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Metabolism > Gastric secretions > Flashcards

Gastric secretions Flashcards

1
Q

What is a mucus neck cell?

A

stem cell compartment

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2
Q

What to parietal cells produce?

A

HCL, Transcobalamine II, intrinsic factors

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3
Q

what do ECL cells produce?

A

Histamines

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4
Q

Where is the proton pump located in the gut? What drives it?

A

Apical membrane of parietal cells.
Driven by ATP
Electroneutral K passes the other way

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5
Q

What are cells of the gastric pit?

A

Parietal cells located at base of gastric pits

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6
Q

What happens when cells of the gastric pit are stimulated?

A

They insert H+-ATPase into the membrane

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7
Q

What is the function of mucus cells?

What is the physical and chimerical barrier of mucus?

A

Mucus cells secrete mucus and bicarbonate to prevent the local low pH from damaging stomach lining

Physical-gel like
Chemical- biocarbonate

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8
Q

What can disrupt the production of mucus?

A

Stress, chemicals, alcohol, NSAIDS

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9
Q

Describe the feedback control of acid secretions when food is ingested

A

Distention of the stomach the the fundus causes parasympathetic stimulation of the parietal cells (vagus nerve, ACh) on M3 receptors which increases activity of the H+-K+ ATPase (proton pump) casuing secretions.
This innervation also stimulates Gastrin production which stimulates ECL cell to produce histamine which also stimulates H+- K+ ATPase in the parietal cells through H2 receptors (M3 mAChR)

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10
Q

Which immune cell prduces histamine?

Which non immune cells secretes histamines?

A

Mast cells during allergic reactions

ECL cells

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11
Q

Describe the feedback control of acid secretions - Which hormone inhibits acid secretions and how?

A

Somatostatin is released from from D cells in the mucosa. Somatostatin is a potent inhibitor of acid secretion; it inhibits gastrin secretion from G cells and histamine secretion from ECL cells.
Acts in a paracrine or endocrine (blood) manner

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12
Q

what is Zollinger-Ellison syndrome?

A

Results in severe gastroesophageal peptic ulcer disease

Caused by gastric acid hyper secretions due to the ectopic secretion of gastrin by a neuroendocrine tumor (gastrinoma)

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13
Q

Where is Zollinger-Ellison syndrome most likely to occur?

A

duodenum or pancreas

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14
Q

Describe the cephalic phase of gastric secretions

A

Sight, smell, taste of food (cerebral cortex) stimulates the the Medullary nuclei
which stimulates the vagus nerve, which causes the secretion of HCL, mucus and pepsinogen.

Oral mechanoreceptors and chemoreceptors stimulate the medullary nuclei which stimulates the parasympathetic innervation of secretions

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15
Q

Describe the Gastric phase of gastric secretions

A

Mechanical distension of
the stomach actiavtes stretch and chemoreceptors which trigger the submucosal and myenteric plexus to produce gut secretions, especially gastrine which increases HCL production.

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16
Q

Which part of the brain does gastric distention secrete back to?

A

Medullary nuclei

17
Q

Describe the Intestinal phase of gastric secretions

A

During feeding, proteins in the chyme act to buffer the pH.
In an emptry stomach drops PH below 3. This causes the sympathetic inhibition of gastric secertions through acting on the medullary nuclei.

Also the activation of D cells to produce somatostatin to reduce production of gastrine

18
Q

Which hormones control bile secretions?

A

Cholecystokinin (CCK) (contracts gall bladder, sphincter of oddi relaxes)- production activated by fatty acids in duodenum
and
Secretin (stimulates biliary ductal cells)- acidic chyme stimulates secretin production

19
Q

What stimulates the production of Cholecystokinin (CCK)

A

Fatty acids in chyme

20
Q

What stimulates the production of Secretin

A

Acid in the chyme located in duodenum

21
Q

Where do Helicobacter pylori infections occur?

A

Duodenum and stomach

22
Q

what does Helicobacter pylori cause?

A

peptic ulcers (combined with stress, smoking,alcohol,NSAIDS)

23
Q

Describe the 4 stages of Helicobacter pylori infection

A
  1. Tunnel through mucus layer
  2. Secrete ammonia to neutralise
  3. Recruit more H pylori
  4. Mucosal damage
24
Q

How is Helicobacter pylori infection diagnosed?

A
  1. Urea breath test: urea C14 is given to patient and H. Pylori converts urea C14 to ammonia (NH3) + C14O2
  2. 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.
  3. Blood antibodies tests against H-pylori
  4. Stool antigens test
25
Q

what is the treatment for H-pylori ?

A

2 antibiotics + 1 Proton pump inhibitor

26
Q

What are the treatment options for peptic ulcer disease?

A

Histamine (H2) antagonists- block H2 receptors on parietal cells to reduce acid secretion (famotideine)

Proton pump inhibitors- (omeprazol)
Prevent H+/K+ ATPase on parietal cell
Reduce acid secretion

Antibiotics- (Amoxycillin + Clarithomycin)
Kill H Pylori bacteria
Eradicate infection

27
Q

Which drugs make up the tripple treatment for H-pylori?

A

Amoxycillin + Clarithomycin+ omeprazol

28
Q

What is the common ending for protein pump inhibitors

A

prazol

29
Q

What is Gastroesophageal reflux disease?

A

When gastric contents flows back into oesophagus causing negative side effects

30
Q

What could possible cause Gastroesophageal reflux disease?

A

Weakened oesophageal epithelium
Increased frequency Lower Oesophageal Sphincter Relaxation
Hypersensitivity of oesophageal pain sensing nerves

31
Q

What are the treatment options for GORD and what do they effect?

A 
Block M3 receptor with pirenzepine
Block H2 receptor with H2RSs
Activate prostoglandin receptor with misoprostol
Inhibit H+/K+ pump with PPI's
Neutralise acids (K+) with antacids

Fundoplication: standard surgical treatment for GORD.
Tightens and reinforces the LOS.
The upper part of the stomach is wrapped around the outside of the lower oesophagus to strengthen the sphincter

32
Q

What are the active ingrideints in gavison and how does it protect the stomach?

A

Active ingredients: Sodium alginate & Potassium hydrogen carbonate

Formation of protective raft over acid pocket (Sodium alginate)

33
Q

Describe the surgical treatments for GORD

A

Fundoplication- Tightens and reinforces the LOS

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

34
Q

Name the two types of Fundoplication

A

Laparoscopic Nissen fundoplication

LINX® magnetic anti-reflux device

35
Q

What will you find in salivery secretions? What is the function of these components?

A

Amylase- Breaks down polysaccharides into disaccharides
Lysozyme- Lyses (destroys) bacterial membranes
Bicarbonate- Buffer, Neutralizes food and bacterial acids
Growth factors- Signalling molecule which stimulates epithelial proliferation
Transcobalamin II- Binds to vitamin B 12

36
Q

Describe the stages of B 12 absorption

A

Bind to Haptocorrin proteins produced in the salivary glands

Must be complexed with stomach derived intrinsic pathway

Absorbed in the terminal ileum

Transported in portal circulation and transferred to transcobalamin II (TC-II/B12)

Degraded in lysosome to allow function

37
Q

What do cheif cells produce?

A

Pepsinogen, chymosin, lipase

38
Q

What activates and inhibits ECL cells?

A

Gastrin activates ECL cell through CCK2 receptor, somatostatin inhibits ECL cell

39
Q

What percentage of the world has H-pylori infection?

A

over 50%

Metabolism (9 decks)

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