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Metabolism > Gastric secretions > Flashcards

Gastric secretions Flashcards

1
Q

what is the function + effect of amylase

A

amylase is an enzyme which breaks down polysaccharides into disaccharides (e.g. starch into maltose)

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2
Q

what is the function + effect of lysozyme

A

lysozyme is an enzyme which ‘lyses’ (destroys) bacterial membranes

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3
Q

what is the function + effect of bicarbonate in stomach

A

bicarbonate is a buffer which neutralizes food + bacterial acids

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4
Q

what is the function + effect of growth factors in stomach

A

GFs in stomach are signalling molecules which stimulate epithelial proliferation. Particularly protective for oesophageal epithelium

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5
Q

what is the function + effect of haptocorrin transcobalamin-1 in stomach

A

haptocorrin transcobalamin-1 is a chaperone which binds + ‘chaperones’ cobalamin (VITAMIN B12)

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6
Q

what is the cerebral (or cephalic) phase of digestion + which nerve (in parasympathetic nervous system) is this mediated by + how this affects acid production

A

cerebral (or cephalic) phase of digestion, whether triggered by the sight, smell, or thought of food , initiates the digestive process with the salivary and gastric secretory responses mediated via the autonomic nervous system

  • Accounts for ~ 20-50% post prandial acid secretion
  • Mediated entirely through VAGUS nerve
  • Affects acid production through several separate pathways:
    • Direct stimulation by acetylcholine on parietal cells – produce HCL
    • Stimulation ECL {Enterochromaffin-like} cells by acteylcholine – indirect stimulation HCL release via parietal cells
    • Stimulation G cells - gastrin release by GRP – Gastrin Releasing Peptide - indirect stimulation HCL release via parietal cells

Acetylcholine from vagus nerve also acts on chief cells to release pepsinogen

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7
Q

what are the ‘acid producing’ cells in the stomach

A

Parietal cells are responsible for gastric acid secretion, which aids in the digestion of food, absorption of minerals, and control of harmful bacteria.

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8
Q

what is pepsinogen + what stimulates chief cells to release it

A

Pepsinogen is a powerful and abundant protein digestive enzyme secreted by the gastric chief cells as a proenzyme and then converted by gastric acid in the gastric lumen to the active enzyme pepsin.

ACETYLCHOLINE from vagus nerve also acts on chief cells to release pepsinogen

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9
Q

cells involved in gastric secretion + their function: surface mucuous cells

A

surface mucuous cells secrete mucus, trefoil peptide + bicarbonate

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10
Q

cells involved in gastric secretion + their function: mucuous neck cells

A

mucous neck cells (MNs) are the anchored pluripotent stem cells that divide to replace all other cell types in the gastric gland.

aka theyre a stem cell compartment that can differentiate into any gastric cell

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11
Q

cells involved in gastric secretion + their function: parietal cells

A

secrete acid + intrinsic factor

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12
Q

cells involved in gastric secretion + their function: ECL cells

A

ECL sells secrete histamines (signalling molecules which cause allergic symptoms

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13
Q

cells involved in gastric secretion + their function: chief cells

A

chief cells secrete pepsinogen when stimulated by Ach

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14
Q

cells involved in gastric secretion + their function: G cells

A

G-cells secrete gastrin into the systemic circulation, which allows the delivery of gastrin to parietal cells and enterochromaffin-like (ECL) cells in the gastric fundus and cardia of stomach. Gastrin stimulates the proliferation of gastric mucosal endocrine cells (parietal cells, ECL cells)

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15
Q

parietal cells make ______ whic is essential for absorption of vitamin b12 ,stomach acid is essential for absorption of positive cations (minerals like _____,____,___) in small intestine

A

parietal cells make intrinsic factor whic is essential for absorption of vitamin b12 ,stomach acid is essential for absorption of positive cations (minerals like iron,zinc + calcium) in small intestine

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16
Q

the majority of D + G cells is in what part of the stomach

A

majority of G + D cells are in gastric antrum of stomach

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17
Q

what would happen if mucuous cells didn’t produce the mucus layer + bicarbonate in stomach. Where in stomach primarily contains mucuous secreting glands?

A

the mucus and bicarbonate layer they produce, protects the stomach from digesting itself!

Cardia + Fundus primarily contains mucuous secreting glands

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18
Q

Gastric glands empty into bottom ____ ____ – openings in gastric mucosa

A

Gastric glands empty into bottom GASTRIC PITS – openings in gastric mucosa

19
Q

why are the chief cells (make pepsinogen) located below the parietal cells (make acid)?

A

because pepsinogen (zymogen) is activated by HCl acid, we can’t have it activated early we need an optimum pH for pepsinogen to be cleaved into pepsin (active enzyme) in the stomach

20
Q

where are the majority of the chief + parietal cells located

A

majority of chief + parietal cells are found in gastric body (corpus) of stomach

21
Q

Zollinger-Ellison syndrome (ZES) caused by

A

Zollinger-Ellison syndrome (ZES): too much gastrin

a neuroendocrine tumour (gastrinoma derived from G cells) making tumours seccrete too much gastrin

results in severe gastroesophageal peptic ulcer disease

usually present in duodenum

(typically non-malignant) but can be malignant rarely

22
Q

why do we have more mucus secreting cells in transition parts of stomach e.g. near oesophagus

A

because we need to protect those parts from the hydrochloric acid of the stomach

23
Q

Ach released by ____ nerve, the Ach binds to ____ receptor on the parietal-cells basolateral membrane. Those parietal cells are stimulated to release ____ into lumen of stomach.
At the same time, the Ach bind to ___ cells which secrete histamine. The histamine binds to parietal cells via ___ receptors.

Drugs we use for ppl with excess acid production/ Peptic ulcer disease are H2 _______ (H2 blockers) that block the receptor which stops the acid release.

A

Ach released by VAGUS nerve, the Ach binds to M3 muscarinic receptor on the parietal-cells basolateral membrane. Those parietal cells are stimulated to release HCl ACID into lumen of stomach.
At the same time, the Ach bind to ECL cells which secrete histamine. The histamine binds to parietal cells via H2 receptors.

Drugs we use for ppl with excess acid production/ Peptic ulcer disease are H2 ANTAGONISTS (H2 blockers) that block the receptor which stops the acid release.

24
Q

aside from ach what else does the vagus nerve release which stimulates ECL histamine production + parietal acid production?

A

vagus nerve also releases GRP (gastrin releasing peptide) which binds to G cells causing them to release gastrin. Gastrin acts on parietal cells to increase acid production. Gastrin also acts on ECL cells to increase histamine production

25
Q

GASTRIC PHASE DIGESTION: continued secretion of HCL, Gastrin, Pepsinogen
Caused by ______ _____ and food breakdown products (all regulated by vagus nerve

A

GASTRIC PHASE DIGESTION: continued secretion of HCL, Gastrin, Pepsinogen
Caused by gastric distention of stomach with food (stretch receptors in stomach which recieve messages from vagus nerve) and food breakdown products (all regulated by vagus nerve

26
Q

when do we refer to food as chyme?

A

after it enters stomach its chyme:
a semi-fluid mass of partly digested food expelled by the stomach, into the duodenum, the upper part of the small intestine

27
Q

When gastrin binds to parietal cells, Ach binds to ___ receptors on parietal cells. The histamine released by ___ cells binds to parietal cells via H2 (histamine-2) receptors. Gastrin binds to parietal cells to stimulate HCl production via _____ receptors.

A

When gastrin binds to parietal cells, Ach binds to M3 receptors on parietal cells. The histamine released by ECL cells binds to parietal cells via H2 (histamine-2) receptors. Gastrin binds to parietal cells to stimulate hcl production via CCK receptors.

28
Q

Where is gastrin made, and where is the majority of these cells located.

where are the effects of gastrin exerted at and what are the functions of gastrin.

A

Gastrin is made by G cells, majority of which are located in antrum of the stomach (cuz these g cells sense the conc of peptides/ conc of acid and tells body whether we need to synthesise more acid)

The effects of gastrin are exerted at CCK2 receptors (also known as gastrin–CCKB receptors). These are found on gastric parietal and ECL cells, some smooth muscle cells, and some central nervous system (CNS) neurons

gastrin functions: stimulates acid production 2 ways
* directly acting on parietal cells to stimulate HCl production
* stimulates histamine production by ECL cells which in turn stimulates hcl production in parietal cells
+ bonus is it stimulates release of pepsinogen

29
Q

What is Somastostatin (SST) and what does it do?

A

Somastostatin (horomone secreted into blood) is the central inhibitor of acid secretion– made by antral D cells

it stops the parietal cells responding to histamine + therefore decreasing HCl production. It also does this by:

  • SST binding to ECL cells= inhibiting release of histamine
  • SST binds to G cells= inhibiting release of gastrin
30
Q

Somatostatin (SST) secretion is stimulated by ________
Somatostatin (SST) secretion is inhibited by ________

A

Somatostatin (SST) secretion is stimulated by low antral pH

Somatostatin (SST) secretion is inhibited by Acetylcholine (PNS)

31
Q

function of Prostaglandins PGE2 + PGI2 they’re synthesised by cox enzyme

A

Prostaglandins PGE2 and PGI2 act directly on parietal cell to decrease acid release + they act on mucus cells to increase mucus + bicarbonate production

32
Q

where is secretin made and what is its function

A

Secretin
* Secreted by epithelial S cells in duodenum

  • Increase production bicarbonate from pancreas AND
  • Inhibits gastric acid secretion after entry of fat and acid into duodenum - reduces acid secretion by three mechanisms:
    1) Inhibition of antral gastrin release,
    2) Stimulation of somatostatin release,
    3) Direct downregulation of parietal-cell H+ secretion
33
Q

where is gastrin made + what is its function

A

Gastrin
* Secreted by epithelial G cells in duodenum

  • Stimulated by high peptide/amino acid load in duodenal chyme
  • Stimulates parietal cells make more HCL
  • Stimulates ECL cells to release histamine that acts on parietal cells to increase HCL

Gastrin also binds to chief cells – release pepsinogen

34
Q

what stimulates the release of gastrin in duodenum

A

lots of broken down bits of protein/ food

aka
Stimulated by high peptide/amino acid load in duodenal chyme

35
Q

How does the parietal cell make HCl (explain proton pump)

A

Parietal cell is full of mitochondria, it has enzyme carbonic anhydrase as well. We have lots of co2 + o2 in the cells as a result of all the mitochondria so the o2 + co2 reacts forming carbonic acid (H2CO3) which rapidly dissociates into H+ and HCO3- ions. The HCO3- is excreted out of parietal cell into the blood in exchange for a chloride ion. Bicarbonate out, chloride in. The H+ (protons) are secreted from parietal cell via proton-potassium ATPase (H-K) pump located on parietal cell. So when H+ excreted out of parietal cell it is replaced by potassium to maintain electrical neutrality. Chloride is excreted out of parietal cell, so the CL- + H+ react together to form HCl acid.

36
Q

pepsinogen is made by chief cells. Why is it a zymogen?

A

A zymogen is the inactive form of an enzyme. Pepsinogen is produced by chief cells in the gastric pits. Hydrochloric acid produced by the parietal cells of the gastric pit work to cleave a peptide bond forming pepsin, which can now work to digest proteins in the stomach.

chief cells, release pepsin in an inactive form, or zymogen form, called pepsinogen. By doing so, the stomach prevents the auto-digestion of protective proteins in the lining of the digestive tract

37
Q

what are the anatomical features that prevent reflux

A

Important anatomical features which prevent reflux are:

  • viable lower oesophageal sphincter seals off stomach from the oesophagus.
  • angle at which oesophagus enters stomach.
  • Contraction of crural diaphragm exerts a ‘pinchcock‘ action at the terminal oesophagus
38
Q

Gastroesophageal reflux disease

A
  • Retrograde flow of gastric contents into oesophagus = Reflux
    GORD (or GERD) = condition develops when reflux of stomach contents causes troublesome symptoms and/or complications

risk:
* Excessive reflux of normal gastric juice (increased frequency of Transient Lower Oesophageal Sphincter Relaxations)
* Weakened lower oesophageal sphincter
* Hiatal hernia
* Obesity
Family history of GORD associated with increased risk

symptoms:
* Heartburn - burning midsternal sensation
* Acid reflux - sour or bitter taste, mainly after meals
* Extra-oesophageal symptoms:
* Cough
* Laryngitis~ (chronic inflammation of voice box/ larynx)
* Asthma
* Dental erosion
CAN BE ASYMPTOMATIC

39
Q

medical options for GORD

A
  • lifetsyle interventions: eat smaller more frequent meals, instead of big meals; avoid NSAIDs/Aspirin which inhibit prostaglandins. Less coffee, chocolate, fatty food, stop smoking
  • proton pump inhibitors PPIs lansoprazole , omeprazole, pantoprazole

*ANTACIDS e.g. gaviscon/rennie

  • surgery sometimes e.g. if ppl don’t wanna be on PPI for long
40
Q

what is a complication of GORD?

A

Barrets oesophagus;
chronic GORD can progress to this where u have mataplasia (one specialised cell from 1 part of body in a part of body u wouldn’t normally find)
so oesophagus usually has squamous epithelium, but in barrets we find metaplasia forming columnar epithelium & goblet cells making mucus to try and protect oesophagus. Metaplastic cells have risk of becoming dysplastic cells= increased risk of adenocarcinoma.

41
Q

What bacteria is a major cause of peptic ulcer (up to 20%) Combined with: smoking, alcohol, NSAIDs

A

Helicobacter pylori
Major cause of peptic ulcer (up to 20%) Combined with: smoking, alcohol, NSAIDs

42
Q

how do we diagnose Helicobacter pylori

A

Helicobacter pylori
* Diagnosis:
* Urea breath test: urea C13 is given to patient and H. Pylori converts urea C13 to ammonia (NH3) + C13O2

* CLO test (Campylobacter-like organism test): biopsy placed in media with urea and pH indicator conversion of urea to ammonia raises pH ( if H. pylori present), which changes  colour of pH indicator. 

* Blood antibody test: antibodies to H. Pylori

Stool antigen test (H. Pylori proteins)

43
Q

What is Peptic Ulcer Disease (PUD)

A

Peptic Ulcer Disease (PUD)

  • Break in mucosal lining of stomach to level submucosa (minimum)
  • Imbalance between factors promoting mucosal damage -gastric acid, pepsin, Helicobacter pylori infection, NSAIDS, smoking and mechanisms promoting gastroduodenal defence - prostaglandins, mucous, bicarbonate, mucosal blood flow
  • Major complications:
    • Pain & Dyspepsia
    • Bleeding –acute and/or chronic
      Perforation - peritonitis
44
Q

What are the treatments for peptic ulcer disease

A

vagotomy
h2 antagonists (cimetidine,ranitidine)
proton pump inhibitors
antibiotic

Metabolism (5 decks)

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