Gastric, Pancreatic, and Intestinal Secretion Flashcards
Pepsinogen Function
digest 10-20% of proteins into peptides
Pepsinogen as inactive proenzyme
pH <5 and autocatalyzes pepsinogen to pepsin
Optimal pH for pepsin activity
1.5-2
Factors that increase pepsinogen secretion
ACh, pH <3, Gastrin
Gastric Lipase Function
digests 15% triglycerides to 2-monoglyceride and 2FFA
Optimal pH for gastric lipase activity
3-8
Gastric lipase in infants
more important bc pancreatic lipase is not abundant
Factors that increase gastric lipase
ACh
Intrinsic Factor Function
Binds Vitamin B12 in duodenum and transporting it to ileum for absorption
Gastric mucosal barrier
mucin glycoproteins and water with trapped HCO3
Function of Gastric mucosal barrier
Protect mucosa from pepsin and H+, slow-back diffusion of H+ into enterocytes, Trap any luminal H+ and buffer with HCO3
Mucin Function
protect mucosa from pepsin, HCl, bacterial invasion, and physical damage, and lubricate food
Mucin secretion
from surface mucus cells and mucus neck cells via exocytosis (continuous) and cell exfoliation (cells replaced every 3 days)
Factors that increase mucin secretion
ACh, gastrin, and prostaglandins
Bicarbonate Secretion Function
buffer H+ that enters the gastric mucosal barrier
Bicarbonate Secretion
from surface mucus cells and mucus neck cells using HCO-Cl antiporter (CA generates HCO)
Factors that increase Bicarbonate Secretion
prostaglandins, H+ in lumen, ACh
ALL surface mucus cells and mucus neck cells secrete
Mucus and HCO
What is the pH at the apical cell surface (beneath the gastric mucosal barrier)?
7
Prostaglandins are cytoprotective, function is
Decrease H+ secretion, increase mucus and HCO secretion, and increase gastric blood flow
Pepsin is inactive within the mucosal barrier, Why? and why is this important
mucosal barrier has a pH of 7 (pepsin inactive at 7), important to avoid digesting stomach lining
Peptic Ulcer Disease
loss of mucosal surface, imbalance of gastric acid and pepsin, and protective elements (mucus, HCO, and prostaglandins)
Causes of PUD
H. pylori, NSAID use
Zollinger-Ellison Syndrome
gastrinoma producing elevated levels of gastrin, causes PUD
H. pylori infection
adheres to and colonizes gastric-type epithelium causing an inflammatory and bacterial response altering cell characteristics
Chronic H. Pylori + pangastritis
results in hypochlorhydia, high levels of gastrin normal level of H+ (cytokines inhibit H+ secretion)
Chronic H. Pylori + antral gastritis
results in hyperchlorhydia, high levels of gastrin AND H+, due to somatostatin dysfunction
H. pylori produces urease
splits urea into ammonia CO2 and HCO3, increasing pH and allowing survival of bacteria and weakening the mucosal barrier
NSAIDs and peptic ulcers
COX inhibitor prevents synthesis of prostaglandins, allowing increased H+ secretion, decreased mucus and HCO secretion, and decreased gastric blood flow
COX2
does not effect GI, but will reduce swelling and pain
Misoprostol (prostaglandin agonist)
treatment for peptic ulcers because it decreases H+ secretion, increases mucus and HCO
Zollinger-Ellison Syndrome
H+ hypersecretion and gastrinoma, diarrhea and steatorrhea due to low pH in sm intestine and inability to absorb B12
In patients with ZES, gastrin release from G cells is
LOW; gastrin is released from gastrinoma
Function of pancreatic secretion
neutralize HCl to protect mucosa, maintain activity of giestive enzymes, secrete digestive enzymes
Pancreatic acinar cell function
electrolytes, amylolytic, lipolytic, nucleolytic, and proteolytic enzymes
Pancreatic acinar cell amylolytic enzymes
amylase (active form) pH 7
Pancreatic acinar cell lipolytic enzymes
Lipase, Pro-phospholipase A2, cholesterol esterase pH 3-8
Pancreatic acinar cell nucleolytic enzymes
ribonucleases, deoxyribonucleases
Pancreatic acinar cell proteolytic enzymes (INACTIVE)
Trypsinogen, Chymotrypsinogen, proelastase, procarboxypeptidase A, procarboxypeptidase B
ALL proteolytic enzymes secreted by the pancreatic acinar cells are secreted as
zymogens, activated by trypsin
what activates trypsin
enterokinase located on the apical membrane of small intestinal enterocytes
pancreatic ductal cell function
modify acinar secretion, secrete Cl, HCO3, and not reabsorb Na, K
What is trypsinogen was active in the pancreas
pancreatitis
Pancreatic Acinar cell secretes peptides that are not enzymes
trypsin inhibitor, procolipase, monitor peptide
Autonomic control of pancreatic secretion
PNS increases secretion (ACh), SNS will decrease secretion (NE)
Hormonal control of pancreatic secretion
CCK (CCK-releasing protein and monitor peptide) and secretin both increase pancreatic secretion
Trypsin
activates all peptidases at start of digestion and inactivates peptides (CCK-RP and monitor protein) at conclusion of digestion to reduce CCK
Pancreatitis
impairment pf endocrine function
Causes of Pancreatitis
alcohol consumption and gall stones blocking pancreatic duct
Small intestine secretion
HCO, Cl, mucus, Secretin
Crypts of Lieberkuhn secrete
HCO and Cl
Brunners glands and goblet cells in crypts secrete
mucus
Cholera toxin
causes diarrhea by increasing intracellular cAMP (excessive Cl secretion)
Secretory diarrhea causes
adenylate cyclase system, not adenylate cyclase system, mucosal injury, neoplasms
adenylate cyclase system
enterotoxin-producing bacteria (e. coli, cholera) and caffeine
Non- adenylate cyclase system
Bacterial endotoxins (staph, shigella, clostridium)
Mucosal injury
IBS, salmonella, e.coli, shigella
Neoplasm
gastrinoma
If a patient’s diarrhea ceases with fasting, is it secretory?
NO - osmotic