenteric plexus release?

Back 52

VIP (vasoactive intestinal polypeptide)

Front 53

Function of VIP releasing neurons:

Back 53

Inhibition of sphincter tone (pyloric and ileocecal valves)

Front 54

General functions of the Sumucosal (meissner's) plexus:

Back 54

-Control of inner intestinal wall functions
-Sensory input from lumen

Front 55

What 3 things are controlled by the submucosal plexus?

Back 55

1. Intestinal secretions
2. Absorption
3. Contraction of submucosal muscle for mucosal infolding

Front 56

2 divisions of the PNS that give autonomic regulation to ENS:

Back 56

-Cranial - mainly vagal
-Sacral - S2-s4

Front 57

What portions of GI tract get
-vagal PNS input
-sacral PNS input

Back 57

Vagal - foregut up to first 1/2 of transverse colon
Sacral - distal 1/2 of colon and beyond

Front 58

What is sacral PNS input important for?

Back 58

Defecation reflexes

Front 59

Where do postganglionic PNS neurons reside?

Back 59

In both ENS plexuses

Front 60

What does PNS stimulation do in general to the GI tract?

Back 60

Stimulates activity

Front 61

Where do SNS preganglionic fibers for GI tract innervation originate? Where do they synapse?

Back 61

-Originate at T5-L2 in spinal paravertebral chain ganglion
-Synapse at prevertebral ganglia

Front 62

What are the prevertebral sympathetic ganglia?

Back 62

-Celiac ganglion
-Mesenteric ganglion

Front 63

What do postganglionic SNS fibers to the ENS release?

Back 63

Norepi

Front 64

How does NE release affect GI functioning?

Back 64

-Directly inhibits intestinal tract sm muscle (minor effect) except for mucosal muscle
-Inhibits ENS NEURONS (major)

Front 65

How does norepinephrine release affect Mucosal muscle?

Back 65

It stimulates it! Hence the exception to NE's otherwise inhibitory effect on GI muscle.

Front 66

2 Types of Afferent systems from the gut:

Back 66

1. Entirely within the ENS
2. Exiting the ENS - cell bodies in ENS extend to prevertebral SNS ganglia and DRG to medulla; elicit Vagal reflex impulses.

Front 67

3 things that stimulate visceral afferents from gut:

Back 67

1. Mucosal irritation
2. Gut distention
3. Chemical presences

Front 68

Where do visceral afferents from the gut go?

Back 68

-Cell bodies in the ENS extend to prevertebral symp ganglia
-Cell bodies in DRG extend to spinal cord or medulla

Front 69

What happens to the afferent impulses transmited by DRG to the spinal cord/medulla?

Back 69

They get integrated and sent back via the Vagus to provide reflex control of GI functions.

Front 70

3 types of GI reflexes:

Back 70

1. Reflexes entirely w/in ENS
2. Reflexes from gut -> prevertebral SNS ganglia -> GUT
3. Reflexes from gut -> SC or brainstem -> Gut

Front 71

4 Reflexes contained entirely within the gut:

Back 71

1. Secretion
2. Peristalsis
3. Mixing contractions
4. Local inhibition

Front 72

What reflexes use the gut -> prevertebral SNS ganglia -> gut reflex?

Back 72

Long distance reflexes for coordinating different areas of the GI tract.

Front 73

3 reflexes that use the prevertebral SNS ganglia:
What is the nature of each type?

Back 73

1. Gastrocolic (stimulatory)
2. Enterogastric (inhibitory)
3. Colonileal (inhibitory)

Front 74

Function of Gastrocolic reflex:

Back 74

Evacuation of the colon when the stomach fills

Front 75

Function of the Enterogastric reflex:

Back 75

Inhibition of stomach motility and secretion when intestins fill.

Front 76

Function of colonoileal reflex:

Back 76

Inhibition of ileal motility when the colon fills

Front 77

3 types of reflexes from the gut to spinal cord/brainstem and back to the GI tract:

Back 77

1. from stomach to control gastric motility/secretions
2. Pain reflexes (inhibit entire GI tract)
3. Defecation reflex

Front 78

What is hormonal most important for? What is it less important for?

Back 78

Most important:Gastric secretion
Less important: GI motility

Front 79

5 hormones that control GI motility (to some extent)

Back 79

1. CCK
2. Secretin
3. GIP
4. Gastrin
5. Motilin

Front 80

Where is CCK made?

Back 80

I cells in duodenal and jejunal mucosa

Front 81

Stimulus for CCK release

Back 81

Fat presence in intestines

Front 82

What does CCK stimulate?

Back 82

-Gall bladder activity/motility to expel bile and emulsfy fats

Front 83

What does CCK inhibit?

Back 83

Stomach motility

Front 84

Where is Secretin made?

Back 84

S cells in duodenal mucosa

Front 85

What stimulates Secretin release?

Back 85

Acid in the duodenum

Front 86

How does Secretin affect GI motility?

Back 86

Mildly inhibits GI motility

Front 87

Where is GIP made? Stimulus for release?

Back 87

in the mucosa of the upper small intestine; stimuladed by FA, AA, and CHO

Front 88

How does GIP affect GI motility?

Back 88

-Decreases stomach motility
-Slows gastric emptying

Front 89

Where is Gastrin made? Stimulus for release?

Back 89

-Made in Gcells of stomach antrum
-stimulated by stomach distention

Front 90

Effect of Gastrin on GI motility:

Back 90

STIMULATES GI motility!!

Front 91

What is special about Motilin?

Back 91

It is the only gastric hormone to stimulate GI motility when the stomach is EMPTY - that is the stimulus for its release.

Front 92

Where is Motilin made?

Back 92

Duodenum.

Front 93

Function of Motilin:

Back 93

prevents stagnation of the intestines in the unfed person

Front 94

2 types of GI motility:

Back 94

-Propulsive/peristaltic
-Mixing

Front 95

Function of propulsion:

Back 95

Moves food along at the appropriate rate for digestion and absorption.

Front 96

What is peristalsis?

Back 96

The forward movement of a contractile ring around the gut wall

Front 97

Stimulus for peristalsis:

Back 97

Distention of the gut

Front 98

What does distention do?

Back 98

Causes the gut to contract 2-3 cm behind where the gut wall stretched.

Front 99

What is MANDATORY for peristalsis?

Back 99

An intact myenteric plexus

Front 100

Why does peristalsis always move forward toward the anus?

Back 100

Because of the law of the gut - retrograde peristalsis dies out.

Front 101

What blocks peristalsis? (2 spcf things)

Back 101

Absence of the myenteric plexus
-Atropine
-Congenital abnormality

Front 102

What is the law of the gut?

Back 102

-Peristalsis is always stimulated BEFORE the site intended for receipt
-Receptive relaxation always occurs AFTER site of constrictn

Front 103

What is the nature of mixing movements within the gut?

Back 103

Heterogenous
-Peristalsis against a closed sphincter causes churning

Front 104

What is the special name for GI bloodflow?

Back 104

Splanchnic circulation

Front 105

Where does splanchnic circulation flow?

Back 105

Through Gut
-Spleen
-Pancreas
-Liver

Front 106

Where does all splanchnic bloodflow drain?

Back 106

Into the portal vein to pass thru sinusoids and leave via the Vena cava.

Front 107

What is the purpose of sending nutrient rich blood through the liver?

Back 107

To allow RES cells to clean out bacteria and particulate matter.

Front 108

Where do the non-fat, water-sol nutrients absorbed by the liver go?

Back 108

Reticuloendothel and Hepatic cells absorb and store 75%

Front 109

Where do fat-based nutrients go?

Back 109

To intestinal lymphatics -> blood via the thoracic duct.
-Bypass the liver

Front 110

What supplies blood to the stomach?

Back 110

Celiac artery

Front 111

What supplies blood to the intestinal wall?

Back 111

Arcades branching from Superior and Inferior mesenteric aa.

Front 112

What 3 structures do the mesenteric arteries serve?

Back 112

1. Muscle bundles
2. Intestinal villi
3. Submucosal vessels

Front 113

What are intestinal villi?

Back 113

Intricate webs of capillaries for absorbing nutrients

Front 114

What is unique about villi vasculature?

Back 114

They have highl muscular walls for tight control of villus bloodflow.

Front 115

What is countercurrent flow in villi refer to?

Back 115

The diffusion of 80% of oxygen directly from artery to vein.

Front 116

What are intestinal villi vulnerable to?

Back 116

Ischemia

Front 117

What is the predominant way to control GI bloodflow?

Back 117

Via metabolic regulation

Front 118

3 cases where GI bloodflow increases:

Back 118

1. After a meal (high local metabolic activity)
2. During nutrient absorption
3. During motility

Front 119

What happens to GI bloodflow between meals?

Back 119

It returns to low resting levels

Front 120

3 Mechanisms for Metabolic regulation of GI bloodflow:

Back 120

1. Release of vasodilators during digestion
2. Secretion of KININS as GI glands secrete other things.
3. Decreased O2 / increased adenosine

Front 121

How do PNS nerves regulate GI bloodflow?

Back 121

Increasing PNS activity increases bloodflow to the GI tract

Front 122

How does SNS stimulation alter GI bloodflow?

Back 122

Decreases it by causing intense vasoconstriction.

Front 123

Why does SNS stimulation vasoconstrict bloodsupply to the GI tract?

Back 123

So that in situations where SNS outflow is high - heavy exercise, circulatory shock, etc, you want to shunt blood AWAY from splanchnics to skel muscle, brain, etc.