How does vomiting occur?
There is reverse peristalsis of gastric and duodenal contents into the esophagus which can push the uppr esophageal spincter open , regulated by the ANS vomiting center (chemoreceptor triggering zone) in the 4th ventricle which can be stimulated via a vaso-vagal affect (sensors in the GI)
What is Ipecac?
extract used as an anti-emetic
What is the effect of vomiting on electrolytes?
metabolic alkalosis and hypokalemia (make sure to add these during a fluid infusion)
Describe the wall of the colon
It consists of both circular (continuous throughout the entire colon) and longitudinal muscle layers (concentrated into flat bands). Contraction of the circular muscle can cause segmentation of the colon (aka haustra) that change constantly
What is the innervation of motility in the colon?
ENS (myenteric plexuses)
Extrinsic (vagua supplies the cecum, ascending, and tranverse and the sympathetic pelvic nerve supplies the descending, sigmoid, and rectum)
Neurocrines (Ach and Substance P is excitatory and NO and VIp are inhibitory)
Normally the il
What kinds of contractions are present in the ascending colon?
-random segmental contractions for mixing
-organized segmental contractions for propulsion
-mass movement/sweeping contractions for quick evacuation of contents that occurs 1-3x/day
T or F. Segmental contractions in the descending colon are much more frequent than the ascending
Describe motility in the descending and sigmoid colon
-Segmental contractions are more frequent
-there is no organized segmentation
-propulsion occurs during mass movement
Normally the rectum is empty but even then there are segmental contractions occuring which prevent entry of contents into it but colonic mass movement will overcome this.
Describe rectal contractions
When a small amount of content enters the rectum you see passive distension which can result in a contraction (increasing pressure) and the internal anal spincter opens and the external sphincter closes
Mg based laxative are osmotically driven
What is one major purpose of pancreatic secretions?
To produce HCO3- to neutralize acid as it moves into the duodenum
Acini apical membranes secrete a small volume of secretions highly rich in protein/pancreatic enzymes (low amounts of fluid though!). The duct consists of epithelial cells and they are the centroacinar cells mainly secrete HCO3- and fluid.
So the HCO3- and the fluid are secreted by the duct and the enzymes by the acinar cells
Note the innervation
Facts about pancreatic duct secretions
1. 90% of HCO3- is derived from plasma
2. This occurs against the electrochemical gradient and ouabain blocks it (involves NaKATPAse)
3. Involves NHE, Cl-HCo3 exchangers, and carbonic anhydrase
4. ECF Cl- is essential
Very high concentration of HCO3- in the lumen!
Remember that HCO3- has to be transferred into the duct lumen again both the concentration AND electrical gradients (more negative in the lumen)
Describe HCO3- secretion into a pancreatic duct lumen
H20 dissociates to OH- and H+ inside the cell and CA produces HCo3- which is pumped into the lumen in exchange for Cl- back into the cell. H+ is then pumped across the basolateral membrane actively in exchange for Na+ (NaH ATPase) OR
there is a basolateral ACTIVE co-transporter of HCO3- and Na+ (the major source of HCO3-)
Water then follows the movement via AQP-1 channels on both the apical and basolateral membranes
Pancreatic will always be isotonic at all flow rates unlike salivary secretions
Higher flow rate= more HCO3- and less Cl- (more exchange)
Na and K remain similar because they passively diffuse through tight junctions
Rapidly secretion of proteins suggest they are secreted even before food enters the stomach (aka a cephalic stage of secretion)
Notice how its different after sham feeding so that only proteins remain elevated without actual food meaning that only the acinar cells are being stimulated. So in the cephalic phase, only acinar cells are stimulated (stimuli could be smell /taste/chewing/hypoglycemia relfex through vagus to release Ach to stimulate acinar cells)
Describe the gastric phase of pancreatic secretions
similar effects to the cephalic phase but its induced by stomach distension (mostly protein elevated again through the same pathway)
What are the main events of the later intestinal phase of pancreatic secretions?
It is only during this final phase that you see significant increases in HCO3- and fluid and this is stimulated by acid entering the duodenum raising the pH. This phase represents about 70-80% of total pancreatic response to a meal and Secretin and CCK account for almost all of the hormonal regulation
Maximum at pH 3
What is the mechanism of the intestinal phase of pancreatic secretions?
The presence of H+ in the duodenum stimulates secretin release into circulation from S cells which then directly binds and promotes secretion of HCO3- and fluid from DUCT cells, while fatty acids, AAs, and peptides in the duodenum stimulate CCK release from I cells which stimulate the vagus nerve to release Ach to act primarily on ACINAR cells to promote more enzyme/protein release
What pH is HCO3- from the pancreas released at?
when the pH of the first part of the duodenum drops below 5 (but in states like Zollinger-Ellison, more distal parts of the GI that are normally too basic to promote HCO3- secretion might become acidic).
Keep in mind that there are S cells throughout the Gi but they are not normally stimulated for the reason above
Notice the potentiation effect of AAs and secretin on pancreatic HCO3-
The synergistic pathway occurs because there are distinct receptors that converge with the same secondary messengers
There's an apical CFTR in duct cells so thats how CF can affect this!