Gastric Secretion and Motility 2 Flashcards

1
Q

LEARNING OBJECTIVES:

*Stomach anatomy and function
*Gastric digestive juice secretion
*HCL secretion
*3 phases of gastric secretion
*Mucosal barrier

A
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2
Q

Stomach Anatomy see slide 3 -> LEARN NB

A

Stomach structure - looking at specialised of a special tube
dilated and turned on its side
Lies in between oesophagus and small intestine the duodenum

Cardia: region where material comes in from oesophagus with stomach
Fundus: top
The major part of stomach is called the body
Pyloric antrum: canal in the centre which leads to opening
guarded by pyloric sphincter: muscle nerve
Opening is called the pyloric orifice
Also the pyloric sphincter, and pyloric constriction

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3
Q

Stomach function? 2

A

1) Storage and Mixing (motility-based functions)

Need to store large material that you consume
expands up to 1L of material
Real capacity to store material
Gives DS time to ingest material
It mixes material

2) Digestion (Secretory function; HCl/pepsinogen/intrinsic factor)

At the fundus: interstitial cells of Cajal: located along DT that produce a wave live motion - this contraction about 3 every minute these contractions occur down through the stomach to allow material go down the body
Storage site the 1/3 part the body
Antrum: greatest mixing of material takes place here
As a wave of contraction moves down through it becomes stronger and stronger, the muscle mass becomes larger as you go through stomach to facilitate more mixing
Pyloric sphincter is tonically opened
Material must be below 2mL in diameter to move through
stomach makes material small enough to pass through

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4
Q

Retropulsion and emptying?

A

Amount of chyme that escapes into duodenum with each peristaltic wave (fundus) before the pyloric sphincter closes depends largely on the strength of antral peristalsis

Causes it to fully close once the contraction meets it after food has gone through
Once sphincter fully closes, the material is churned on itself and this is called retropulsion and then again when it leaves and this is called emptying

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5
Q

Gastric Juice secretion
1. How much a day?
2. What are the 2 major collection of cells inside the stomach?
How do they differentiate

A
  1. 2 litres of gastric juice a day
  2. Collection of cells - inside of stomach - the inner lining of the tube: 2 major
    Oxyntic mucosa: inner lining of stomach the fundus
    Pyloric gland area: mucosal lining in the antrum

They contain different collection of gastric cells however they are both mucosa cells

We have gastric pits - invaginations deepening down into surface from surface into mucosa and at base of pits sis gastric glands which make different products of gastric juice
Mixed into substance of stomach from mucosa

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6
Q

MOST IMPORTANT SLIDE 7
The stomach mucosa and gastric glands
1. Exocrine cells: 3 and what do they secrete?
2. Endocrine/paracrine cells and what do they secrete?

A
  1. Mucous cells- line the invaginations: protective role - alkaline mucus, chief cells- inactive enzyme that becomes active, protein breakdown - pepsinogen, parietal cells-dots within submucosa, they make acid HCL is key for protein digestion it activates pepsinogen - HCL and intrinsic factor - made by parietal cells
    important for filament absorption
  2. ECL cells: Enterochromaffin like cells - histamine - activator of PARIETAL CELLS - in oxyntic mucosa
    G cells - Gastrin - released into circulation and stimulates ECL parietal and chief cells, D cells - somatostatin - inhibitor, inhibits g cells and ECL and parietal cells

There is a complex between cross talk between different cell types

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7
Q

Where do exocrine cells secrete from?
Where do endocrine cells secrete from?

A

In oxyntic mucosa
In pyloric gland area

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8
Q

Stimulation of HCL secretion?

A

Diagram slide 8 shows inter talk between all cells

Gastrin, histamine + ACh all stimulate HCL secretion by stimulating parietal cells

Gastrin releasing peptide (GRP) → gastrin release
Gastrin (G) released by Gm cells → histamine (H) release from ECL cells
Ach (A) released by neurons → histamine release

Neuron make neuropeptide: makes GRP - cranial nerve: vagus the 10th one

Vagus nerve stimulates G cells

NT labelled A is seen: Ach - localised released by neurons by intrinsic nerves - the enteric NS, can also release ECL cells which is a stimulator for secretion of HCL

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9
Q

Vagus nerve - CN X?
Where does it arise?

A

Orginates in brainstem in medulla on left and right
Exits cranial cavity back of the skull goes through the body
it has abdominal branches that innervate the digestive system - it has 10 branches throughout the body
Transits output to/from viscera: 80-90% afferent
In the medulla

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10
Q

HCL secretion slide 10

A

Q - Know cellular mechanism by which HCL is actually regulated:

Parietal cells within stomach make HCL
Lumen membrane is seen curved and on the other side is the basolateral membrane
Its not plasma it is Interstitial fluid
Want to make HCL in lumen - primary active transport and secondary active transport
ATPase pump is how H ^+ ions gain entry into lumen they pump them out against this gradient vs K^+ ions
Water within the cell donates H ions for this and also donates OH ions
These cells have Ca - carbonic anhydrase which is very important it combines OH and CO2- which is taken in from plasma by diffusion or made by cellular metabolism
Product of these is HCO3 -> KEY for Cl^- gaining entry to lumen
Secondary active transport mechanism here in basolateral membrane that moves bicarbonate out down the electrochemical gradient for reaching of bringing Cl into cell against electrical gradient then Cl^- moves by diffusion by lumen membrane and once it is in lumen it combines with H ions and makes HCL in gastric lumen
VERY DEPENDENT ON ENZUME Canaliculus

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11
Q

Explain cephalic phase of control of gastric secretion:

A

Cephalic means head
This is stimulated in the head
Feedforward mechanism that prepares body for food that is being made
Stimuli in cranial region: vagus is key - vagal nerve feeds down to the stomach to stimulate G cells to make Gastrin which promote gastric secretion and indirectly it stimulates ECL cells which make histamine which makes chief parietal cells
Vagal nerve also causes positive effect on intrinsic nerves so increases Ach which stimulates chief and parietal cells to also increase gastric secretion

SHERWOOD at top the all black diagram is the 1 to know for EXAMS -> HAS MORE DETAIL

Initial stimulus of sight, smell, taste of food, chewing and swallowing causes physiological response: Increased parasympathetic activity by vagus nerve: 2 things occur -
(1) Increased ACh increases chief and parietal cells which increases gastric secretion
(2) G cells cause increased gastrin secretion and increased plasma gastrin which causes parietal and chief cells to increase acid and pepsinogen secretion and thus increase gastric secretion

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12
Q

SLIDE 11 SEE

A
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13
Q

With Cephalic phase what activation stimulates multiple cell responses via neurotransmitters?

A

Vagal Activation

See slide 13

Vagal input
Vagus is also at GRP at the right hand side
G major stimulator for many cells

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14
Q

What components of the gastric mucosal barrier enables the stomach to contain acid with injuring itself?

A
  1. The luminal membrane of the gastric mucosal cells are impermeable to H^+ so that HCL cannot penetrate into the cells.
  2. The cells are joined by tight junctions that prevent HCL from penetrating between them.
  3. A mucus coating over the gastric mucosa offers further protection
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15
Q

Protection of gastric mucosa?

A

Mucosal barrier - Secretion of mucus/HCO3 by epithelial cells forms a barrier that protects stomach from low pH and from digestion by pepsin
Replacement of the entire stomach lining every 3 days

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16
Q

4 important factors in the control of motility and secretion in the central role of neural and endocrine pathways?

A
  1. Autonomous smooth muscle function
  2. Intrinsic nerves
  3. Extrinsic nerves
  4. Gastrointestinal hormones - switching off secretion
17
Q

Receptor activation alters digestive activity how?

A

Via neural and hormonal pathways

18
Q

What is gastroparesis?
Signs and symptoms? 6
Cause?
Treatment?

A

Collection of disorders involving delayed gastric emptying
1. Vomiting/ Nausea
2. Abdominal bloating
3. Abdominal pain
4. Changes in blood sugar levels - not a cause of diabetes but can make diabetes worse
5. Lack of appetite
6. Weight loss
Damage to the vagus (diabetes- can alter neural surergy and alter blood vessels for neurons and damage vagus nerve/surgery)
Treatment involved changes in diet- smaller meals, etc, diphenhydramine, therapies such as Reglan used to stimulate gastric muscle

SEVERE CASES-> A J tube can be used which by passes the stomach and goes straight to Small intestine and deliver fluids but only in severe cases

19
Q

Slide 23 see - Summary of all gastric secretion v important

A
20
Q

How often is entire stomach lining changed?

A

Every 3 days

21
Q

SLIDE 14 GASTRIC PHASE explain:

A

See diagram at the top
Major stimulator for this is food, especially protein
Overlapping stimulatory pathway - amplified by previous steps
food is now in stomach want to enhance secretion more
vagus is still activated
There are lots of overlapping pathways

Stimuli in the stomach: protein - peptide fragments are picked up and also the stimulants caffeine and alcohol cause distension
Causes an effect on vagus nerves which stimulates intrinsic nerves and G cells
G cells stimulate increase in gastrin which has a positive effect on chief and parietal cells leading to increased gastric secretion and on ECL cells which stimulate histamine which also have an effect on chief and parietal cells thus increasing gastric secretion.
Intrinsic nerves cause an increase in ACh which cause an stimulate chief and parietal cells which then increase gastrin secretion.

22
Q

2 stimulants for gastric secretion?

A

Caffeine and alcohol are natural stimulants of gastric secrtion
very acidic environment

23
Q

slide 15 - Gastric Secretion: intestinal phase - explain what switches off gastric secretion
1. What happens in Body and Antrum?
2. What happens in Antrum and duodenum?
3. What happens in duodenum: the intestinal phase of gastric secretion?

A

Inhibitory phase is the last phase - intestinal phase
there inhibitory factors that switch off gastric secretion
Food has left stomach so no longer need gastric juice

  1. In the body and antrum, the body then no longer has stimuli - such as protein so the intrinsic nerves, G cells and vagus nerve are all being inhibited and that stops secretion. G cells do this by decreasing gastrin secretion thus decreasing histamine thus causing a decrease in gastric secretion.
  2. In the antrum and duodenum there is an accumulation of acid which causes D cells to become activated. D cells causes an increase in somatostatin, which is an inhibitor which turns off these cells Parietal, G and ECL cells thus decreasing gastric secretion.
    Acid normally lies on surface of D cells - if food is longer there than acidic lies on surface of stomach which causes D cells and turns off secretion. so acid doesn’t destroy stomach
  3. Then goes into duodenum for the last part - Fat, acid, hypertonicity and distention promotes increased production of enterogastrones (cholecystokinin and secretion which are key players in digestive control - what they do here is they switch off secretion of lots of different cells - inhibitory cells) They cause decrease in parietal cells, chief cells and smooth muscle cells thus decreasing gastric secretion and motility.
    This ^ along with the Entrogastric reflex being promoted which has the same affect on these cells thus decreasing secretion.
24
Q

What is the negative feedback control of gastric secretion?

A

Key thing is change in pH - acid is accumulating - food is no longer there and this is what stimulates D cells which are inhibitory cells and turn off this secretion
Lower pH stimulates somatostatin secretion by these D cells and SST inhibits secretion by G, ECL, Parietal and chief cells

25
Q

Very acidic enviornent how deos this not damage our stomach?

A

Many different barriers that protect it

3 layers of protection: mucous coat acts as physical barrier to HCL
Cells in stomach such as parietal cells are held very closed together by tight junctions which stop HCL moving between the cells connection between cells very tight in stomach
Hydrogen ions cannot physcially cross lumenal membrane of the stomach
Huge reparation mechanism of the stomach as we replace our lining every 3 days
Excessive acid production causes erosion in surface and causes peptic ulcers:
Gastric reflex - comes back to oesophagus and oesphogeal organs
we do have protective mechanism to ensure this does’nt happen

26
Q

slide 20

A

pacemaker cells in inner circualr muscle in funuds make wave like contractions taht shuttle material down stoamch and causeing repuslion and emptuing of materual

27
Q

Oxyntic mucosa and pyloric gland area are found where?

A

Oxyntic mucosa: fundus and Pyloric gland area: antrum

28
Q

During Gastric secretion, in the cephalic phase - where are Pepsinogen and HCL found?
Histamine?
Gastrin?

A

Pepsinogen and HCL in the lumen
Histamine in the laminar propria
Gastrin in the blood

29
Q

What effect do entergastrones: cholecystokinin and secretin have?

A

They reduce the strength of atrial peristalsis: feedback mechanism from duodenum back to stomach that is all we need to know - lowering the strength of emptying

30
Q

GI motility - how does it move?
What are the pacemaker cells called?

A

*Inner circular layer generates slow, spontaneous, graded depolarizations known as slow waves
Peristalsis
*Basic electrical rhythm (BER)
*Pacemaker cells known as interstitial cells of Cajal