physiology Flashcards
describe the 3 main methods of protein digestion.
protein to peptides to amino acids by luminal enzymes. Amino acid moved across cell in enterocyte by apical membrane transporters. Transported to the blood by basolateral membrane transporters.
Protein to peptide by luminal enzymes. Peptide to amino acid by brush border enzymes. Same as previous from now on.
Protein to peptide by luminal enzymes. Peptide to peptide in enterocyte by apical membrane transporters. Converted to amino acid in enterocytes by intracellular hydrolysis. Basolateral membrane transporters take to blood.
what is the function of the orad of the stomach?
To store food and allow further carbohydrate digestion by salivary amylase.
what type of contraction occurs in the orad and why?
constant low amplitude contraction to allow food to enter the caudad intermittently, this minimal mixing allows further carbohydrate digestion by salivary amylase
which part of the stomach makes up the caudad?
distal body and antrum
what is the function of the caudad of the stomach?
to mix and churn the food, beginning protein digestion, and to expell the chyme into the duodenum
what type of contraction occurs in the caudad and why?
intermittent, phasic contractions caused by slow waves reaching threshold. They propel chyme towards the pyloric sphincter
what nerve stimulates relaxation of the orad during swallowing?
the vagus nerve
in which part of the stomach is there slow wave activity?
the caudad
Describe how and why retropulsion occurs in the stomach.
The contraction of the muscle overtakes the velocity of the chyme. Resulting in chyme hitting the already contracted caudad wall and bouncing back into the antrum, so only a small amount gets through. Retropulsion occurs to allow maximum mixing of the chyme into small particles.
Describe the effect fat has on gastric emptying.
it delays gastric emptying as fat takes longer to digest and absorb
describe the effect acid has on gastric emptying.
it slows gastric emptying to allow time for the acid to be neutralised by the bicarb from the pancreatic enzymes to prevent damage to the duodenum
what is the function of HCl secretions in the stomach?
to activate pepsinogen to pepsin, denature proteins and kill injested microorganisms
what is the function of pepsinogen in the stomach?
it is the inactive form of pepsin, once activated it creates an amplification loop converting more
what is the function of the intrinsic factor and gastroferrin?
to bind B12 and Fe2+ to facillitate their absorption
what is the function of histamine secretion in the stomach?
it stimulates the release of HCl
what do parietal, enterochromaffin-like and chief cells secrete?
parietal: HCl and intrinsic factor and gastroferrin
enterochromaffin-like: histamine
chief cells: pepsinogen
what do D and G cells secrete?
D cells: somatostatin
G cells: gastrin
what is the function of gastrin?
to stimulate HCl secretion
what is the function of somatostatin?
to inhibit HCl secretion
describe how HCl is secreted from parietal cells.
carbonic anhydrase within the cell converts H20 and CO2 into carbonic acid which quickly dissociates into bicarbonate and hydrogen ions. The bicarbonate exits the cell via a Cl/HCO3 antiporter. The Cl is now inside the cell and exits at the apical membrane through the CFTR channel.
The H+ from the carbonic anhydrase exits the apical membrane via a proton pump.
K+ and Na+ regulate the cell pH
what 3 things induce acid secretion from parietal cells?
ACh
gastrin
histamine
describe the direct and indirect pathway of ACh, gastrin and histamine.
Direct= they all act on the parietal cells to trigger secretions of H+ ions Indirect = ACh and gastrin act on the enterchromaffin-like cells stimulating release of histamine which stimulates the release of H+ from the parietal cells
where does ACh come from and which receptors does it act on to induce H+ release (both direct and indirect)
from the vagus nerve
acts on M3 or M1 ACh receptors
what receptor does histamine act on to increase H+ secretion?
H2 histamine receptors
which receptors do gastrin act on to increase H+ secretion (both direct and indirect are the same)?
CCK2 gastrin receptors
what do gastrin and ACh act on to stimulate H+ secretion from parietal cells?
PLC and IP3
what does histamine act on to stimulate H+ secretion from parietal cells?
cAMP and PKA signalling pathways
by which signalling pathways do somatostatin and prostaglandins inhibit secretion of H+ from parietal cells?
cAMP and PKA signalling pathways
what happens to the proton pumps when the parietal cell is stimulated?
they move from within the cytoplasmic tubulovesicles to the apical membrane in the extended microvilli
what are the three phases of gastric acid secretion?
cephalic
gastric
intestinal
describe the three phases of gastric acid secretion.
CEPHALIC is driven by the CNS and CNX and prepares the stomach to receive food
GASTRIC occurs when food is in the stomach and involves physical and chemical mechanism
INTESTINAL occurs after food has left the stomach as chyme entering the SI causes weak stimulation of gastric secretion via neuronal and hormonal mechanisms
describe the cephalic phase of gastric acid secretion.
vagus nerve stimulates enteric neurons which: release ACh directly activating parietal cells. AND via the release of GRP causing the release of gastrin from G cells into systemic circulation which then activated the parietal cells AND by increasing the ACh by the enteric neuron that stimulates histamine secretion from ECL cells.
ALSO enteric neuron releases ACh inhibiting D cells and therefore decreasing the inhibitory effect of SS on G cells, increasing the gastrin in the blood increasing parietal cell secretion
describe what happens in the gastric phase of gastric acid secretion.
distension of the stomach as the food enters activates reflexes via mechanoceptors causing acid secretion (same as cephalic phase).
food buffers the pH meaning inhibitory effect of ss is increased.
Amino acids stimulate G cells to release more gastrin
describe the three phases of gastric acid secretion inhibition.
CEPHALIC: vagal nerve activity decreases when stop eating and following stomach emptying.
GASTRIC: antral pH falls when food exits stomach recommencing release of SS from D cells reducing gastrin secretion (decreasing parietal cells secretion)
AND PGE2 locally reduces histamine and gastrin mediated HCl secretion
INTESTINAL: reduces gastric motility, reducing gastric secretion
what is the function of the small intestine?
digestion and absorption
what types of motility occur in the small intestine and why?
segmentation: to mix
peristalsis: to move aborally
MMC (migrating motor complex): to remove undigested residues to the large intestine
describe segmentation in the small intestine (what it is and how it works).
there is alternating contraction and relaxation of circular muscle to move the chyme back and forth.
Pacemaker cells initiate it by causing a continuous basic electrical rhythm. Contraction is achieved by a spike in the slow wave (as Ca2+ dependent APs)
what is segmentation activated by?
distension by chyme
what is peristalsis caused by?
a few localised contractions
Describe the migrating motor complex (MMC)
it occurs between meals to clear debris into the large intestine.
It is caused by a strong peristaltic contraction slowly passing the length of the intestine.
what is the migrating motor complex (MMC) inhibited and suppressed by?
inhibited by eating and vagal activity
suppressed by gastrin and CCK
what is the migrating motor complex (MMC) triggered by?
motilin
what effect does circular and longitudinal contraction have on the lumen?
circular contraction = narrower and longer
longitudinal contraction = wider and shorter
Smooth muscle of the GIT is electrically coupled. True or false?
true
describe how smooth muscle in the GIT can be excited (including spontaneous)
adjacent smooth muscle cells are coupled by gap junctions. Once one is excited will start a synchronous wave as it excited all the other cells it is in contact with.
Spontaneous activity is driven by pacemaker cells.
what are pacemaker cells in the GIT modulated by?
enteric and autonomic nerves and hormones
where in the GIT does spontaneous electrical activity occur as slow waves?
stomach and intesitnes
what are slow waves?
rhythmic patterns of depolarisation and repolarisation that spread from cells to cell via gap junctions
what are the pacemaker cells of the GIT called?
interstitial cells of Cajal
where are the pacemaker cells of the GIT located mostly?
between the circular and longitudinal muscle layers
describe how slow waves cause smooth muscle contraction in the intestines.
they are always present and dont always cause contraction.
contraction in the intestines ONLY occurs if the slow wave amplitude reaches threshold causing a Ca2+ mediated AP (spike). BUT the amplitude of the slow wave remains mostly the same, the starting point of each slow wave increases instead due to neuronal, hormonal and mechanical stimuli.
what does the myenteric/auerbach’s plexus modulate mainly?
motility and sphincters
what does the submucosal/Meissner’s plexus modulate mainly?
the epithelia and blood vessels
what hormones does the small intestine secrete?
gastrin secretin cholecystokinin (CCK) gastric inhibitory peptide (GIP) glucagon like peptide 1 (GLP-1) motilin ghrelin
what do all peptide hormones released from the small intestine act on?
G protein coupled receptors
what type of cell releases gastrin and what does it do?
G cell (found in stomach and duodenum) stimulates H+ secretion by parietal cells AND stimulates growth of gastric mucosa
what type of cell releases secretin, where are these cells found and what does secretin do?
S cells (found in duodenum) released in response to H+ and fatty acids in the lumen to increase secretion of pancreatic and biliary HCO3-
what type of cell releases CCK, where are these cells found and what does CCK do?
I cells (in duodenum and jejunum)
released in response to monoglycerides, free fatty acids, amino acids and small peptides in the lumen.
Inhibits gastric emptying, causes secretion of pancreatic enzymes, stimulates relaxation of sphincter of Oddi and contraction of gallbladder to eject bile, increases the action of secretin
what type of cell releases GIP, where are these cells found and what does GIP do?
K cells (found in duodenum and jejunum) released in response to glucose, amino acids and fatty acids. Stimulates the release of insulin from pancreatic beta cells AND inhibits gastric emptying
what type of cell releases GLP-1, where are these cells found and what does GLP-1 do?
L cells (small intestine) stimulates insulin secretion, inhibits glucagon secretion, decreases gastric emptying and appetite
what type of cell releases motilin, where are these cells found and what does motilin do?
M cells (duodenum and jejunum)
secreted during fasting state
initiates the MMC
what type of cell releases ghrelin, where are these cells found and what does ghrelin do?
Gr cells (stomach, SI and elsewhere) stimulates appetite
what increases the secretions (juice of the intestine produced into the tract) from the small intestine?
distention/irritation, gastrin, CCK, secretin and para nerve activity
what decreases secretions (juice of the intestine produced into the tract) from the small intestine?
symp activity
what does the secretion (juice) of the small intestine contain and why and where are they produced?
mucous for protection from goblet cells
aqueous slat for enzymative digestion mostly from crypts of Lieberkuhn
describe how aqueous salts are secreted from the small intestines (note if too much secreted will get diarrhoea).
Cl- enters the cell via a Na+/K+/2Cl- co-transporter on the basal surface.
The Cl- travels to the apical membrane and exits via the CFTR channel.
The -ve lumen now attracts Na+ and therefore H20 through the gaps in the cells. (note Na+ exits cell again via Na+/K+ ATPase)
what does the pancreas secrete?
insulin and glucagon into the blood (endocrine)
digestive enzymes, aqueous NaHCO3- solution (pancreatic juice - exocrine)
