Lecture 15: Introduction to GI tract Physiology Flashcards
Describe the components of the enteric nervous system
- Myenteric and Meissner’s plexuses
- Collectively form the enteric nervous system of the gut tract
- can operate autonomously via intrinsic regulation and sensory reflexes
- work with sympathetic and parasympathetic (mostly vagus nerve) systems
- Parasympathetic system generally increases GI tract activity
- Sympathetic system generally decreases GI tract activity
- Neurons are supported by intrinsic glial cells
Differentiate between the myenteric plexus (Auerbach’s plexus) and Meissner’s plexus (submucosal plexus)
- Myenteric (Auerbach’s) plexus:
- Located between longitudinal and smooth muscle layers
- Primarily controls intestinal smooth muscle and participates in tonic and rhythmic contractions
- Consists of a linear chain of interconnecting neurons
- Extends the entire length of the G.I. tract
- Mostly excitatory (Ach/NO)
- some inhibitory signals may inhibit intestinal sphincter muscles
- Effects
- Increased tonic contraction of gut wall
- increased intensity of rhythmical contractions
- slightly increased rate of rhythmical contraction
- increased velocity of excitatory waves
- Meissner’s (Submucosal) Plexus
- Controls mainly GI secretion, absorption and local blood flow
- Mainly concerned with controlling function within inner wall of each minute segment of the intestine
- Helps in control of local secretion, local absorption, and local contraction of submucosal muscle
Compare the effects of parasympathetic stimulation and sympathetic stimulation
- Parasympathetic system generally increases GI tract activity
- Sympathetic system generally decreases GI tract activity
Compare propulsive movements to mixing (segmentation) movements
- Propulsive movements
- Stimulation at any point in the gut can cause a contractile ring to occur
- Contractile ring moves forward after it appears
- usually stimulus is distension
- Stimulus 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
- Enterochromaffin cells in intestine sense food and release serotonin
- serotonin binds to receptors on primary afferent neurons, initiating peristaltic reflex
- Mixing (segmental) movements
- Mix intestinal contents by sending chyme in both directions without a net forward movement
- may be caused by peristaltic contractions themselves
- at other times local intermittent constrictive contractions occur every few centimeters in the gut wall
Describe and differentiate between slow contraction waves and spike potentials
- Slow contraction waves
- are not action potentials
- slow waves are slow, oscillating potentials inherent to the smooth muscle itself in some parts of the digestive tract
- slow waves occur spontaneously
- Slow waves orginate in intestinal cells of Cajal (pacemakers)
- Intesnity varies between 5 and 15 mV
- Frequency ranges form 3 to 12 per minute (increases form stomach to duodenum)
- slow waves set the maximum frequency of contraction for each part of the GI tract
- May be caused by complex interactions among the smooth muscle cells and the interstitial cells of Cajal (smooth muslce cell electrical pacemakers)
- cells of Cajal undergo cyclic changes that periodically open and produce inward (pacemaker) crrents that may generate slow wave activity
- Slow waves excite the appearance of intermittent spike potentials
- Spike potentials excite muscle contraction
- Spike Potentials
- Are true action potentials
- occur automatically when resting membrane potential of GI smooth muscle becomes more positive than -40mV
- 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 (10-20ms)
- Spike potentials are responsible for opening calcium channels and smaller number of sodium channels in GI smooth muscle cells
- Channels open slowly and close rapidly
List factors that cause hyperpolarization and depolarization
- Factors that cause hyperpolarization
- Norepinephrine and epinephrine
- Stimulation of sympathetic nerves
- Factors that cause depolarization
- Stretching of muscle
- Stimulation by acetylcholine (parasympathetic)
- Stimulation by specific GI hormones
List causes of tonic contraction
- Continuous repetitive spike potentials
- Hormones
- Continuous entry of calcium ions
List the three kinds of gastrointestinal reflexes and give examples
- Reflexes that are integrated entirely within the gut wall enteric nervous system
- Much of the GI secretion
- Peristalsis
- Mixing contractions
- Local inhibitory effects
- Reflexes from the gut to the prevertebral sympathetic ganglia and then back to the GI tract
- transmit signals long distance to other areas of the gut tract
- Cause evacuation of the colon (gastrocolic reflex)
- Inhibit stomach motility and secretion (enterogastric reflex)
- empty ileal contents into the colon (colonoileal reflex)
- Reflexes from the gut to the spinal cord or brain stem and then back to the GI tract
- Reflexes from the stomach and duodenum to brain stem and back to the stomach control gastric motor and secretory activity
- Pain reflexes cause general inhibition of the entire GI tract
- Defecation reflexes from the colon to the rectum to the spinal cord and back
Stimulus for secretion, site of secretion, target, and action of Gastrin
- Stimulus for secretion
- Small peptides and amino acids in stomach lumen, especialy phenylalanine and tryptophan
- Distension of stomach
- Vagal Stimulation mediated by GRP (gastrin-releasing peptide)
- Inhibition of secretion
- Acid from stomach
- Somatostatin
- Site of secretion
- Secreted from G cells of antrum, duodenum, jejunum (in response to stimuli associated with ingestion of a meal (i.e., stomach distension or gastrin releasing peptide))
- Actions
- Stimulates gastric acid secretion by parietal cells
- Stimulates mucosal growth by stimulating synthesis of RNA and new protein
- Pathology
- Patients with gastrin-secreting tumors have hypertrophy and hyperplasia of gastric mucosa
- Zollinger-Ellison syndrome occurs from gastrin-secreting non-beta cell tumors of pancreas
Stimulus for secretion, site of secretion, target, and action of CCK (cholecystokinin)
- Stimulus for secretion
- Small peptides and amino acids
- Fatty acids and monoglycerides
- (note triglycerides cannot cross intestinal cell membranes and do not stimulate release of CCK)
- Site of secretion
- I cells of duodenum, jejunum, and ileum
- Actions
- Stimulates pancreatic enzyme secretion
- Stimulates pancreatic bicarbonate secretion
- Stimulates growth of exocrine pancreas
- Inhibits gastric emptying
- Inhibits appetite
- Stimulates contraction of gallbladder and relaxation of sphincter of Oddi for secretion of bile
Stimulus for secretion, site of secretion, target, and action of Secretin
- Stimulus for secretion
- Acid and fat in lumen of duodenum
- Site of secretion
- S cells of the duodenum, jejunum, and ileum
- Actions
- Stimulates pepsin secretion
- stimulates pancreatic bicarbonate secretion
- stimulates biliary bicarbonate secretion
- stimulates growth of exocrine pancreas
- inhibits gastric acid secretion by parietal cells
Stimulus for secretion, site of secretion, target, and action of Gastric inhibitory Peptide (GIP)
- Stimulus for secretion
- Only GI hormone released in response to protein, fat, and carbohydrates
- Released in response to orally administered glucose
- Site of Secretion
- K cells of duodenum and jejunum
- Actions
- stimulates insulin release
- Inhibits gastric acid secretion by parietal cells
Stimulus for secretion, site of secretion, target, and action of Motilin
- Stimulus for secretion
- Fat, acid, nerve action
- Site of secretion
- M cells of duodenum and jejunum
- Actions
- Stimulates gastric and intestinal motility
- secreted during fasting
What are the four official GI hormones
- Gastrin
- CCK
- Secretin
- Gastric Inhibitory Peptide (GIP)
- Trace the formation and destination of the portal vein
- What does it transport?
- All the blood that courses through the gu, spleen, andpancreas flows immediately into the liver by way of the portal vein. In the liver, the blood passes through millions of minute liver sinusoids and finally leaves the liver by way of hepatic veins that empty into the vena caa of the general circulationthis flow allows reticuloendothelial cells that line the liver sinusoids to remove bacteria and other particulate matter that might enter the blood from the GI tract
- The nonfat, water-soluble nutrients absorbed from the gut (such as carbohydrates and proteins) are transported in the portal venous blood to the same liver sinusoids.