Lecture 56 Flashcards
List the steps for stimulation of HCl secretion by using the direct path of vagal stimulation
Vagus nerve sends a signal to the parietal cells
The parietal cells release Ach to then release HCl
OR
The vagus nerve activates GRP to stimulate G cells
The G cells will then release gastrin
What are the steps of the indirect path of vagal stimulation (for HCl secretion)
Gastrin from the G cells goes into systemic circulation
This then causes a release of HCl from Parietal cells
T/F: Atropine WILL block HCl secretion completely b/c it DOES have an effect on the direct paths of vagal stimulation
F
What percent of HCl comes from the cephalic phase of HCl secretion
0.3
What percent of HCl comes from the gastric phase of HCl secretion
0.6
What percent of HCl comes from the Intestinal phase of HCl secretion
0.1
What is the stimuli for the cephalic phase of HCl secretion
Smelling, tasting, chewing, swallowing, & conditioned reflexes
What is the stimuli for the Gastric phase of HCl secretion
Distention of the stomach & the presence of AAs and amino acids
What is the stimuli for the Intestinal phase of HCl secretion
Products of protein digestion
What are the mechanisms of the Cephalic phase
Direct stimulation of parietal cells by the vagus nerve (Ach)
Indirect stimulation via gastrin
What are the mechanisms of the Gastric phase
Distension (causes vagal stimulation which stimulates parietal cells)
indirect stimulation via gastrin
Distension of the antrum causes gastrin
Aas and peptides stimulate gastrin
Caffeine and alcohol stimulates gastrin
When is HCl secretion inhibited
When it is no longer needed for the conversion of pepsinogen to pepsin
How can decreased pH of gastric contents inhibit HCl secretion
pH decreases when food enters the stomach (food does buffer the pH a little)
When food leave the pH falls more & starts to inhibit further gastrin release
How does somatostatin inhibit HCl releease
Can be a direct inhibition by binding to the parietal cells - this antagonizes the histamine pathway by decreasing cAMP
Can be indirect inhibition by inhibiting both histamine & gastrin release
How do prostaglandins inhibit HCl secretion
By reducing cAMP to antagonize histamine
Definition: “Ulcerative lesion of the gastric or duodenal mucosa. Is caused by a loss of mucus & an excessive amount of H & pepsin secretion. Can be b/c of other damaging factors like helicobacter pylori infection or stress”
Peptic ulcer disease
What causes Gastric ulcers
The mucosal barriers are defective & hydrogen ion penetrat/pepsin digest the mucosa
Why can H.pylori colonize & cause gastric ulcers
Because they make urease to increase the pH of the enviroment so that they can bind to cells
Urease allows H.pylori to survive in the stomach
Definition: “An enzyme that converts urea to NH3 to decrease the pH of the local enviornment
Urease
T/F: Most dogs & cats are positive for pylori but they rarely have ulcers
T
Why do duodenal ulcers occur
Because the H+ secretory rate is higher than normal (this overwhelms the buffering capacity of the pancreas)
What occurs in Gastrinoma (Zollinger-Ellison syndrome)
High rates of H+ secretion ocurs due to high amounts of gastrin
Delivery of the high rates of H+ to the duodenmen causes steatorrhea
What does gastrinoma cause steatorrhea
Because the decrease in pH of the intestine inactiv ates enzymes such as lipase so there is very little to no fat digested
What are the components of pancreatic secretions
aqueous component (very high in bicarb)
enzymatic component
Pancreatic secretion comprises how much of the pancreas
0.9
What is the enzymatic component of pancreas secretions do
Digest major nutrients like carbs, proteins, & fat
What are the important structures of the exocrine pancreas glands
Acinus lined w/ acinar cells
ducts lined with ductal cells & centroacinar cells
What does the acinus of the exocrine pancrease secrete
Enzymes
What does the centroacinar cells and duct cells of the exocrine pancrease secrete
Both secrete the aqueous portion