Gastric Mucosal Barrier

Front 1

Four specific factors that help the gastric mucosa & gland maintain integrity in acidic environment w/ a lot of pepsin ; (4)

Back 1

bicarbonate micro climate
mucus layer
low passive permeability of mucosal membrane
rich blood supply

Front 2

Why does the gastric mucosal barrier need to exist?

Back 2

b/c H/K ATPase can drive the gastric pH to 1 or less

Front 3

What protective mechanisms can be found at the gastric mucosal surface?

Back 3

bicarbonate micro climate
mucus layer

Front 4

Bicarbonate micro climate is located

Back 4

adjacent to surface epithelium
found on epithelium of body & antrum

Front 5

Rate of bicarbonate secretion is ____ but needs, its partner _____

Back 5

rapid, mucus layer

Front 6

Mucus layer is composed of

Back 6

insoluble mucus secreted by mucus neck cells

Front 7

The mucus layer creates a buffer zone by

Back 7

forming a sticky coat, 200 micrometers thick, which resists gastric mixing.

Front 8

Regulation of bicarbonate & mucus are

Back 8

regulated in similar ways

Front 9

When are bicarbonate & mucus secretion increased?

Back 9

when sensing chemical acidity
when abrasive substances enter the stomach

Front 10

Bicarbonate & mucus are regulated

Back 10

vagally (most organs in lower GI)
Vagus goes to lower system & affects liver, pancreas, gall bladder, & intestine.

Front 11

Why is Prostagliandin E2 an important gastric mucosal layer?

Back 11

b/c it stimulates both bicarbonate & mucus secretion

Front 12

How is mucus secretion inhibited?

Back 12

via sympathetic stimulation

Front 13

Parietal cells don't have a lot of mucus - so how do they remain intact?

Back 13

located at base of gland, so they have a diff function: @ the base of the gland there are fewer parietal cells (less density).

Front 14

Functional Difference of parietal cells @ base of gland -

Back 14

have H/K ATPase with very weak activity - so these cells are relatively week secretors of acid

Front 15

Parietal cells at bottom of gland don't have _____

Back 15

basolateral bicarbonate/Cl exchanger.

Front 16

What do the parietal cells at the bottom of the gland have instead of the basolateral bicarbonate/Cl exchanger?

Back 16

Na/K/2Cl transporter
Can transport large amounts of Cl across the cell,

Front 17

When the Cl reaches the lumen from the Na/K/2Cl transporter, it combines w/

Back 17

w/ K & Na instead of H - thus you have less HCl activity at the base than at the top.

Front 18

Mucus plug is present in

Back 18

bottom of parietal cells in----

Front 19

How are things released from the gastric gland to the gastric lumen?

Back 19

secreted volume that comes out is under pressure.
Volume that is secreted rises to the surface under pressure - tunnels its way under pressure.

Front 20

Low passive permeability of mucosal membrane

Back 20

cells tightly packed w/ small pores

Front 21

Function of Rich blood supply
Assisted by

Back 21

keeps integrity of epithelium
Assisted by prostaglandins

Front 22

When substances disrupt the gastric mucosal barrier it is known as

Back 22

breaking the gastric mucosal barrier

Front 23

How is mucosal damage repaired at a rapid level?

Back 23

b/c stomach cells are so active, cells on top exfoliate at a rapid rate (natural consequence). Surface cells get replaced by migration of cell from down in the pits.

Front 24

G cells in the epithelium

Back 24

secret gastrin & promote restorative effects. - assist in mucosal damage repair

Front 25

When the epithelium doesn't repair itself, it b/c

Back 25

inflammed

Front 26

Acute gastritis

Back 26

occurs if mucosa can repair itself by upward migration & gastrin.

Front 27

Ulcers can result from

Back 27

the mucosa being unable to repair itself

Front 28

Drugs that cause ulcers

Back 28

NSAIDs - non sterodial anti inflammatory drugs

Front 29

Example of NSAIDS

Back 29

asprin

Front 30

% of people getting ulcers from taking NSAIDS

Back 30

20%

Front 31

Aspirin irritates

Back 31

irritates gastric mucosa, irritates gastric mucosal barrier

Front 32

When you take aspirin, what form passes across the gastric membrane quickly?

Back 32

undissociated form

Front 33

Where does aspirin dissociate?

Back 33

in the cytosol

Front 34

How can aspirin dissociating in the cytosol cause problems?

Back 34

it releases H in the cytosol, which raises pH.

Front 35

While aspirin is dissociating, what happens?

Back 35

H buffers get exhausted. pH rises to a certain level, causing transport to stop.

Front 36

What is sensitive to acidic cytosolic pH?

Back 36

Na/K pump

Front 37

What happens to the Na/K when the cytosol b/c acidic?

Back 37

loses potential difference & prob that the cell will remain viable is small.

Front 38

What happens when H dissociates

Back 38

decreased membrane permeability of gastric cells & acid contents begin to flow & infect the cell - & can cross the epithelium.

Front 39

when H crosses the epithelium membrane, it causes

Back 39

inflammation.

Front 40

Tight junctions of the gastric mucosal barrier b/c ______ when H crosses the epithelium

Back 40

leaky -

Front 41

when the mucosal barrier b/c leaky, acid can flow where

Back 41

into an area that will attack the basolateral surface of the epithelium. - Histamine release - inflammation.

Front 42

Aspirin interferes w/

Back 42

COX enzyme pathways

Front 43

COX 1 enzyme generates

Back 43

cyto-protective products = prostacyclins & prostoglandins.

Front 44

COX 2 generates

Back 44

inflammation response.

Front 45

Aspirin & Cox 1

Back 45

aspirin irreversibly binds to COX 1 - inhibits mucus production, bicarbonate secretion, blood flow by inhibiting cytoprotective products

Front 46

Aspirin & Cox 2

Back 46

inhibits COX 2, preventing inflammation.

Front 47

Dentists usually give acetaminophen instead of aspirin b/c

Back 47

acetaminophen is an anti inflammatory but does not inhibit COX 1.

Front 48

Celebrex

Back 48

NSAID which inhibits enzymes that mediate inflammation & doesn't inhibit cyto protectins.

Front 49

Why do NSAIDs cause problems?

Back 49

Pepsins - cleave peptide bonds in the mucus - making it less visous

Front 50

Pepsins create a problem in the

Back 50

stomach b/c this where pepsin is located & where hydrogen conversion occurs.
lesser of a problem in the duodenum, where pepsin is inactivated.

Front 51

Alpha adrenergic agonist

Back 51

reduces bicarbonate secretion., pouring out high levels of catecholamins - causes stress ulcer.