Gastro Physiology Flashcards
Gastric mucosa 3 layers
Mucuosal consists of epithelial cells (absorptive & secretory functions), lamina propia (conncetive tissue, blood/ lymph vessels), muscalaris mucosae (smooth muscles)
Gastric Submucosa
collagen, elastin, most of the blood vessels & the submucosal plexus (Meissner’s
Gastric hormones (4)
released from endocrine cells (free cells or clusters spread over large areas but not concentrated in glands) of GI into portal circulation, pass thru liver to systemic circulation & target cells in the GI (gastrin, CCK, secretin, GIP)
Gastric paracrine
peptides that act a short distance from where they are released; only paracrine is somatostatin which inhibits actions throughout GI (histamine acts locally but it is not a peptide)
from cholinergic neurons: contract smooth muscle in wall & relax sphincters, increase salivary, gastric, pancreatic secretion
Ach
from adrenergic neurons: relax smooth msucle in wall and contract sphincter, increases salivary secretion
NE
NT that increases gastric secretion
GRP
from neurons of mucosa & smooth muscle: contraction of smooth muscle, decreases intestinal secretion
Enkephalin (opiates)
neurons of mucosa and smooth muscle, relaxes smooth muscle, decreases intestinal secretion
Neuropeptide Y
cosecreted with Ach, contracts smooth muscle increasing salivary secretion
Substance P
Gastrin - 2 types
little gastrin (G-17 secreted by G cells in atrum in response to food & G34 between meals – both come from different biosynthetic pathways); the C-terminal tetrapeptide is minimal fragment necessary for activity (1/6 as active as the entire gastrin molecule); functions to increase H+ secretion and growth of gastric mucosa (small peptides and amino acids in stomach (esp. aromatics like tryptophan and phenylalanine), distention of stomach, vagal stimulation through GRP causes release; inhibited by low gastric acid pH
CCK
promotes fat digestion & absorption; has the same C-terminal as gastrin & therefore some gastrin activity (but you need the C-terminal heptapeptide); secreted by the I cells of the duodenal and jejunal mucosa; response to presence of monoglycerides/ FFAs but NOT TAGS, and to small peptides (fat & protein stimuli) 5 actions: increases secretion of pancreatic enzymes, bicarb, inhibits gastric emptying, stimulates gall bladder contraction & also relaxation of the sphincter fo Oddi, stimualtes growth of exocrine gall bladder and pancreas
Secretin
needs the entire molecule to be active; from the S cells of the duodenum in reponse to H+ and DDAs in the lumen; pancreatic lipases function optimally at pH of 6-8 and are inactivated at pH < 3; secretin inhibits the effect of gastrin
Gastrin Inhibitory Peptide (GIP)
from cells of duodenal and jejunal mucosa in response to all 3 nutrients (carbs, peptides, fats), stimulates insulin secretion
motilin
from upper duodenum during fasting states; initiates the gastrointestinal motility- the interdigestive myoelectric complexes at 90 minute intervals
pancreatic polypeptide
response to nutrients fat, protein, carbs to inhibit pancreatic secretion of bicarb and enzymes
Frequency of slow waves along GI tract
stomach with the lowest rate, duodenum with the highest rate; frequency of waves is not influenced by hormones (but the APs/ contractions are influenced)
Origin of slow waves (pacemaker?)
interstitial cells of Cajal in the myenteric plexus
Phases of swallowing
oral (tongue pushes food to pharynx w/ high density of somatosensory receptors to initiate involuntary swallowing reflex in medulla)
pharyngeal (pharynx upper esophageal sphincter opens by swallowing reflex and inhibit breathing), esophageal by reflexes)
esophageal phase (primary peristaltic wave coordinated by swallowing reflex, but if food not cleared, a secondary peristaltic wave is initiated by distention of the esophagus (mediated by the enteric NS)
Lower esophageal sphincter opens by
by vagal N, which is petidergic and releases VIP to relax LES
Receptive Relaxation
VIP also relaxes the orad region of the stomach
Esophagus intrathoracic location (only the LES is in the abdomen), intraesophageal pressure is loess than atm P & lower than abdominal pressure problem of keeping air out and no GERD resolved w/ …?
upper and lower esophageal sphincters
The thickness of the stomach muscle wall increases …
distally
fundus, proximal body of stomach; receptive relaxation (vagovagal reflex - VIP) increases the volume to accommodate up to 1.5L food
Orad region
distal body & antrum (caudad has a much thicker wall & more forceful contractions); retropulsion propels gastric contents back into stomach for further mixing
Caudal region
Migrating myoelectric complexes
at 90 minute intervals function to clear the stomach (3-4 min interval frequency), PNS (gastrin & motilin as well) increases APs and SNS (secretin, GIP) decrease APs
Neurocrins from PNS - name 3
VIP, enkephalins, motilin
2 kinds of contractions in small intestine
segmentation: mixing chyme w/o forward movement & peristaltic – forward movement
Orad contraction involves 2 compounds?
ACh and Substance P
Caudal relaxation involves 2 compounds?
VIP and NO