Study Guide Flashcards
explain the neural mechanisms controlling GI functions - local, short, long
- local: myenteric -> muscle (peristalsis)
- short: afferent to ganglion outside CNS (DRG) -> muscle (anatomical sphincter stuff)
- long: afferent vagus -> solitary tract -> DMVN -> efferent vagal to muscle (peristalsis)
explain the neural mechanisms controlling GI functions - peristalsis, rhythmic segmentation, tonic contractions
- peristalsis: local reflex
- rhythmic segmentation: local and long reflex to mix shit
- tonic contractions: local reflex to move things aborally
understand how intrinsic neural connections can generate intrinsic reflexes
local reflexes, so stretch receptor stimulates inhibitory motor neuron and excitatory motor neuron
- inhibitory: VIP, NO relaxation aborally
- excitatory: ACh contraction towards mouth
describe mechanisms involved in swallowing
RRGSP: raise soft palate, resp stopped, glottis closed, sphincters relaxed (UES, LES), peristalsis of bolus to epiglottis, over epiglottis and into esophagus
what is the swallowing reflex?
pressure sensors in pharynx sense food -> medulla swallowing center coordinates relaxation of UES and LES
what is voluntary about swallowing?
raising soft palate
what controls the LES?
local reflexes, VIP and NO
what are some of the problems with esophageal function?
- achalasia: LES has too much tension, lower esophagus gets super dilated
- GERD: LES not closed, gastric reflux into esophagus
what is receptive relaxation and where does it occur?
bolus in the esophagus (long reflex) stimulates relaxation of proximal stomach to make room for incoming food
what neural mechanisms control receptive relaxation?
long reflexes
explain neural control of gastric emptying
distention of duodenum (long reflex) inhibits gastric emptying
what are other non-neural controls that regulate gastric emptying?
- excitatory (from gastric): gastrin, distention
- inhibitory (from intestine): acidic duodenal pH, hypertonic chyme, fat digestion
how is the pattern of gastric contractions immediately after eating different from that seen after fasting for several hours?
-interdigestive phase: MMC (migrating motility complex) controlled by motilin/deals w/ circular muscle
how does this influence GI functions: gastrin
- increases parietal secretions
- increases chief cell secretions
how does this influence GI functions: glucagon
- increases lipolysis
- increases gluconeogenesis
- inhibits glycogenesis
how does this influence GI functions: secretin
(from duodenum)
- inhibits gastric emptying
- inhibits gastrin
- decreased parietal cell secretion
- increases chief cell secretion
- increase HCO3- secretion from pancreas
how does this influence GI functions: CCK
(from duodenum… response to fat)
- relaxes sphincter of Oddi
- contracts gallbladder
- slows gastric emptying
- stimulates pancreatic lipase
- stimulates HCO3-
how does this influence GI functions: GIP
- stimulates somatostatin
- inhibits gastric emptying
- decreases gastrin (via somatostatin)
how does this influence GI functions: motilin
-regulates MMC
how does this influence GI functions: VIP
-SM relaxation
how does this influence GI functions: somatostatin
- slows gastric emptying
- down-regulates gastrin
- inhibits chief and parietal statin
how does this influence GI functions: GRP (from vagus)
-stimulates endocrine cells to release gastrin
describe the function of slow waves. what cells and membrane events are responsible for generating slow waves?
BER (basal electrical rhythm) - interstitial cells of Cajal and pacemaker type cells in proximal stomach -> spreads to longitudinal muscle -> spreads to myenteric plexus -> circular muscle -> travels along these fibers via gap junctions, which changes membrane potential
what contractile behaviors are seen in the small intestine and what neural mechanisms control these contractions?
- interdigestive: MMC (motilin)
- digestive: MMC stops
- peristalsis, rhythmic segmentation, tonic contraction
what is gastric sieving?
pyloric sphincter closes as bolus approaches -> only a small amount of fluid gets through, while most fluid and solids remain in stomach for more mixing
what regulates movement of chyme from the small to large intestine?
ileocecal junction - distention of ileum causes relaxation of sphincter and vice versa, mediated by myenteric plexus
what happens in the colon?
- water absorption
- electrolyte absorption
- evacuation of feces
what motility patterns are seen in the colon, and what functions do they serve? (6)
- haustral shuttling: annular contractions of circular mm. to mix back and forth between haustra
- haustral propulsion: haustra contract sequentially to go to anus
- multihaustral propulsion: simultaneous contraction of many
- mass propulsion (peristalsis): infrequent, longer distance
- gastro-colic reflex: colonic movement soon after a meal (ACh, gastrin, CCK)
- defecation: parasympathetic long arc (rectum relaxes and distends), internal anal sphincter relaxes, external contracts at first then relaxes
what is a mass movement and what does it accomplish?
getting things through fast after you eat
explain what the defecation reflex is and what might enhance it
enhancement of reflex from increased intra-abdominal pressure due to contraction of chest and abdominal muscles
describe composition of saliva
- acinar cells secrete stuff into water and form presaliva that is isotonic to plasma
- as it’s going across ductal cells, Na and Cl get pulled out and K and HCO3 go in -> makes saliva hypotonic to plasma
- acinar cells also put in alpha-amylase and salivary lipase
describe cellular processes in acinar and duct cells responsible for salivary secretions
-ACh binds muscarinic receptors -> rise in intracellular Ca2+ that leads to solute flux
-VIP binds to receptor and leads to protein kinase activity that leads to amylase vesicle secretion
(stimulus (excitation)-secretion coupling)
what are the neural mechanisms controlling salivation and what sorts of stimuli excite or inhibit salivation?
- CN 7, 9
- excite: see, smell, taste
- inhibit: dehydration
explain the physiological functions of gastric juice
- HCl- lowers pH, CT dissolved, denatures proteins
- gastrin: stimulates gastric emptying, stimulates chief and parietal cells
how is HCl produced in the stomach?
- CO2 and water make H2CO3 via CA
- H+/K+ ATPase on apical side -> H+ into lumen
- HCl/Cl exchanger on basal side, then Cl- and K+ channels on apical side -> Cl- into lumen
- H+ and Cl- combine in lumen
describe the neural mechanisms that regulate the secretion of HCl in the stomach
vagal (ACh) - cephalic phase
describe the hormonal mechanisms that regulate secretion of HCl in the stomach
ACh acts directly on parietal cells, gastrin, histamine (activates AC to cause HCl secretion from parietal cell, from ECL cells)
how is stomach pH regulated?
- secretion produced in duodenum -> inhibitory to parietal cells
- somatostatin (from GIP) inhibitory to parietal cells
- secreted in response to fat in duodenum
explain the importance of mucus and bicarbonate in creating a gastric mucosal protective barrier
- prevents stomach mucosal epithelial cells from being destroyed by digestive enzymes
- mucus is mechanical barrier, stops bacterial adhesion
what are the intestinal secretory cells and what do they secrete?
- I cells (CCK)
- S cells (secretin)
- K cells (GIP)
what are the pancreatic secretory cells and what parts of pancreatic juice do they secrete?
-acinar: pancreatic enzymes, ductal readjustments - HCO3- is high
how does the composition of pancreatic juice change as flow increases?
increased flow = more bicarb
what is the mechanism for pancreatic production of bicarbonate?
duct cells of pancreas have CA on either side (not inside), so the bicarb is made in the blood and the lumen
explain the physiological functions of pancreatic juice components
- secrete inactive enzymes that will be activated in the duodenum
- HCO3 secretion
what are the components of bile?
- bile salts (glycocholate, lysolecithin, monocyceride)
- TG
- phospholipids
- cholesterol esters
what are the physiological functions of bile components in digestion?
bile salts for fat travel in blood (emulsify lipids)
what is the role of Kupffer cells in the liver?
macrophages
what neural and hormonal mechanisms regulate secretion of bile?
CCK - contracts gallbladder
vagal stimulation to gallbladder
where is the sphincter of Oddi and what does it do?
common bile duct into duodenum -> relaxes to let bile and all pancreatic shit through
how are bile components recycled?
reabsorbed in terminal ileum -> blood -> liver to be reused
what role does the liver play in excretion of wastes?
detox and conjugation
what is bilirubin and where does it come from?
globulin portion of Hb - comes from apoptotic RBCs
if there was a decrease in pH of chyme entering duodenum, what would happen to liver, pancreatic, and stomach functions?
- liver: nothing
- pancreas: secretin increases bicarb
- stomach: secretin inhibits gastrin and inhibits parietal cells (and increased chief cells)
where are amylases produced in the body and how do they work?
salivary, pancreatic - cleave internal 1,4 alpha linkage
what limits carbohydrate digestion by salivary amylase?
- acid in stomach degrades it
- still the 1,6 alpha and terminal 1,4 alpha linkages
where do digestion and absorption of carbohydrates take place?
small intestine
describe digestion of sucrose, lactose, and branched starch molecules
sucrose, lactase
what are oligosaccharidases and what role do they play on brush border membrane cells?
degraded by enzymes in the brush border
how are monosaccharides transported in the small intestinal brush border cells?
- glucose/galactose: with Na and an independent glucose transporter
- fructose: facilitated diffusion
- facilitated diffusion on basal side to get into blood
what are pepsins, where are they produced, and what role do they play in total protein digestion?
- chief cells
- break peptide bonds into free aa, dipeptides and tripeptides
what role does gastric acid play in protein digestion?
- activates pepsinogen -> pepsin
- activates pancreatic alpha-amylase
- ribo/deoxyribo
what are the pancreatic proteases/peptidases?
- trypsin (activated by enteropeptidases)
- chymotrypsin
- elastase
- carboxypeptidases A/B
- aminopeptidases
how are some peptidases functionally unique?
- trypsin - basic aa
- chymotrypsin - aromatic aa, large hydrophobic aa
- elastase - peptide bonds
- carboxypeptidase A/B - peptide bones on carboxy end
- aminopeptidases - peptide bones on amino ends
what prevents the pancreatic enzymes from digesting the cellular apparatus of the pancreas?
they are zymogens - only become activated by trypsin, CI, or enteropeptidases
how do peptides and amino acids get absorbed at the brush border membrane?
- free aa, di and tripeptides are cotransported with Na via secondary active transport (Asp, Glu move via facilitated diffusion)
- all move by facilitated diffusion to the blood
where does most dietary protein get digested and absorbed?
small intestine?
what are the different fat digestion enzymes, where do they originate and how do they work? (6)
- lingual lipase: lingual gland, breaks down TG
- gastric lipase: endocrine glands?, breaks down TG
- colipase: pancreas, attach to fat droplets
- pancreatic lipase: pancreas, breakd 1,3 position of TG
- cholesterol ester hydrolase: pancreas, breaks water-soluble lipids
- phospholipase A2: breaks phospholipids
where does most dietary fat get digested?
proximal small intestine
where are lipids absorbed mainly?
proximal small intestine
what roles do bile salts and lecithin play in fat digestion?
- bile salts emulsify fat for transport
- lecithin is a type of bile salt?
what happens to lipids inside the intestinal epithelial cell
free, but then packaged into micelles with apoproteins
what are chylomicrons and what special role do they play?
make micelles with the free fatty acids in the intestinal mucosal cells and transport the lipids from the cell to the lymph
how do chylomicrons get into the circulatory system?
thoracic duct
what role would tight junctions play in intestinal water and electrolyte fluxes?
water goes through, Na and I… sodium does this in early small intestine more so, K exclusively moves across tight jxn, and water can move across tight jxn
explain how electrolyte transport is similar and different in the small and large intestine
- SI: cotransport, active transport, passively
- LI: electrogenic transport only (down its electrochemical gradient)
what mechanisms are important for the absorption of calcium in the GI tract?
Ca binding protein in brush border that binds Ca and gets moved into the cell via CA ATPase (2 in for 1ATP)
-active vit D is a steroid hormone that activates translation of mRNA -> Ca binding protein -> makes Ca absorption easier
what mechanisms are important for the absorption of Fe in the GI tract?
- DMT in the DUODENUM absorbs free iron
- heme is facilitated diffusion
what is unique about the absorption of vit B12 and why is this so important in humans?
B12 needs IF to bind to recognize site on mucosal cell, B12 needed for neuro shit…. in ILEUM
how do disease states disrupt water and electrolyte balance?
cholera - upregulates cAMP, Gs, inhibits Na/Cl symport so it keeps the Na in the lumen -> diarrhea
how is the absorption of water-soluble vitamins different from fat-soluble vitamins?
- water soluble in distal SI: facilitated diffusion, cotransport, active transport
- fat soluble in proximal SI: facilitated diffusion, cotransport, active transport
How do pancreatic hormones control nutrient traffic during the fed and fasted states?
glucagon:
- increased gluconeogenesis, lipolysis, glycogenolysis, protein breakdown
- decreased glycogen synthase
insulin:
- increased glycogen synthase, lipogenesis
- decreased gluconeogenesis
which gut hormones are important in regulating food intake?
ghrelin stimulates LH? to increase feeding
what are the important brain regions involved in control of ingestive behavior and what controls do they exert?
LH - hunger, lesion = anorexia
VM - satiety, lesion = over-eating
how do different gut signals get to brain areas that control appetite?
BBB
what role do pancreatic hormones play in the control of food intake?
- insulin - decrease feeding, excessive increases feeding
- glucagon - increase feeding? not on the list
- ghrelin - increase feeding
what are the endocrine and metabolic changes associated with T1DM?
Ab’s against beta cells of pancreas -> decreased insulin, so glucose can’t get into cells (hyperglycemia)
what are the endocrine and metabolic changes associated with T2DM?
insulin resistance or down-regulation of insulin receptors
how is the control of food intake altered in uncontrolled diabetes?
excess insulin - causes hunger
how are signals of adiposity important in body weight control and how do they work?
leptin decreases neuropeptide Y, and CRH increases SNS, leading to increased insulin
how can we use our knowledge of basic physiological findings to devise better treatments for obesity?
- amphetamines: directly inhibit feeding center in brain
- sibutramine: decreases food intake
- leptin agonist, ghrelin antagonist
- orlistat: lipase inhibitor (reduce intestinal digestion of fat)
