Wk3 Pancreas, Gall Bladder, Liver Physiology Flashcards
I cells
location:
respond to?
release?
duodenum
release CCK in response to fat and amino acids
S cells
location:
respond to?
release?
duodenum
respond to H+
release SECRETIN
What does secretin do?
causes pancreatic ductal cells to release bicarb
Neuro activation of pancreatic acinar cells?
vagus –> Ach –> M3 receptors
look at slide 10
Monitor peptide
Master regulator of duodenal cluster unit:
CCK
CCK –> gallbladder?
contraction
CCK –> Pancreas?
Acinar secretion
CCK –> stomach?
reduced emptying
CCK –> sphincter of Oddi?
relaxation
CCK –> brain?
decreased hunger/food intake
Brush border enzyme that activates trypsinogen?
enteropeptidase
Where do pancreatic duct cells get bicarb? (2 places)
blood (from alkali tide of stomach) –> Na+/2HCO3- symporter
intracellular CA
Hoe does bicarb get from duct cell into lumen?
Cl-/bicarb exchangers
How does Cl- get into lumen for exchange with bicarb?
CFTR
**activated by secretin
**this is why CF patients have decreased bicarb secretion
3 causes of pancreatitis:
- CF
- Occlusion fo pancreatic duct (gallstones, malignancy)
- EtOH –> hyperstimulation of acinar cells –> intracellular trypsin activation –> cell death
Regulator of nutrient assimilation:
hypothalamus
GLP-1 general role:
increase insulin
decrease glucagon
**direct- pancreas
**indirect- hypothalamus
GLP-1 cell of origin:
intestinal L cells
GIP role and cell of origin:
K cells –> pancreatic beta and alpha cells –> increased insulin, decreased glucagon
Two negative regulators of pancreatic beta cell secretion of insulin:
somatostatin
NE
4 satiety signal acting on hypothalamus:
- GLP1
- CCK
- Insulin
- Leptin (adipose tissue)
hormone produced in fundus of stomach (and hypothalamus) during fasting to stimulate appetite:
grehlin
great summary chart on
slide 22
hardening of liver due to irreversible deposition of excess collagen:
cirrhosis
Pathology of cirrhosis:
oxidative stress (infx, EtOH) –> Kupffer cells release cytokines –> induce collagen production by stellate cells
Bile review
slide 30 –> end of ppt