L29 Flashcards
what is Helicobacter pylori
a common, Gram negative bacterium
who does Helicobacter pylori not get destroyed by stomach acid
We produce a lot of urea because that is the non toxic version of amino groups from proteins. If we didnt produce this then it would end up as ammonia which can get through Na channels and therefore is toxic
Urea is in the blood and is the main osmotic force in the urine
What HP does is use urease to convert urea
into HCO3
urea has a bicarbonate attached and what the bacteria does is break the bicarbonate off the urea and holds it around itself so that the acid cannot kill it
what dies Helicobacter pylori cause
Can also lead to internal bleeding which can cause death
Ulcers lead to anemia as the cells cannot secrete intrinsic factor which effect’s the RBC formation
Secretion of bicarbonate into the stomach lumen
A. depends on a basolateral K+ gradient in parietal cells.
B. requires a basolateral Cl- gradient in surface cells.
C. changes with apical K+ conductance in parietal cells.
D. protects the surface epithelium against bacteria such as
Helicobacter pylori.
E. is mainly facilitated by chief cells.
A. K is involved in acid secretion not HCO3-
B. parietal cells
D. no
E. parietal cells
C is correct
what turns gastric secretions on and off
arrival of food in the stomach
gastric secretion is a very coordinated process
what are the 2 ways that this coordination is achieved
neurocrine
endocrine and paracrine functions
what is parietal secretion stimulated by
ACh (neurocrine) from postganglionic ENS fibers
gastrin (endocrine) from G cells located in antral regions
histamine (paracrine) secreted from ECL cells
what part of the stomach secretes acids and what part gastrin
body = acid
antrum = gastrin
what kind of input do ECL cells get
they get nervous input from ENS (ACh) and hormonal input (gastrin) from G cells
describe the nervous imput to the ECL cells
The ENS is the mediator (from the parasympathetic system)
The PNS is the main driver of gastric secretion (vagal input)
Acetylcholine is released by postganglionic neurones of ENS in response to….
vagal stimulation involving external reflex
local enteric nervous system reflex
how does ACh stimulate the parietal cell
directly via M3 receptors which increase in [Ca2+]
indirectly via ECL cells and histamine (main effect)
where can gastrin effect
ECL cell (causing histomine release)
or
parietal cell
through CCK receptors
ACH leads to the release of histamine which further leads to an increase in gastric acid secretion (this is known as the turbo boost)
Gastrin also boots the response
k
Gastrin is produced by G cells in the antrum in response to…..
products of protein digestion