GI Physiology Flashcards
1
Q
What is the splanchnic blood system?
A
from heart through abdominal organs back to heart
2
Q
What things increase blood flow during increase GI activity?
A
effect of gut activity and metabolic factors; release of dilator substance (CCK, VIP, gastrin, secretin), release of kinins (bradykinin-dilator peptide), decreased oxygen concentration in the gut wall (adenosine); more sensitive to ischemia than other tissues
3
Q
What is the use of the countercurrent blood flow in the villi? complications from this?
A
blood can be shunted from one side to the other bypassing some tissue during exercise or shock; short term cells will die and be replace by stem cells; long term leads to necrosis and then sepsis
4
Q
How does the neural system control blood flow through the GI?
A
PS- stomach, SI, LI, increases blood flow and glandular secretions; Symp- direct effect on entire GI via intense vasoconstriction of arterioles and reduction of flow
5
Q
What are the 4 main systems controlling splanchnic circulation?
A
autonimics (PS, S, enteric, and sensory), cardiovascular (CO, art press, BV), Digestive system control (vasodilator metabolites and paracrines, local mech- myogenic, posprandial hyperemia, O2 countercurrent) and endocrine and paracrine control (vasoconstrictor and GI hormones, immunologic paracrines)
6
Q
What are the five distinct functions of the GI tract?
A
secretion, motility, digestion, absorption, immunity
7
Q
What role does the GI system play in immunity?
A
largest area of the body with direct contact with infectious/toxic substances, 80% immunoglobulin producing cells are in the SI; also have acid, mucous and motility to protect
8
Q
What are the sphincters under total CNS control?
A
upper and lower esophageal sphincter, ileocecal and anal
9
Q
Which sphincters are under minimal CNS control?
A
pyloric and oddi
10
Q
What is the swallowing reflex?
A
UES opens due to pressure generated by bolus of food pushed back followed by peristaltic waves of relaxation and contraction
11
Q
What is the function of the LES?
A
prevent stomach acid and contents from entering the esophagus
12
Q
What is GERD?
A
failure of LES to contract following ingestion, heartburn feeling due to stomach contraction pushing stomach contents into the esophagus, antihistamines can be used to reduce acid (H2 receptor antagonist) or proton pump inhibitor (H-K-ATPase)
13
Q
What is achalasia?
A
absence of relaxation of LES or impaired peristalsis in distal esophagus; probly loss of Vagal inhibitory
14
Q
What is the function of the pyloric valve?
A
regulates movement of chime from stomach into small intestine to ensure adequate digestion
15
Q
What is the function of the sphincter of oddi? What mechanism causes it to open?
A
guards exit of common bile duct and pancreatic duct; CCK produces contraction of gall bladder driving bile down the duct; when chime enters the duodenum, this sphincter prevents chime from entering the ducts
16
Q
What is the function of the internal anal sphincter?
A
circular and longitudinal smooth muscle under involuntary control; prevent movement of fecal matter through anus unless external anal sphincter is relaxed; forced open by pressure
17
Q
What is the function of the external anal sphincter?
A
Encircles rectum, contains only striated muscle, under voluntary control; pelvic cholinergic nerves cause tonic contraction to hold everything in
18
Q
What is the general function of the myenteric plexus?
A
controls GI movements
19
Q
What are the two divisions of the enteric nervous system?
A
submucosal plexus (meissner’s) and myenteric plexus (auerbachs)
20
Q
What is BER?
A
basic electrical rhythm; cycling of RMP from -60 to -40 to -60 etc.
21
Q
What stimuli cause depolarization in the enteric NS
A
stretch, ACh, PS
22
Q
What stimuli cause hyperpolarization of the enteric NS?
A
noradrenaline, sympathetics
23
Q
Where is the myenteric plexus located? main type of neurons found there?
A
between circular and longitudinal muscle layers, most are motor neurons
24
Q
What is the excitatory role of the myenteric plexus?
A
control movement of GI tract; when stimulated it increases intensity of rhythmic contractions, increases rate of rhythmic contractions, increases velocity of conduction of excitatory waves along the gut wall (more peristalsis); motor excitatory neurons release ACh and substance P onto smooth muscle receptors
25
What is the inhibitory role of the myenteric plexus?
some neurons secrete VIP and NO that inhibit contraction of GI smooth muscle, inhibit movements of GI tract
26
Where is the submucosal plexus found? What do most of the neurons do?
in submucosal layer; regulate glandular, endocrine and epithelial cell secretion and GI blood flow, mostly sensory, release Ach onto glandular or epithelial cells to stimulate secretion; receives signals from epithelium and stretch receptors
27
Where do chemo and stretch receptors in the GI epithelium synapse to ?
enteric system, prevertebral ganglia, spinal cord and brain
28
What PS nerves affect the enteric NS?
pelvic (just myenteric) and vagus (myenteric, submucosal and epithelial cells)
29
What are the different types of neurons in the myenteric plexus and their corresponding NT?
stimulatory motor-ACh, inhibitory motor-NO, Ascending and descending interneurons-ACh, 5-HT, and sensory neurons- substance P
30
What are the different types of neurons in the submucosal plexus and their corresponding NT?
noncholinergic secretomotor- VIP, cholinergic secretomotor- ACh, sensory neurons- substance P (small peptide, pain and vasodilator)
31
What are the localized GI reflexes?
entirely in the enteric NS, GI secretions, peristalsis, and mixing, intrinsic, travel short distances and distention is the usual stimulus
32
What is the gastrocolic reflec?
from stomach(during emptying of stomach after ingestion of meal) to colon in order to evacuate the colon; probly mediated by gastrin; well developed in infants
33
What is the enterogastric reflex?
from colon or SI to stomach, inhibit gastric motility and secretions, release of gastrin is shut off; probably stimulated by acid in the duodenum
34
what is the colonoileal reflex?
from colon to ileum, inhibit contents at ileocecal valve from emptying into the colon
35
What systems act on the extrinsic reflexes of the GI?
components contained within GI, can be modulated by extrinsic factors
36
What are some general features of neurohormonal regulation of the GI tract?
mediated by peptides, amino acid derivatives, lipids and steroids; GI hormones are peptides but not all peptides are hormones; mediators have both membrane and intracellular targets, intricate and redundant, crosstalk between systems allow for integrated regulation
37
What methods of signaling are used in neurohormonal control of the GI?
endocrine, paracrine, neurocrine, immune/juxtacrine
38
What 4 things establish the existence of GI hormones?
event in one segment alters activity of another (except autocrine), effect persists after neural connections have been severed (except neurocrine), capable of reproducing the effect if injected into the blood (must be isolated from site of stimulation), hormone must be id chemically and structure confirmed by synthesis
39
What is the source, stimuli for release and main action of gastrin?
G cells (somach, prox SI), peptides, AA, neural (GRP, vagal), stretch, inhibited by acid; increases HCl secretion, parietal cell growth (make pepsin and enzymes)
40
What is the source, stimuli for release and main action of CCK?
CCK cells (I cells) duodenum and jejunum; CCK-RP, fatty acid, AA, neural; pancreatic enzyme secretion, gallbladder contraction, pancreatic growth, inhibits gastric motility
41
What is the source, stimuli for release and main action of secretin?
S cells in duodenum and jejunum; luminal pH <4 and FA; ductal secretion in pancreas (HCO3) and bile ducts, pancreatic growth, inhibits acid secretion; more potent than CCK
42
What is the source, stimuli for release and main action of somatostatin?
D cells, nerves; fat, protein, low pH; decreases acid, enzyme secretion and inhibits gastrin
43
What are the endocrine mediators involved in response to meal?
CCK, gastrin, GIP, pancreatic polypeptide
44
What are the neurpcrine mediators involved in response to meal?
ACh, CCK, GRP (gastrin releasing peptide), NO, Substance P, VIP, 5-hydroxytryptamine
45
What are the paracrine mediators involved in response to meal?
CCK, Histamine, 5-hydroxytryptamine, somatostatin
46
What are the two CCK receptor types? What do they bind with?
CCK A just CCK; CCK B (smaller binding site, gastrin 2 sites and CCK
47
What are some general feature of the secretin family?
peptides with structural homology to secretin (VIP, glucagon, GIP; effects presumably mediated via cAMP or similar signaling system
48
what does GIP do?
stimulates insulin release, inhibits acid secretion
49
What does motilin do?
stimulates gastric and intestinal motility
50
What are the general structural features of CCK/gastrin family?
peptides, particularly similar at C termini; amidated C termini- protect against carboypeptidase activity
51
Where is gastrin secreted in GI tract? Where doe it taper off and where is it last found?
antrum of stomach, duodenum, jejunum
52
Where is CCK secreted in GI tract? Where doe it taper off and where is it last found?
duodenum, ileum, ileum
53
Where is secretin secreted in GI tract? Where doe it taper off and where is it last found?
duodenum, jejunum, ileum
54
Where is GIP secreted in GI tract? Where is it last found?
duodenum, jejunum
55
Where is motilin secreted in GI tract? Where is it last found?
duodenum, jejunum
56
What factors stimulate GIP secretion?
FA and glucose
57
What factor stimulate motilin secretion? inhibit?
neural; protein/AA, FA, glucose
58
What are the major contributors to neurocrine? function?
VIP, NO-relaxation of smooth muscle; ACh- multi stimulatory, mediate vagal and vagovagal effects; GRP- increases gastrin release; ekephalins- increased smooth muscle tone, slow transit
59
What percent of GI secretions are excreted?
1%
60
What are the functions of chewing and salivary secretions?
food in smaller particles, formation of bolus, initiation of starch (lipid?) digestion, facilitation of taste, cleansing of mouth and selective antibac action, clearance and neutralization of refluxed gastric acid, regulation of food intake and eating behavior, aids in speech
61
What transporters are active in the salivary ductal cells? what disease affects which transporter? What is the product?
NA reabsorption- ENaC, NHE; HCO3 excretion via CL exchange, K secretion via K/H exchange, CFTR channel secreting CL; CFTR affected in cystic fibrosis; hypotonic KHCO3 rich and NaCl poor
62
How is the flow rate of saliva and the rate of Na reabsorption related?
as flow rate increases, NA reabsorption rate increases
63
What are the organic constituents of saliva ?
mucins, amylase, lipase, lysozyme, IgA, nerve growth factor, epidermal growth factor
64
What things are affected by PS and Symp input on salivary glands?
secretion, vasodilation, myoepithelial contraction, metabolism, growth
65
How does the sympathetic system act on the salivary gland? (source, mediator, cell signaling)
superior cervical gang, norepi, cAMP
66
How does the parasympathetic system act on the salivary gland? (source, mediator, cell signaling)
savilary nucleus of the medulla, ACh, M3 muscarinic receptor, Ca2+
67
What things have a negative effect on salivary nucleus of medulla (PS)?
fatigue, sleep, fear, dehydration
68
What things have a positive effect on salivary nucleus of medulla (PS)?
condition reflexes, smell, taste, pressure, nausea
69
What is the make up and function of esophageal secretions?
entirely mucus, provide lubrication for swallowing and protection from acid that might enter lower part
70
What are the components of the gastric secretions?
main: HCl, pepsin, mucus, intrinsic factor and bicarbonate ion
71
What is the make up of LES/cardia secretions?and function of the region
mucus and HCO3; prevention of reflux, entry of food, regulation of belching
72
What is the make up of fundus and body secretions? and function of region?
H+, intrinsic factor, mucus, HCO3, pepsinogens, lipase; resvoir, tonic force during emptying
73
What is the make up of fundus and body secretions? and function of region?
mucus, HCO3; mixing, grinding, sieving, regulation of emptying
74
What are the phases of gastric acid secretion?
cephalic (anticipatory effect), gastric (food enters), intestinal (some movement into intestine, but some remains)
75
What are the vagal effects on GI responses during the cephalic phase?
DVC receives stimulus (anticipation, smell, sight, taste);motor- relaxation of stomach smooth muscle and oddi, contracton of Gallbladder; secretory: HCl, pepsinogen, intrinsic factor, gastrin, pancreatic enzymes
76
Gastric distention triggers what responses mediated by the vago-vagal reflexes?
DVC receives distention stimuli, causes receptive relaxation, acid secretion, pepsinogen secretion, antral contraction, gastrin secretion and via protein break down by pepsin to oligopeptides (feeds back to stimulate parietal and chief cells, intrinsic neural path), pancreatic enzyme secretion, sphincter oddi relaxation
77
what stimulates the parietal cell? to secrete what?
neuron releases GRP on G cell which secretes gastrin travels via blood and stimulates parietal cell and stimulates ECL cell which releases histamine paracrine through lamina propria stimulation of parietal cell; neuron releases ACh on ECL stimulating histamine signal and ACh directly stimulate parietal cell which secretes HCl
78
What cellular transporters are involved in the parietal cells secretion of H+?
apical: CL channel, and H/K ATPase; basal side: HCO3/Cl (HCO3 to IS) CO2 diffusion in and reaction with H2O via carbonic anhydrase
79
What are all the mediators that stimulate parietal secretion of HCl? inhibit?
stimulate: gastrin, ACh, Ca, Histamine, inhibit: Somatostatin, Prostaglandins
80
What is the makeup of the pancreatic secretions and from which cells?
digestive enzymes in proenzymes form from acini; HCO3 from ductal cells
81
What are the different enzymes secreted by the pancreatic ancinar cells? category?
Proteases: trypsinogen, chyotrypsinogen, proelstase, procarboxypeptidase A and B; Amylolytic enzyme: amylase; Lipase: Lipase, lipase related proteins, non-specific sterase; Nucleases: deoxyribonuclease, ribonuclease; Other: procolipase, trypsin inhibitors, monitor peptide
82
What method is used by pancreatic acini to secrete and what is it dependent on?
vesicular, Ca->calmodulin->degranulation
83
What medators effect the ductal cell secretion? acini?
ACh and secretin; ACh, CCK, GRP, VIP
84
What factors effect the pH in the duodenum?
H+ from stomach, H+ absorption, HCO3 secretion from pancreatic ductal cells and in bile, dietary buffer: protein, peptides, FA
85
WHat is the method for HCO3 secretion?
apical HCO3/Cl exchange, CFTR; basal, HCO3/NA cotransport, CO2 and H2O (CA in cell to make HCO3) secretin most powerful stimulus start cAMP cascade inserting CFTR in apical side
86
Hwo does CCK activate neural and hormonal path affecting pancreatic secretion?
CCK acts on vagal nerve to DVC down Vagus to pancreas releasing ACh, VIP, and GRP via enteric plexus; CCK also enters circulation and acts on pancreas; both cause secretion
87
what occurs in the cephalic and gastric phase of pancreatic secretion?
stimuli to DVC: sight, taste, smell, stomach distention; vagus causes g cell release of gastrin which activates CCKA receptor in pancreas and ACh release from vagus in pancreas on M3 receptor; cause release of H2O, enzymes and HCO3
88
What occurs in the intestinal phase of pancreatic secretion?
protein and lipid breakdown stimulate vago-vagal reflex primarily on acinar cells; H+ stimulates S cells to secrete secretin in duodenum, acts on receptors in duct to secrete HCO3
89
What are the secretions of the SI? function? what glands?
isotonic alkaline fluid, secretes bicarbonate to neutralize acid, mucus for lubrication and prevent passage of microorganism into mucosa; brunner's , crypts of lieberkurn, microvilli
90
What transporters are involved in electrogenic chloride secretion in crypt cells?
apical: CFTR (VIP and PG stimuli); basal: Na/Cl/K tritransporter, Na paracellularly
91
What are the three types of diarrhea and their cause?
inflammatory- decrease surface area for absorption of H2O and electrolytes; osmotic- deficiency of absorption of products of digestion (ex lactose intolerance); secretory- bacterial infections, specifically stimulate cAMP to increase chloride ion secretion, water follows
92
What are the secretions of the large intestine? How?
mucus, chloride (similar mech. to SI CFTR), K (passive paracellular and active Na/Katpase tritransporter basal and apical ion channel), and HCO3 (Cl-HCO3 or coupled NaHE and Cl-HCO3E)
93
WHat inactivates salivary amylase? How long does pancreatic lipase take to digest all carbs?
low pH; 15-30 min
94
What affects the rate of luminal carb hydrolysis in SI? Brush border?
source of carbs, effect of fiber and protein; proximity of enzymes to transport path improves uptake efficacy, mediated by heavily glycosylated membrane proteins anchored via single transmembrane segment
95
How is gastric proteolysis achieved?
pepsin- stored and secreted in chief cells, autolytic cleavage of N-terminal peptideyeilds active at low pH, cleavage at neutral AA preferable esp large alipathic and aromatic, inactivated at 4.5, non-essential, products mainly large and non-absorbable peptides
96
What are the enzymes in proteolytic activity in SI?
endopeptidases (attack from middle), ectopeptidases/carboxypeptidases (attack carboxy terminus), initial actiation is cleavage of N-terminus peptide from trypsin (mediated by enterokinase on enterocyte membrane)
97
Where are proteolytic brush border enzymes found? why are they needed?
only on villi enterocytes not in crypts; 60-70% of luminal product is small oligopeptides and only 30% free AA
98
How are AA absorbed?
dipeptide can sometimes be faster and important immunologically for infants; patients with specific AA transport defects do not become deficient due to di peptide uptake, tri and di peptide transporters cotransport with H, AA transporters co transport with Na
99
What happes to absorbed di and tripeptides in the cytosol of the enterocyte?
peptidases break them down; glycine and proline containing ones are resistant
100
What are the two comonpenents of signals in peristalsis?
stimulatory above food to propel food with contraction (secondary), inhibitory stimulus to relax smooth muscle below the food (primary)
101
How is mixing achieved?
segmental contraction
102
What are the components of the chewing reflex?
presence of food causes reflex inhibition of muscles droping the jaw which initiates a stretch reflex causing rebound contraction which pushes bolus against palate causing relax, continues until voluntary pushing of bolus back to pharynx
103
What are the stages of swallowing?
voluntary food into pharynx, reflex involuntary- pharyngeal muscular contraction, soft palate moves up, palatopharyngeal folds pulled to center to form slit, larynx pulled up and anterior, epiglottis closes over the trachea, UES relaxes, esophageal peristalsis
104
What causes mixing in the stomach and what else does it do?
weak peristaltic waves generated; upper part show a low frequency sustained contractions that are responsible for generating a basal pressure and a pressure gradient leading to gastric emptying; increase in peristaltic strength of contraction in antrum, these are stimulated by distension and squirt chime into the SI
105
What causes vomiting?
glottis closed, larynx raised, UES open, diaphragm contracted down creating negative pressure, abdominal muscle contraction squeezes stomach increasing intragastric pressure, facilitates opening of LES, reverse peristalsis
106
What stimuli cause vomiting?
pain, sights, anticipation, motion, vertigo all act on brain stem vomiting center, pharyngeal stimuli, ipecac, cytotoxic drugs and irritants act on NTS and the BSVC
107
What facilitates the gastroenteric reflex?
distention in stomach through myenteric plexus, gastrin, serotonin, CCK enhance stomach motility; glucagon inhibits SI motility
108
What is the intrinsic defecation reflex?
feces enter rectum, distention initiates afferent signal through myenteric plexus initiate peristaltic contractions in descending, sigmoid and rectum, wave approaches intrernal sphincter and it reflexively relaxes, if external is voluntarily relaxed defecation will occur (weak)
109
What is parasympathetic defecation reflex?
enhances peristaltic waves and relaxation of internal anal sphincter, still need external to be relaxed; reflexes die after minutes if external is not relaxed can be reinitiated by deep breath and abdominal contraction
110
What happens if the spinal cord is damaged?
urge to defecate not felt, can result in distension of rectum resulting in megacolon
111
What gas is produced in the stomach? where does it go?
nitrogen and CO2 usually from swallowing, belch
112
What gas is produced in the SI? where does it go?
CO2, absorbed
113
What gas is produced in the LI? where does it go?
CO2, methane, hydrogen, nitrogen, oxygen; some absorbed; O2, methane, and H very explosive and cause flatus
114
What is hirshsprung's disease?
congenital megacolon; absence of enteric NS in colon, internal anal sphincter tone increased
115
What is IBS?
abdominal pain with constipation or diarrhea
116
What is Crohn's disease?
chronic inflammation unknown origin, may be genetic component, damage to intestinal layers, may be related to B or virus; thickening of intestinal mucosa (malabsortpion), ulcerations (some rectal bleeding) and diarrhea; surgery and steroids
117
What is ulcerative colitis?
inflammation of colon, rectal bleeding, can involve entire colon (unlike Crohns), usually diarrhea, very diffuse disease, usually involves mucosa, steroids and antibiotics
