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
what are G cells stimulated by
stimulated by enteric neurones
GRP (gastrin releasing peptide)
gastin is a true hormone. what does this mean
as a true hormone is secreted into the blood
circulates in blood supply
It then finds the ECL cell and the parietal cell to boost gastric acid secretion
When food arrives in the stomach , the food absorbs all of the fluid in there therefore the stomach will need to secrete more
k
how does gastrin increase gastric secretion
as a true hormone is secreted into the blood, circulates in blood supply and when it reaches the parietal cells in the body/fundus stimulates acid secretion directly (CCKB receptor on parietal cells) and indirectly via ECL cells and histamine
ECL cells have the main effect
intracellular second messenger of gastrin in parietal cell is the increase in [Ca2+]
when is gastrin produced/in response to/is stimulated by
Gastrin is produced by G cells in the antrum in response to products of protein digestion
it is stimulated by enteric neurones
- GRP (gastrin releasing peptide)
The CCK receptor and the gastrin receptor are the same
Gastrin and Ach cause the release of histomine for the ECL cell
Gastrin can also bind to the parietal cell which causes an increase H+ production which then will het pumped out into the stomach for more acid
Histomine also makes more H+
NOTE that when they bind to the receptor they increase intracellular Ca which then goes to produce more H+
what are the receptors of histamine, ACh and gastrin
ACH = M2 receptor
histamine = H2 receptor
gastrin = CCK receptor
what is histomine
a paracrine transmitter secreted by ECL cells
what is the most potent stimulus for acid secretion
histamine
because both gastrin and ACh stimulate histamine release
how does histamine cause an increase in gastric secretions
operates via H2
receptors on apical membrane of parietal cells
this activates intracellular second messenger cAMP which activates PKA which phosphorylates vesicles which insertes more H/K ATPases into the membrane
what are the intracellular messangers for histomin, ACh and gastrin
ACh and gastrin = Ca
histamine = cAMP
what is cimetidine
an H2 blocker
Blocks histamine effects
They block the H2 receptors so that you block the H2 receptors so that you release less gastric acid into the stomach
omeprazole is more popular because it blocks the H/K ATPase receptor specifically therefore you don’t use cimetidine as much because we have histamine receptors everywhere
Gastric acid secretion
A. is stimulated by gastrin release from ECL cells.
B. is inhibited by histamine.
C. is stimulated by acetylcholine from enteric nerve system.
D. is stimulated by histamine release from G-cells in the antrum.
E. is inhibited by luminal amino acids and digested protein.
A. G cells
B. stimulated
D. ECL cells in the body
E. stimulated
C is correct
