ICL 2.4: Physiology of the GI Tract Flashcards
(74 cards)
1
Q
what does the GI system consist of?
A
- GI tract
2. accessory exocrine glands
2
Q
what are the parts of the GI tract?
A
- the mouth
- esophagus
- stomach
- small intestine
- large intestine
3
Q
what are the major accessory glands in the GI system?
A
- salivary glands
- liver
- gall baldder
- pancreas
4
Q
what are the salivary glands in the mouth?
A
- parotid
- submandibular
- sublingual
submandibular and sublingual glands both empty saliva into the floor of the mouth through small ducts
5
Q
what is the function of saliva?
A
- lubrication of oral cavity
- thermal and chemical insulation
- chewing
- swallowing
- antimicrobial activity
6
Q
what is saliva composed of?
A
- salivary amylase
- lingual lipase
- lysozyme and antibodies
- mucins
- bicarbonate
- water
7
Q
what is the function of salivary amylase?
A
begins starch digestion
but it’s inactivated by low pH of stomach so there’s not much digestive function
8
Q
what’s the function of lingual lipase?
A
triglyceride digestion
important in babies
9
Q
what’s the function of lysozyme and antibodies in saliva?
A
antimicrobials
10
Q
what’s the function of mucins in saliva?
A
lubrication
11
Q
what is the function of water in saliva?
A
- facilitates taste and dissolution of nutrients
- aids in swallowing
- speech
12
Q
what type of solution is saliva?
A
saliva secreted by acinar cells is isotonic so it’s the same osmolality as plasma
but as it passes though the intercalated ducts, ductal cells reabsorb Na+ and Cl- it becomes hypotonic compared to plasma by the time it’s secreted into your mouth
there’s also an HCO3/Cl exchanger that’s balancing out all the (+) ions being absorbed
13
Q
what part of the nervous system controls the salivary glands?
A
autonomic nervous system
sympathetic stimulation is less important –> when stimulated, decreased saliva production by acinar cells and decreased blood flow to the glands
parasympathetic stimulation –> mediated by muscarinic M3 receptors and when they’re stimulated, it leads to the release ofacetylcholineonto (M)3muscarinic receptors resulting in:
- acinar cellsincrease secretion of saliva
- duct cells increase HCO3–secretion
- increased blood flow to the salivary glands
- increased rate of expulsion of saliva
overall, increased parasympathetic stimulation results in an increased flow of saliva that is more watery in composition
14
Q
what is the esophagus?
A
a relaxed structure that transfers food from mouth to stomach –> pressure in the esophagus is low which helps because stuff moves from high to low pressure!
movement of materials aided by gravity, but depends onperistalsis –> this is why when you’re hanging upside down your food doesn’t fall out
there are sphincters at bond ends which cooperate in the act of swallowing, ordeglutition and prevent backflow of gastric contents
retrograde movement is only seen during belching and vomiting
15
Q
which structures serve as antireflux barriers?
A
- upper esophageal sphincter (UES)
2. lower esophageal sphincter (LES)
16
Q
what is the upper esophageal sphincter?
A
aka inferior pharyngeal sphincter
it’s located at the lower end of pharynx and guards the entrance into the esophagus
it’s composed of striated skeletal muscles
exhibits tone and contracts due to the excitatory nerves
it relaxes with swallowing andwith Transient LES relaxation (TLESR)
17
Q
what are the 2 major functions of the upper esophageal sphincter?
A
- to prevent air from entering into the esophagus during breathing
- to prevent reflux of esophageal contents into the pharynx to guard airway aspiration
18
Q
what is the lower esophageal sphincter?
A
it’s composed of smooth muscles and maintains tonic contraction unless otherwise stimulated to relax
it functions as an antireflux barrier protecting the esophagus from the caustic gastric content
during swallowing or belching, the LES muscle must relax briefly to allow passage of food or air- “transient lower esophageal sphincter relaxation” (TLESR)
19
Q
when does the lower esophageal sphincter relax?
A
it relaxes due to vagal nerve mediated inhibition (involving NO)
also when the LES opens, so does the UES! that’s why you’re able to belch
20
Q
what is esophageal achalasia?
A
loss of inhibitory mechanisms of lower esophageal sphincter
relaxation doesn’t happen so the food can’t move past the LES
21
Q
what is GERD?
A
increased frequency of transient lower esophageal sphincter relaxation (TLESR)
gastric contents reach the esophagus!
22
Q
what is the function of the stomach?
A
food breakdown!
23
Q
what are the only 2 things absorbed in the stomach?
A
- alcohol
2. aspirin
24
Q
what regulates gastric juice in the stomach?
A
gastric juice is regulated by neural and hormonal factors
the presence of food or rising pH causes the release of the hormone gastrin
gastrin increases the secretion of protein-digesting enzymes, mucus, and HCl
acidic pH allows for protein digestion and creates a hostile environment for microorganisms
25
what are the 2 types of tubular glands in the stomach mucosa?
1. oxyntic
| 2. pyloric
26
what are oxyntic tubular glands?
they are one of the two types of tubular glands in the stomach mucosa
they are acid-forming glands on the inside surfaces of the body and fundus of the stomach—> proximal 80% of the stomach
they secrete HCl, pepsinogen, intrinsic factor, and mucus
27
what are pyloric tubular glands?
they are one of the two types of tubular glands in the stomach mucosa
they are glands located in the antral portion of the stomach—> distal 20% of the stomach
they secrete mucus and the hormone gastrin
28
what are oxyntic glands composed of?
1. mucous neck cells, which secrete mucus;
2. peptic (or chief) cells, which secrete pepsinogen
3. parietal (or oxyntic) cells, which secrete hydrochloric acid and intrinsic factor
29
what do parietal cells secrete and what's the function of the secretion?
HCl and intrinsic factor
1. kills microbes and activates pepsinogen
2. binds vitamin B12 to allow for its absorption
30
what do chief cells secrete and what's the function of the secretion?
pepsinogen and gastric lipase
1. protein digestion
2. fat digestions
31
what do G cells secrete and what's the function of the secretion?
gastrin
stimulates gastric acid secretion
32
what do ECL cells secrete and what's the function of the secretion?
histamine
stimulates gastric acid secretion
33
what do muscus-neck cells secrete and what's the function of the secretion?
mucus and bicarbonate
protects stomach epithelium from acid
34
what do D cells secrete and what's the function of the secretion?
somatostatin
inhibits gastric acid secretion
35
what are the 3 basic factors that stimulate gastric secretion?
1. acetylcholine
2. gastrinc
3. histamine
36
how does acetylcholine stimulate gastric secretion?
ACh is released by parasympathetic stimulation via the vagus nerve
it excites secretion of pepsinogen by chief cells, HCl by parietal cells, and mucus by mucous cells
37
how does gastrin stimulate gastric secretion?
it's released by G cells in response to:
1. distention of the stomach
2. the products of proteins
3. gastrin releasing peptide (GRP) released by the nerves of the gastric mucosa during vagal stimulation
gastrin and histamine strongly stimulate parietal cells (secretion of acid) with very little effect on other cells
38
how does histamine stimulate gastric secretion?
it's released by ECL cells in response to acetylcholine and gastrin
gastrin and histamine strongly stimulate parietal cells (secretion of acid) with very little effect on other cells
39
what stimulates acid secretion in the GI system?
1. gastrin, secreted by gastrin cells (G cells) located in the pyloric glands, is transported to the ECL cells by vigorous mixing of gastric juices
2. gastrin binds to its receptors (CCKb) and causes release of histamine
vagus nerve also stimulates histamine secretion through acetylcholine binding to muscarinic acid (M3) receptors
3. the gastrin, acetyl choline and histamine then acts quickly to directly stimulate gastric HCl secretion via the parietal cells
rate of HCl secretion is directly related to the amount of histamine secreted
40
what is the pH of an empty stomach?
2
41
what are the steps in stimulation of acid secretion?
distention of the stomach by food --> local ENS reflexes and vasovagal reflexes stimulated --> ACh and GRP --> G cell releases gastrin, ACh stimulates ECL cell to release histamine --> gastrin stimulates ECL cell to release histamine which then stimulates parietal cell and gastrin also directly stimulates parietal cell to secrete HCl
42
what is the mechanism of HCl secretion including the transporters?
the key player is the H+/K+ ATPase or "proton pump" located in the cannalicular membrane
H+ ions are generated within the parietal cell from dissociation of water. The OH- ions rapidly combine with CO2 to form HCO3- ion, cataylzed by carbonic anhydrase
HCO3- is transported out of the basolateral membrane in exchange for Cl-
the outflow of HCO3- into blood results in a slight elevation of blood pH known as the "alkaline tide". This process serves to maintain intracellular pH in the parietal cell
Cl- and K+ ions are transported into the lumen of the cannaliculus
H+ ion is pumped out of the cell, into the lumen, in exchange for K+ through the action of the proton pump; K+ is thus recycled
accumulation of H+ ion in the cannaliculus generates an osmotic gradient across the membrane that results in outward diffusion of water
43
how is acid secretion controlled by gastrin and ACh?
gastrin binding to CCKb receptor and ACh binds to M3 receptors
this activates G protein coupled receptors (GPCR) by binding to Gq subunit resulting in Ca2+ release from ER and PKC mediated signaling
PKC and Ca+2 lead to the activation of the H/K ATPase pump that pumps H+ out and K+ in
44
how is acid secretion controlled by histamine?
histamine binds to H2 receptors
this activate GPCR by binding to Gs subunit leading to the activation of adenylate cyclase and increasing cAMP-PKA mediated signaling
PKA leads to the activation of the H/K ATPase pump that pumps H+ out and K+ in
45
how is acid secretion controlled by somatostatin and prostaglandins?
somatostatin and prostaglandins bind to their respective receptors
this activates GPCR by binding to the Gi subunit and inhibiting cAMP-PKA pathway
this inhibits acid secretion
46
which drugs target acid secretion?
1. atropine
2. cimetidine
3. omeprazole
47
how does atropine effect acid secretion?
atropine blocks M3 receptors so that means ACh can't activate the Gq pathway to increase IP3/Ca+2 and activate the H/K ATPase pump
48
how does cimetidine effect acid secretion?
cimetidine blocks histamine binding to H2 receptors which decreases Gs activation --> this means there isn't increased cAMP to activate the H/K ATPase pump and therefore decreases H+ secretion
49
how does omeprazole effect acid secretion?
omeprazole blocks the H/K ATPase pump so H+ isn't secreted
50
what is the function of surface mucous cells in the stomach?
surface mucous cells secrete mucus that coats the stomach mucosa with a gel layer of mucus (> 1 mm thick) which provides:
1. protection for the stomach wall
2. lubrication of food transport
mucus is alkaline protecting stomach wall from the highly acidic, proteolytic stomach secretion --> the slightest contact with food or any irritation of the mucosa directly stimulates additional secretion of thick viscous mucus
51
what is the gastric diffusion barrier?
the gastric mucosal barrier enables the stomach to contain acid without injuring itself
the luminal membranes of the gastric mucosal cells are impermeable to H+ so that HCl cannot penetrate into the cells due to tight junctions --> a mucosa coating over the gastric mucosa offers further protection
the mucus gell is embedded with HCO3 which diffuses out into the stomach lining and combines with H+ to neutralize it
52
how/when is pepsin secreted?
pepsinogen is activated to form active pepsin in contact with HCl --> pepsinogen is secreted by chief cells in gastric pits
pepsin autocatalytically sustains the cascade in the absence of acid at pH < 3.5
pepsin is most active at pH 2 to 3, and activity declines as acidity diminishes
pepsin digests up to 10% of protein in the diet at acid pH
53
what is the function of intrinsic factor? which cells secrete it?
it's essential for vitamin B12 absorption in the ileum
it's secreted by the parietal cells
54
what is pernicious anemia?
when the parietal cells of the stomach that secrete intrinsic factor are destroyed (chronic gastritis), pernicious anemia often develops
this is due to the failure of red blood cell maturation in the absence of stimulation of the bone marrow by vitamin B12
intrinsic factor is essential for vitamin B12 absorption in the ileum
55
what are the 3 phases of gastric secretion?
1. cephalic phase
30% of the gastric secretion; results from sight, smell, thought or taste of food via the vagus which leads to parasympathetic pepsin and acid production
2. gastric phase
60% of the total gastric secretion due to local nervous secretory reflexes, vagal reflexes, and gastrin-histamine stimulation
3. intestinal phase
10% of the acid response to a meal and occurs via nervous and hormonal mechanisms when there is presence of food in the upper portion of the small intestine, particularly in the duodenum
56
how is gastric secretion inhibited?
intestinal chyme slightly stimulates gastric secretion during the early intestinal phase but inhibits gastric secretion at other times
this inhibitor effect is mediated by:
1. reverse enterogastric reflex
2. secretin
3. other hormones (slight to moderate effects) = glucose-dependent insulinotropic peptide (gastric inhibitory peptide), vasoactive intestinal polypeptide, somatostatin
57
what is the reverse enterogastric reflex?
it inhibits gastric secretion and is initiated by:
1. distension of the small bowel
2. presence of acid in the upper intestine
3. presence of protein breakdown products
4. irritation of the mucosa
58
how does secretin effect gastric secretion?
it inhibits gastric secretion and is released by the presence of:
1. acid, fat, protein breakdown products
2. hyperosmotic or hypo-osmotic fluids
3. any irritating factor in the upper small intestine
59
what are the stimulatory and inhibitor events involving gastric secretion during the cephalic phase?
STIMULATORY
1. sight and thought of food --> cerebral cortex --> conditioned reflex activates hypothalamus and medulla oblongata --> vagus nerve --> stomach secretion
2. stimulation of taste and smell receptors --> hypothalamus and medulla oblongata --> vagus nerve --> stomach secretion
INHIBITORY
loss of appetite depression --> cerebral cortex --> lack of stimulatory impulses to parasympathetic center
60
what are the stimulatory and inhibitor events involving gastric secretion during the gastric phase?
STIMULATORY
1. stomach distention activates stretch receptors --> local reflexes activate stomach secretory activity but also vasovagal reflexes activate the medulla then the vagus nerve which also activates stomach secretory activity
2. food chemicals and rising pH activate chemoreceptors --> G cells release gastrin into the blood which activates stomach secretory activity
INHIBITORY
1. excessive acidity <3 in the stomach leads to inhibition of the G cells so gastrin secretion declines and also does stomach secretory activity
2. emotional upset activates the SNS which overrides parasympathetic controls and decreases stomach secretory activity
61
what are the stimulatory and inhibitor events involving gastric secretion during the intestinal phase?
STIMULATORY
1. presence of low pH and partially digested foods in the duodenum when stomach begins to empty activates intestinal gastrin release into the blood which leads to stomach secretory activity
INHIBITORY
1. distention of the duodenum, presence of fatty, acidic, hypertonic, chyme and/or irritants in the duodenum leads to inhibition of local reflexes, vagal nuclei in the medulla and the pyloric sphincter which activates the enterogastric reflex which inhibits stomach secretory activity
2. distention, presence of fatty, acidic, partially digested food i the duodenum leads to release of intestinal hormones like secretin, gastric inhibitor peptide, cholecystokinin, vasoactive intestinal peptide which inhibit stomach secretory activity
62
what happens to gastric secretion during the interdigestive period?
composed mainly of mucus but little pepsin and almost no acid
may be increased by emotional stimuli (highly peptic and acidic)
believed to contribute to the development of peptic ulcers
63
other than gastric acid production, what are the other functions of the stomach?
1. storage = retention and slow delivery of food particles to the duodenum
2. signaling = delivers important information to downstream segments
3. motor functions = mechanical break down of ingested food
4. motility = distinct functions during the fasted state known as the migrating motor complex or MMC
64
what is the migrating motor complex?
the MMC removes undigested material or ingested foreign objects
it's mediated by motion
65
what are the motor functions of the stomach?
grinding is the most vigorous peristalsis and mixing action and occurs close to the pylorus aka end of the stomach
waves of peristalsis occur from the fundus to the pylorus forcing food past the pyloric sphincter
the pyloric end of the stomach acts as a pump that delivers small amounts of chyme into the duodenum
66
what are the 2 types of electrical activity in the GI smooth muscle?
1. slow waves
rhythmic and continuous variations in the smooth muscle action potential but they're not actually AP themselves; Interstitial cells of cajal are the pacemakers --> not regulated by hormonal or neural signals
2. spike potentials
true action potentials that appear at the peak of slow waves --> regulated by hormonal or neural signals
67
what are mixing waves?
weak peristaltic waves in the mid to upper portion of the stomach that are initiated by the "slow waves" in the stomach wall
they occur every 15-20 seconds
68
what are peristaltic action potential-driven constrictor rings?
intense, powerful waves in response to a stimuli
they force astral contents under high pressure towards the pylorus
69
what is retropulsion?
as the peristaltic wave reaches pylorus, the pyloric muscle contracts and most of the antral contents are squeezed upstream toward the body of the stomach
aka they go backwards
70
what is responsible for gastric emptying?
the pyloric pump!!
it causes intense strong astral peristaltic contractions that begin in the mid stomach and spread through the caudad stomach
it's regulated by signals from both the stomach and duodenum but the duodenum provides more potent signals
71
what are the steps of gastric emptying?
1. a peristaltic contraction originates in the upper funds and sweep down towards the pyloric sphincter
2. the contraction becomes more vigorous as it reaches the thick muscled antrum
3. the strong astral peristaltic contraction propels the chyme forward
4. a small portion of chyme is pushed through the partially open sphincter into the duodenum -- the stronger the astral contraction, the more chyme is emptied with each contractile wave
GASTRIC MIXING
5. when the peristaltic contraction reaches the pyloric sphincter, the sphincter is tightly closed and no further emptying takes place
6. when chyme that was being propelled forward hits the closed sphincter it's tossed back into the antrum -- mixing of chyme is accomplished as chyme is propelled forward and tossed back into the antrum with each peristaltic contraction
72
what factors promote gastric emptying?
1. food volume
increased food volume in the stomach stretches the stomach wall and increases the activity of the pyloric pump and at the same time inhibit the pylorus
2. hormone gastrin
gastrin also has mild to moderate stimulatory effects on motor functions; it enhance the activity of the pyloric pump
73
what duodenal factors inhibit stomach emptying?
1. enterogastric nervous reflex
2. hormonal feedback
cholecystokinin (CCK), secretin and glucose-dependent insulinotropic peptide aka gastric inhibitory peptide (GIP)
74
what is the enterogastric nervous reflex?
it inhibits the “pyloric pump” propulsive contractions, and increases the tone of the pyloric sphincter
it's activated by:
1. distention of the duodenum
2. presence of any irritation of the duodenal mucosa
3. acidity of the duodenal chyme
4. osmolality of the chyme
5. presence of breakdown products of proteins and fats in the chyme
