Biol 2420 Lecture 28

note that we do not secrete the ready enzyme because we would digest ourselves

when we have too much secretin: we can get a peptic ulcer - disrupting the alkaline mucous layer

digestion of mucosa and submucosa etc. by acid and pepsin

Bacteria:

Heliobacter Pylori

promotes peptic ulcers

30% of pop has this

movbile - takes cover from low pH in mucosal barrier

urease - used as a pH buffer

releases toxins causing inflammation

destroys tight junctions

GastroEsophageal Reflux Disease

HKATPase in Parietal Cells is responsible for acid secretion into the lumen

multiple secretagogues increase secretion

ACh (PNS)

Gastrin (G cells)

Histamine (Enterolike Cells)

Antisecretagogues

prostaglandin

NE
CO2 and H2O are converted to HCO3

H then excreted into lumen (K into the cell, diffuses back)

HCO3 and Cl have a changer on the other side of the cell

Cl is transported into the lumen

= HCl

Prevention of Acid Secretion

2 major targets to lower gastric acid

1. Histamine receptor blockers

Tagamet, Zantac, Pepcid

Adenylene Cyclase and Protein Kinases

Reversible Receptor competition

2. Proton pump inhibitors

Prilosec, Prevacid

Directly block pump

most effective, but irreversible

Other Gastric Secretions

Protein Digestion - HCl and Pepsin hydrolyze, denature and break down Proteins to peptides

Parietal Cells secrete substance to help with Vitamin B12 uptake

Goblet cells produce thick alkaline mucous for protection

Pyloric Cells produce thin mucous to coat food

Alkaline Tide

from Parietal cells. H+ across apical membrane, HCO3 across basolateral to blood (buffer blood)
Control of secretions

Cephalic phase

thought, smell, taste

the medulla oblongata to ENS via the Vagus nerve

stimulate Parietal cells - acid production

stimulates G cells and Enterolike cells - gastrin and histamine

Gastrin - HCl and pepsinogen

Histamine - acid secretion

Gastric Phase

triggered by food in the stomach

stom notices stretch and a-as

does the gastrogastric

mucus, HCl, pepsinogen, intrinsic factor (B12) gastrin

*if pH is lower than 2, acid secretion stops

AA and Vagus = G cells = Gastrin

Gastrin and Vagus = ECL = Histamine

Histamine = Parietal = HCl

too much HCl = neg feedback (somatostatin??)

Intestinal Phase

Enterogastric reflex

triggered by acidic chyme and lipids in the duodenum

shuts off acid production in stomach

Secretin released inhibits parietal and chief cells

Gastrin Inhibitory peptide (inhibits gastrin lol)

 CCK - same effects, not as strong as GIP

also slows motility

Fluid Secretion in Small Intestine

Pancreas - incredible organ. Endocrine and Exocrine functions

Islets of Langerhans - ENDOCRINE

Beta insulin

Alpha glucagon

Acini cells - EXOCRINE

Pancreatic Juice (nasty stuff, 1500mL a day)

Alkaline - increases pH from 3 to 7

K, Na, bicarbonate, H2O

Enzymes: need activation though

Trypsinogen

Chemotrypsinogen

Pancreatic Amylase

Pancreatic Lipase

Controlled by the vagus nerve (more para = more enzymes)

CCK also increases enzyme secretion by the pancreas

stimulated by fatty acids and other fats in the duodenum

also stimulates gall bladder contraction and stomach emptying

Secretin stimulates more H2CO3 to buffer pH - stimulated by acidic chyme