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88 Cards in this Set

  • Front
  • Back
what determines the amount of food we eat? what determines what type of food we eat?
hunger; appetite
what centers in the CNS control the regulation of food? (5)
hypothalamus, nucleus tractus solitarius (brainstem), amygdala, the cortex prefrontalis, and the area postrema
what two hormones in the endocrine system control the regulation of food?
insulin and leptin
what are the three hormones of the GI system that regulate food intake?
cholecystokinin, ghrelin, peptide YY
what is the key region in the CNS that is involved in feedback control of appetite and food intake?
hypothalamus
where is the feeding or hunger center? what is it involved in?
lateral hypothalamic area; involved in stimulation of food intake and storage of calories
where is the satiety center? what is it involved in?
ventromedial nuclei; involved in the limitation of food intake or satiety.
what are the two hypothalamic pathways that exist to regulate food intake? what purposes do they serve?
melanocortin pathway: increase metabolism and inhibit food intake; neuropeptide Y: stimulate food intake and decrease metabolism.
what is the purpose of NTS?
to serve as a gateway for neural signals from the GI tract to the hypothalamic feeding centers
what is the source, site of action and clinical effect of insulin?
source: pancrease
Site of action: hypothalamus
clinical effect: decreased appetite and increase metabolism
what is the source, site of action and clinical effect of Leptin?
source: fat cell
site of action: hypothalamus
clinical effect: decreased appetite and increased metabolism
what is the source, site of action and clinical effect of CCK?
source: duodenum
site of action: vagal afferents
clinical effect: decreased appetite and decreased gastric emptying
what is the source, site of action and clinical effect of PYY?
source: ileum and colon
site of action: hypothalamus
clinical effect: decreased appetite and increased metabolism
what is the source, site of action and clinical effect of Ghrelin?
source: stomach
site of action: hypothalamus
clinical effect: increased appetite and decreased metabolism.
what are the four functions of the digestive system?
motility, secretion, digestion and absorption
what is the function of the oral cavity? what does it prevent?
food intake, mixing and size reduction; food propulsion; taste. Prevents pulmonary aspiration.
what is the function of the esophagus? what does it prevent?
food bolus propulsion into the stomach. Prevents gastric reflux.
what is the function of stomach?
nutrient storage; mixing; homogenization and propulsion; secretion.
what is the function of small intestine?
major site of nutrient digestion and absorption, mixing and propulsion of chyme; secretion
what is the function of large intestine?
mixing and propulsion; final water and electrolytes absorption
what is the function of the rectum?
storage of fecal material
what is the function of the anus?
control of defecation
The functional structure of the GI wall contains 7 layers, name them in order.
serosa, longitudinal muscle layer (smooth), myenteric plexus of enteric NS, circular muscle layer (smooth muscle cells), submucosal plexus of the enteric NS, submucosa, mucosal muscle cellls and mucosa.
what are the voluntary muscles of the upper tract? lower tract?
upper: mouth, pharynx, and first 1/3 of esophagus.
lower: external anal sphincter.
what action does the longitudinal muscle perform?
peristalsis, food propulsion
what does the action of the circular muscle produce?
segmentation, mixing
what does the action of mucosal muscle produce?
surface area and lymph flow
what are the five hormones that regulate GI functions?
Gastrin, CCK, secretin, gastric inhibitory peptide, motilin
what are the two paracrines released for regulation of the GI functions?
somatostatin and histamine
what are the four neurocrines released for regulation of the GI functions?
substance P, VIP, gastrin-releasing peptide, enkephalins
what is the primary action of gastrin?
increased HCL secretion and increased pepsinogen secretion
what is the primary action of secretin?
increased water and bicarb secretion by pancreatic ductal cells and biliary tract
what is the primary action of the CCK?
increased enzyme secretion by pancreatic acinar cells, increased contraction of the gallbladder
what is the primary action of the Gastric inhibitory peptide?
inhibit gastric secretion, motility, and emptying
what is the primary action of Motilin?
increased motility and initiate the migrating motor complex MMC
what is the main example of intrinsic control of neural control of GI functions?
enteric NS
what is the 2 main examples of extrinsic control of neural control of GI functions?
autonomic NS and CNS
Parasympathetic pathways generally have an _________ influence on the functions of the GI tract.
Excitatory
what time of receptors do the afferent fibers come from?
chemo- or mechano receptors
where do the preganglionic fibers synpase in parasympathetic pathways in the GI?
cells of the enteric plexuses
what effect does the parasympathetic pathway have on GI smooth muscle, mucosal secretory and/or endocrine, and vascular smooth muscle cells?
GI smooth muscle: increased GI motility, decreased tone of GI smooth muscle sphincters
Mucosal secretory and/or endocrine cells: increased secretion
Vascular smooth muscle cells: vasodilation and increased blood flow.
Sympathetic stimulation generally has an _____________ influence on the functions of the GI tract.
inhibitory
what receptors do the afferent fibers come from? where do they connect to?
mucosal and smooth muscle receptors directly to the prevertebral ganglia and/ or to spinal cord.
where do the efferent preganglionic fibers synapse? postganglionic fibers?
outside of the GI tract with prevertebral ganglia; neurons located with the enteric nerve plexi
Most efferent sympathetic pathways are what type of ganglionic fiber?
postganglionic
what are the effects sympathetic nerves on vascular smooth muscle cells, GI smooth muscle, and mucosal secretory and/or endocrine cells.
Vascular smooth muscle: Vasoconstriction, decreased blood flow
GI smooth muscle: decreased GI motility, increased tone of GI smooth muscle sphincters.
Mucosal secretory and/or endocrine cells: decreased secretion activity
what are the two examples of reflexes regulated by the CNS?
Long reflexes: pain, defecation
where is the enteric nervous system located?
entirely within the GI tract : from esophagus to anus
what are the two plexi contained under the enteric nervous system umbrella?
myenteric plexus (auerbach's plexus) and submucosal plexus (Meissner's plexus)
T/F
The enteric Nervous system can function autonomously.
TRUE
what does the submucosal plexus innervate?
glandular epithelium, intestinal endocrine cells and submucosal blood vessels.
what is the primary control of the submucosal plexus?
primarily controls GI secretion and local blood flow
what does the submucosal plexus regulate?
contraction of the muscularis mucosae.
what does the myenteric plexus primarily control? what does it regulate?
GI movements. the local and inter-regional motility activity through regulation of contraction/ relaxation of circular and longitudinal smooth muscle layers.
what are the major neurotransmitters of the enteric NS? are they inhibitory or excitatory?
ACH: excitatory; NE: inhibitory
what are the 8 non-peptide neurotransmitters of the enteric nervous system?
ATP, NO (Both inhibitory), adenosine, serotonin, GABA, histamine, glycine, dopamine
what are the 2 peptide neurotransmitters of the enteric nervous system?
VIP (inhibitory) and substance P (excitatory)
what are the 4 signals for sensory neurons?
mechanical, thermal, osmotic and chemical
what are the effector cells for motor neurons?
smooth muscle, secretory cells and I endocrine cells
what are the interneurons mainly responsible?
for integrating information (from sensory to motor)
what controls the short reflexes of the gut? what are the short reflexes responsible for?
Enteric NS. Controls secretion, peristalsis, mixing contraction
what controls the long reflexes of the gut? where do they travel?
CNS and ENS.
reflexes are from the gut to the prevertebral sympathetic ganglia and then back to the GI tract (gastrocolic, enterogastric, and colonoileal reflexes); from the stomach and duodenum to the CNS;
what is controlled by the long reflexes?
controls gastric motor and secretory activity, pain reflexes (general inhibition of entire GI), and defecation reflexes
how are smooth muscle cells electrically connected?
gap junctions
what are the interstitial cells of Cajal connected to?
one another, smooth muscle cells and nerve endings
where are ICC's pace-maker cells?
caudad stomach and intestine
T/F
Initiation of GI smooth muscle contraction is dependent of neural or hormonal input.
FALSE:

its independent
what is the spontaneous cycles of depolarization and repolarization of GI smooth muscle known as?
electrical slow waves or Basic electrical Rhythm (BER)
T/F
the frequency of the BER is the same throughout the entire digestive system.
FALSE.

It varies by region. (ie 3/in in stomach and 12/min in duodenum
what causes muscle contractions?
action potentials "spikes"
what generates the BER or electrical smooth waves?
ICC: interstitial cells of Cajal
what is the range of the spontaneous rhythmic fluctuation of the "resting" membrane potential of smooth muscle?
-65- (-45) mV
what is the depolarization phase of smooth muscle due to? Repolarization phase?
Na influx; K+ efflux
where are these slow wave potentials generated in the GI tract?
from mid stomach to rectum
where are their no slow waves?
esophagus and proximal portion of stomach
T/F
slow waves initiate contraction in the intestine?
FALSE.

They may (rarely) cause muscle contraction in stomach, but not intestine
T/F
slow waves are influenced by body temperature and metabolic activity.
True!
the spike is formed by both depolarization and repolarization, what is influxing in depolarization and what is effluxing in repolarization?
Ca2+ and K+
What is the force of the contraction directly related to? what about the duration?
force is directly related to frequency of APs. Duration of contraction is releated to number of AP.
what are two depolarizing factors that stimulate GI smooth muscle contraction?
stretching of the muscle and stimulation by parasympathetic nerves (ach)
what are two hyperpolarizing factors that will inhibit GI smooth muscle contraction?
stimulation by sympathetic nerves (norepi) and epi
____ increase the number of spikes and increases _______ of the smooth muscle
Ach; tension
what is another name for tonic contraction of GI smooth muscle?
basal myogenic tone
T/F
Tonic contraction of the GI is characterized by very high ATP consumption.
FALSE
very low --> latch mechanism
what increases the intensity of the tonic contraction? (3)
an increased number of action potentials, factors that cause partial depolarization of SM membrane and factors that increase Ca influx.
what is the function of the orad stomach?
tonic contraction of proximal stomach
what is the function of the sphincter of oddi?
separates pancreatobiliary ducts from duodenum
what is the function of internal anal sphincter?
control defecation