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Alimentary System > Gastric Secretion, Gastric Motility and Pancreatic Function > Flashcards

Gastric Secretion, Gastric Motility and Pancreatic Function Flashcards

1
Q

What is the function of the Fundus, Body and Antrum

A

▷Fundus: Storage

▷Body: Storage, Mucus, HCl, Pepsinogen, Intrinsic Factor

▷Antrum: Mixing/Grinding, Gastrin

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2
Q

What cells make up the Gastric Glands?

What do each secrete?

A

▷Mucous Neck cells: mucus

▷Parietal/Oxyntic cells: HCl + Intrinsic Factor

▷Chief cells: Pepsinogens

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3
Q

What is the importance of Gastric Acid secretion?

A

▷Inactivates swallowed organisms -> preventing them from reaching the small intestine

▷Aids Digestion -> creates optimal pH for pepsin and gastric lipase, and also stimulates pancreatic HCO3- secretion

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4
Q

Which hormonal and neural mechanisms responsible for the control of Gastric Acid secretion?

A

▷Distension of food in the stomach -> Vagus/Local (enteric) reflexes → Ach

▷Peptides in Lumen -> G cells → Gastrin

▷Gastrin/Ach -> ECL cells → Histamine

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5
Q

Which cell is responsible for Gastric Acid secretion?

A

Parietal/Oxyntic cells!

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6
Q

How is Gastric Acid pumped into Stomach Lumen?

A

▷H+-K+-ATPase: H+ ions are pumped out of cells in exchange for K+ ions

▷Open Chloride channels: Cl- ions follow the electrical gradient of H+ ions out of the cell

▷Paracellular Pathway: Water follows the osmotic gradient created by the ions in the lumen of the stomach

NET EFFECT = HCl secretion in the stomach lumen!!

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7
Q

What is an Alkaline Tide?

A

▷Due to transient increase in HCO3- ions released into the blood after meals (post-prandially), transiently increasing blood pH

▷Occurs bc while HCl is being secreted into the lumen after meals, CO2 is being absorbed by the parietal cells from the bloodstream -> Carbonic Anhydrase inside cells combines it with H2O to form Carbonic acid, which rapidly dissociates to form HCO3- and H+ ions -> HCO3- leaves the cell in exchange for Cl- ions -> transient alkalisation of blood while Gastric acid is being secreted post-prandially!

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8
Q

What is the action of PPIs (ie. Omeprazole)?

A

▷Inhibits the H+-K+-ATPase

▷Used to treat over-secretion of gastric acid by Parietal cells

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9
Q

Which factors are involved in increasing proton pump activity?

Describe the intracellular effects of these factors.

A

▷Gastrin: (hormone) G cells -> increase intracellular Ca2+ -> Protein Kinase C -> increases Proton Pump activity!

▷Ach: (NT) Vagus nerve -> M3 Receptor -> increase intracellular Ca2+ -> Protein Kinase C -> increases Proton Pump activity!

▷Histamine: (inflammatory mediator) -> ECL cells -> H2 Receptor -> G protein (GS) -> Adenylate Cyclase converts ATP to cAMP -> protein kinase A -> increases Proton Pump activity!

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10
Q

Which factors are involved in decreasing proton pump activity?

Describe the intracellular effects of this factor.

A

▷Prostaglandins: (inflammatory mediator) -> its own receptor -> G protein (GI) -> inhibits Adenylate Cyclase conversion of ATP to cAMP -> therefore, inhibits protein kinase A -> inhibits Proton Pump activity!

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11
Q

What is the Cephalic phase of Gastric Acid secretion?

A

▷Sight, smell, taste of food

▷Stimulates the Vagus Nerve

(which stimulates G cells, and both stimulate ECL cells to release their various chemicals and trigger gastric acid secretion from the parietal cells)

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12
Q

What is the Gastric phase of Gastric Acid secretion?

A

▷Distension of stomach (Arrival of food) -> Vagus nerve -> Ach

▷Peptides in Lumen -> G cells -> Ach

▷Gastrin/ Ach -> ECL cells -> Histamine

All stimulate Parietal cells to secrete Gastric Acid!

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13
Q

What is the Intestinal phase of Gastric Acid secretion?

A

▷Acid in the Duodenum -> triggers Enterogastric (splanchnic) reflex an Secretin release -> decreases Gastrin secretion from G cells

▷Fat/CHO in the Duodenum -> triggers GIP release -> decreases Gastrin secretion from G cells

Both decrease Gastrin stimulation of Parietal cells -> reduces Gastric acid secretion!!

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14
Q

What are Enterogastrones?

What triggers their release?

A

▷Hormones released from Gland cells in the Duodenal mucosa -> Secretin, CCK, GIP

▷Released in response to acid, hypertonic solutions, Monoglycerides or FAs in the Duodenum

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15
Q

What do Enterogastrones do?

A

▷They all collectively act to prevent further acid build-up in the Duodenum

▷They do this in 2 ways:

  1. Inhibit gastric acid secretion
  2. Reduce gastric emptying -> (inhibit motility/contract pyloric sphincter)
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16
Q

What is Pepsinogen?

How is it activated, and what is the role of its activated form?

A

▷Pepsinogen is a zymogen released from chief cells in the Gastric mucosa

▷It is activated to Pepsin when exposed to low pH environments

▷Pepsin is an endopeptidase -> it is needed to break down proteins into smaller peptides

17
Q

What stimulates Pepsinogen secretion?

A

▷Ach

▷Gastrin

▷Histamine

(NB. same as Gastric Acid secretion!)

18
Q

What is the role of Gastric Mucus?

A

Cytoprotective Role:

▷Protects mucosal surface from mechanical injury

▷Neutralises pH (HCO3-) → Protects the stomach against gastric acid corrosion and pepsin digestion (pepsin activated at low pH -> protects the stomach from that!)

19
Q

Which cells produce Intrinsic Factor?

What is the function of Intrinsic Factor?

What happens if Parietal cells are damaged and you don’t get any Intrinsic Factor production?

A

▷Parietal cells

▷Vitamin B12 absorption in the distal/terminal ileum

▷Pernicious Anaemia (bc no B12 complex created, and hence B12 can’t get absorbed!)

20
Q

Where are Brunner’s Glands found?

What is the function of its secretions?

A

▷Duodenal Submucosa

▷It secretes HCO3- -> important for Gastric Acid neutralisation

21
Q

What triggers HCO3- secretion?

A

▷Long (vagal) & short (ENS) reflexes

▷Release of Secretin from S cells

22
Q

What is the function of Secretin?

A

▷Stimulates HCO3- secretion

▷Inhibits Gastric emptying and acid secretion

23
Q

What inhibits Secretin release?

A

▷Acid neutralisation

negative feedback control!

24
Q

What mechanisms increase Gastric emptying?

A

▷Gastrin → increases contraction of GIT

▷Distension of stomach wall → long (vagal)/short (ENS) reflexes → increases contraction of GIT

25
Q

What mechanism decreases Gastric emptying?

A

▷Fat/acid/amino acid/hypertonicity in duodenum → inhibition of motility

26
Q

What generates Peristaltic rhythm in the GIT?

What propagates it?

A

▷Pacemaker cells in the Longitudinal muscle layer

▷Propagated by the BER (basal electrical rhythm) -> Slow wave rhythm (spontaneous depolarisation/repolarisation along the longitudinal muscle layer)

27
Q

What is the function of the Endocrine and Exocrine Pancreas?

A

▷Endocrine Pancreas (Islets of Langerhans) = creates + releases hormones into the bloodstream (insulin, glucagon and somatostatin)

▷Exocrine Pancreas (duct + acinar cells) = responsible for the digestive function of the Pancreas

28
Q

What is the function of the duct and acinar cells of the Pancreas?

A

▷Duct cells = secretes HCO3- ions

▷Acinar cells = secretes digestive enzymes (as inactive zymogen granules)

29
Q

What is the action of Secretin?

What stimulates its release?

A

▷It stimulates HCO3- secretion from the Pancreas, Duodenum

▷It is released in response to Gastric Acid in the Duodenum

It’s release is switched off by neutralisation of the Gastric Acid -> Negative Feedback!

30
Q

What is the action of CCK?

What stimulates its release?

A

▷It stimulates Pancreatic zymogen secretion

▷It is released in response to Fat/AAs in the Duodenum

31
Q

What is the role of Enterokinase?

Where is it present?

A

▷Converts Trypsinogen to Trypsin

▷It is present on the brush border membrane of Duodenal enterocytes

32
Q

What is the role of Trypsin?

What activates it?

A

▷It converts all other zymogens to their active forms

▷It is activated by Enterokinase from Trypsinogen (from the Pancreas)

Alimentary System (11 decks)

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