Exam 4: Lecture 56: Gastric, pancreatic and Bile secretion Flashcards
vagus nerve releases Ach on parietal cells which then release
HCl
vagus nerve releases gastrin-releasing peptide (GRP) on G cells which release
gastrin
Gastrin from G cells goes into the systemic circulation and HCl from parietal cells causes ________ secretion
HCl
________ will not block HCl secretion
atropine
atropine will not block HCl secretion, why?
because you only affect a small path.
using GSP to release G cells = still have same effect
30% of total HCl stimulated by smelling, tasting, chewing, swallowing, and conditioned reflexes during the ________ phase
cephalic
60% of total HCl release is stimulated by distension of the stomach and the presence of amino acids during the ________ phase
gastric
alcohol and caffeine stimulate ________ secretion during gastric phase
HCl
10% of total HCl release steamed by products of proteins into the intestines = increase ________ of acid production during the ________ phase
inhibition
intestinal phase
HCl secretion is inhibited when no longer needed and converts ________ to ________
pepsinogen
pepsin
for pepsinogen to convert to pepsin the ________ must be low
pH
somatotatin directly binds parietal cells and ________ histamine pathway = decreasing ________
antagonizes
cAMP
somatotatin indirectly inhibits both ________ and ________ release
histamine
gastrin
prostaglandins antagonizes ________ by reducing ________
histamine
cAMP
the two main barriers to acid and pepsin damage to gastric mucosa are
bicarbonate
mucus
________ and ________ are in the gastric stomach within/on gastric epithelial cells and mucosal neck cells = secrete ________ which is trapped in ________ = anything/acid become neutralized in mucous = ________ becomes inactivated/deactivated
HCO3-
Mucus
HCO3-
mucosal
pepsin
peptic ulcer disease is where ulcer lesions of ________ or ________ mucosa because acidic levels are high
gastric
duodenal
peptic ulcer disease is cased by a loss of ________, excrete excess ________ and ________ or a combinataton of both
mucus
H+
pepsin
gastric ulcers form because the mucosal barrier is
defective
H. pylori colonizes gastric mucus and attaches to ________ cells. and release ________
epithelial cells
cytotoxins
H. pylori survives in ________ environments because it has the ________ enzyme
acidic
urease
what converts the urea to ammonia, increases pH level of local environment so H. pylori can survive and bind cells instead of being shed from the body. prevents ________ and ________ from working
urease enzyme
HCl and pepsin from doing job
most dogs and cats are positive for H. pylori, but they rarely have ________
ulcers
duodenal ulcers and Zollinger Ellison syndrome occur when ________ secretory rate is higher than normal
H+
When H+ secretion is higher than it should be = overwhelming the ________ and ________ capacities
pancreas
buffering
define the disease
- high rates of H+ secretion due to high gastrin (gastrin always releasing)
- delivery of H+ into duodenum
- cause steatorrhea (decrease pH in SI big issue with enzymes = inactive ________, decrease fat ________ and increase ________ in poop)
gastrinoma
lipase
digestion
fat
increase in CO3- in aqueous solution from the exocrine pancreas is used for
neutralization
what digests major nutrient groups such as carbs, proteins, and fat from the exocrine pancreas
enzymatic components
exocrine pancreas such as aqueous and enzymatic components are about/comprise ________ of the pancreas
90%
exocrine glands lined with acinus lined with ________ cells
acinar
exocrine glands ducts lined with ________ cells
ductal
exocrine glands lined with ________ cells to secrete the aqueous portion in which HCO3- is the major component
centroacinar
SNS innervates the ________ and ________ ________ to inhibit the exocrine cells of the pancreas
celiac and superior mesenteric
PSNS innervates the ________ nerve to stimulate the exocrine cells of the pancreas
vagus