Gastric secretions Flashcards

1
Q

name the volume of secretions that happen in the gut

A
  • Ingested water (2L)
  • Liver and pancreatic secretions (2L)
  • Salivary gland secretions (1.5L)
  • Secretions by glands of the stomach and small intestines (3.5L)
  • Small intestines absorbs 8.5L
  • Colon 400ml
  • Faeces 100ml
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2
Q

what is the function and effect of amylase

A

Function: Enzyme
Effect:Breaks down polysaccharides into disaccharides
(e.g. starch to maltose)

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3
Q

what is the function and effect of lysozyme

A

Function: Enzyme
Effect: Lyses (destroys) bacterial membranes

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4
Q

what is the function and effect of bicarbonate

A

Function: Buffer
Effect: Neutralizes food and bacterial acids

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5
Q

what is the function and effect of growth factors

A

Function: signalling molecule
Effect: Stimulate epithelial proliferation Particularly protective for oesophageal epithelium

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6
Q

what is the function and effect of transcobalmin II

A

Function: chaperone
Effect: Binds and chaperones cobalamin (vitamin B12)

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7
Q

what are the salivary secretions

A
  • amylase
  • lysozyme
  • bicarbonate
  • growth factors
  • transcobalamin
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8
Q

what are the gastric secretions

A
  • mucus
  • acid (HCl)
  • pepsinogen
  • chymosin
  • lipase
  • intrinsic factor
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9
Q

where is Mucus secreted from and what is its effect

A

Secreted from: Mucous cells (cover luminal surface, extend into glands as mucous neck cells)
Effect: Secrete bicarbonate-rich mucus that coats and lubricates the gastric surface, and protects the epithelium from the acid that we need to properly digest the food Bicarbonate acts as a buffer prevents gastric acid being in direct contact with the epithelium

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10
Q

where is acid secreted from and what is its effect

A

secreted from: Parietal cells
effect:Activation of pepsinogen
Inactivation of ingested microorganisms such as bacteria
Produces acid

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11
Q

where is pepsinogen secreted from and what is its effect

A

secreted from: Mucous cells and chief cells

effect: activated by low pH into active protease pepsin - digestion of proteins

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12
Q

where is chymosin(renin) secreted from and what is its effect

A

secreted from: Chief cells

effect: Coagulates milk protein and is used to make cheese

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13
Q

where is lipase secreted from and what is its effect

A

secreted from: Chief cells

effect: Initiates triglyceride digestion

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14
Q

where is intrinsic factor secreted from and what is its effect

A

secreted from: Parietal and chief cells

effect: Glycoprotein- binds vitamin B12 in intestine for absorption

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15
Q

describe how B12 absorption takes place

A
  • Bind to haptocorrin proteins produced in the salivary gland
  • Must be complexed with the IF
  • IF is released by the stomach
  • Absorbed in the terminal ileum
  • Transported in portal circulation and transferred to transcobalamin II (TCII/B12)
  • Degraded in lysosome to allow function as a cofactor
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16
Q

what do the gastric epithelial cells secrete

A
  • Surface mucus cells = secrete mucus, trefoil peptides (associated with mucus), bicarbonate
  • Mucus neck cells = stem cell compartment
  • Parietal cells = secrete acid, intrinsic factor
  • ECL cells – secrete histamine
  • Chief cells. – pepsinogen, chymosin, lipase
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17
Q

what are the gastric epithelial cells

A
  • surface mucus cells
  • mucus neck cells
  • parietal cells
  • ECL cells
  • chief cells
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18
Q

what causes gastric acid secretion

A
  • parietal cells
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19
Q

how is HCl made

A
  1. Carbonic anhydrase takes carbon is acid that dissociates with carbon dioxide and water
  2. Water can easily cross the membrane using aquaporins via facilitated diffusion
  3. Carbon dioxide can diffuse by simple diffusion as it is a gas
  4. Then carbonic anhydrase reassembles carbon dioxide into bicarbonate and the bicarbonate is taken back into the blood
  5. The proton that is created is pumped out through the potassium proton pump
  6. Need to use an ATP driven pump to pump the hydrogen ions against the concentration gradient
  7. This produces the proton to make HCL
  8. Chloride is pumped in when bicarbonate is pumped out in order to maintain electroneutrality
  9. Therefore the CFTR pumps chloride out straight away as you do not want it in the cell
  10. Proton combines with the chloride and makes HCl
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20
Q

where is the proton pump located

A
  • located on the apical membrane of the parietal cell
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21
Q

describe the proton pump

A
  • Driven by energy released by ATP
  • Electroneutral K+ goes the other way
  • Has a crystal structure
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22
Q

what structure does the proton pump have

A

crystal structure

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23
Q

what cells are located int he gastric pits

A

parietal cells

24
Q

why do the parietal cells have lots of ATP

A
  • Lots of mitochondria in the gastric pits in order to generate the ATP for HCL secretion, this is used only when the stomach is informed for example by hormones
25
Q

what would happen without mucus

A
  • Without mucus the acid would interact with the cells directly and cause pain and injury
26
Q

what does mucus do

A
  • mucus along with bicarbonate is used to counteract pH
  • the bicarbonate is released by the surface mucus cells
  • mucus layer forms a physical barrier which is the gel layer and a chemical barrier which is the bicarbonate Laye
27
Q

what can disrupt mucus acid control

A
  • This can be disrupted by Stress/chemicals/alcohol/NSAIDS
28
Q

what are ECL cells whole name

A

Enterochromaffin like cells

29
Q

describe how acid secretion is controlled

A
  • When food is in the stomach there is a distension from the Vagus nerve
  • This relays through the enteric nervous system
  • Produces acetylcholine which binds to M3
  • M3 is on the parietal cells and ECL cells
  • The Vagus nerve stimulates parietal cells to produce acid
  • It has an indirect effect on the ECL cells,
  • The ECL cells release histamine and this is the second stimulation of acid secretion which binds to the H2 receptors on the parietal cells and causes them to produce HCl
  • ECL cells are also influenced by gastrin receptor CCK2 and Somatostatin receptor
  • Gastrin receptors – enhances the system and makes it activate producing more stomach acid and HCL
30
Q

what releases histamine

A
  • ECL cells

- Mast cells

31
Q

what does histamine do

A
  • Responsible for allergic response

- Activate visceral pain pathways

32
Q

describe feedback control of acid secretion in D cells

A
  • Somatostatin is released from the D cell
  • Acetylcholine binds to the M3 which is on the D cell, this inhibits the D cell from working and therefore increases HCL secretion
  • Somatostatin – it binds to the parietal and prevents cells to stop the acid system and it binds to the ECL to stop the release of histamine
33
Q

what happens in the antrum in the stomach

A
  • this is where gastrin is important
  • can see partially digested protein
  • lot of protein is not completely digested in the stomach
  • in order to digest protein need acid to activate pepsin to break down protein G cells to make gastrin
  • D cells in the antrum – if there is too much acid they release somatostain and feedback through the blood and attach to the parietal cells and prevent them from making acid
34
Q

what activates HCL production

A

Gastrin, acetylcholine and histamine activate HCL production

35
Q

what inactivates HCL production

A

Somatostatin and prostagladins inactivate HCL

36
Q

describe Zollinger Ellison syndrome

A
  • Caused by gastric acid hypersecretion
  • Results in severe gastroesophageal peptic ulcer disease
  • Due to the ectopic secretion of gastrin by a neuroendocrine tumor (gastrinoma)
  • Neuroendocrine tumours secrete excess hormones
  • Usually present in the duodenum or pancreas
  • If acid gets out of control then it damages its own body
37
Q

what are the parts of the neural control of gastric secretions

A
  • cephalic phase
  • gastric phase
  • intestinal phase
38
Q

describe the neural control of gastric secretions

A

o Cephalic phase activates secretion
o Gastric phase – distends stomach and activates the vagus nerve the increase secretions
o Acid in small intestine inhibits secretion by sympathetic outflow

39
Q

what are the two hormones that control bile secretion

A

Cholecystokinin (CCK

secretin

40
Q

when is Cholecystokinin (CCK) secreted

A
  • Fatty acids in duodenum
  • Gall bladder contraction
  • Sphincter of Oddi relaxation
41
Q

when is secretin secreted

A
  • Acid chyme in duodenum

* Stimulates biliary ductal cells

42
Q

where does H.Pylori infect

A

• Duodenum and stomach

43
Q

what does H.Pylori cause

A

• Major cause of peptic ulcer (up to 20%)

- Combined with: stress, smoking, alcohol, NSAIDs

44
Q

what are the 4 stages of how H.pylori enter the cells

A
  • Tunnel through mucus layer
  • Secrete ammonia to neutralise, it changes the pH
  • Recruit more H pylori as the environment has been changed
  • Mucosal damage is caused
  • Urease combined with water and urea forms carbon dioxide and ammonia and this neutralises the gastric acid and results in de-gel of the mucin
45
Q

How do you diagnose H.Pylori

A
  • Urea breath test: urea C14 is given to patient and H. Pylori converts urea C14 to ammonia (NH3) + C14O2
  • CLO test: biopsy placed in media with urea and pH indicator conversion of urea to ammonia raises pH ( if H. pylori present), which changes the colour of pH indicator.
  • blood antibody test: antibodies to H. Pylori
  • stool antigen test (H. Pylori proteins)
46
Q

what is the treatment of H.Pylori

A

Triple therapy: 2 antibiotics + 1 Proton pump inhibitor – this helps the mucosa to recover

47
Q

Name the treatment options for peptic ulcer disease

A
  • Vagotomy
  • Histamine
  • Proton pump inhibitor
  • Antibiotics
48
Q

describe the mechanism of action of vagotomy

A
  • Reduces ACh secretion from enteric neurones
  • Reduce acid secretion
  • This is no longer done
  • This removed the vagus nerve
49
Q

describe the mechanism of action of proton pump inhibitors

A

omeprazole

  • Prevent H+/K+ ATPase on parietal cell
  • Reduce acid secretion
50
Q

describe the mechanism of action of antibiotics

A

Amoxycillin + Clarithomycin

  • Kill H Pylori bacteria
  • Eradicate infection
51
Q

what is Gastrooesophageal reflux disease

A

a condition that develops when the reflux of stomach contents causes troublesome symptoms and/or complications
- it is not caused by excessive HCl secretion

52
Q

what is GORD caused by

A
  • Excessive reflux of normal gastric juice (increased frequency of Transient Lower Oesophageal Sphincter Relaxations)
  • Weakened oesophageal epithelium
  • Hiatal hernia
  • Hypersensitivity of oesophageal pain sensing nerves
53
Q

how do you prevent and treat GORD

A
- proton pump inhibitors 
Can block 
-	Histamine receptor 
-	Inhibit the protons pumped
-	Neurtralise antacids by prevent potassium move out
54
Q

what is gavascion made up of

A
  • Potassium hydrogen carbonate and sodium alginate
55
Q

what are the surgical treatment for GORD

A

Fundoplication

magnetic anti-reflux device

56
Q

how doe fundoplication work

A
  • Tightens and reinforces the LOS.

* The upper part of the stomach is wrapped around the outside of the lower oesophagus to strengthen the sphincter.

57
Q

How does the magnetic anti-reflux device work

A

this extends when the chyme goes through and restricts when nothing is going through via magents