L29 Flashcards

1
Q

what is Helicobacter pylori

A

a common, Gram negative bacterium

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2
Q

who does Helicobacter pylori not get destroyed by stomach acid

A

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

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3
Q

what dies Helicobacter pylori cause

A

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

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4
Q

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

A. K is involved in acid secretion not HCO3-

B. parietal cells

D. no

E. parietal cells

C is correct

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5
Q

what turns gastric secretions on and off

A

arrival of food in the stomach

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6
Q

gastric secretion is a very coordinated process

what are the 2 ways that this coordination is achieved

A

neurocrine

endocrine and paracrine functions

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7
Q

what is parietal secretion stimulated by

A

ACh (neurocrine) from postganglionic ENS fibers

gastrin (endocrine) from G cells located in antral regions

histamine (paracrine) secreted from ECL cells

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8
Q

what part of the stomach secretes acids and what part gastrin

A

body = acid

antrum = gastrin

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9
Q

what kind of input do ECL cells get

A

they get nervous input from ENS (ACh) and hormonal input (gastrin) from G cells

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10
Q

describe the nervous imput to the ECL cells

A

The ENS is the mediator (from the parasympathetic system)

The PNS is the main driver of gastric secretion (vagal input)

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11
Q

Acetylcholine is released by postganglionic neurones of ENS in response to….

A

 vagal stimulation involving external reflex

 local enteric nervous system reflex

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12
Q

how does ACh stimulate the parietal cell

A

 directly via M3 receptors which increase in [Ca2+]

 indirectly via ECL cells and histamine (main effect)

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13
Q

where can gastrin effect

A

ECL cell (causing histomine release)

or

parietal cell

through CCK receptors

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14
Q

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

A

k

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15
Q

Gastrin is produced by G cells in the antrum in response to…..

A

products of protein digestion

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16
Q

what are G cells stimulated by

A

 stimulated by enteric neurones

 GRP (gastrin releasing peptide)

17
Q

gastin is a true hormone. what does this mean

A

 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

18
Q

When food arrives in the stomach , the food absorbs all of the fluid in there therefore the stomach will need to secrete more

A

k

19
Q

how does gastrin increase gastric secretion

A
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+]

20
Q

when is gastrin produced/in response to/is stimulated by

A

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)

21
Q

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+

A

NOTE that when they bind to the receptor they increase intracellular Ca which then goes to produce more H+

22
Q

what are the receptors of histamine, ACh and gastrin

A

ACH = M2 receptor

histamine = H2 receptor

gastrin = CCK receptor

23
Q

what is histomine

A

a paracrine transmitter secreted by ECL cells

24
Q

what is the most potent stimulus for acid secretion

A

histamine

because both gastrin and ACh stimulate histamine release

25
Q

how does histamine cause an increase in gastric secretions

A

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

26
Q

what are the intracellular messangers for histomin, ACh and gastrin

A

ACh and gastrin = Ca

histamine = cAMP

27
Q

what is cimetidine

A

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

28
Q

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

A. G cells

B. stimulated

D. ECL cells in the body

E. stimulated

C is correct