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Yr2 GI Joe > Gastric secretion > Flashcards

Gastric secretion Flashcards

1
Q

What is the function of the Fundus of the stomach?

A

Storage

  • Rugae make it stretchy so it can accomodate stuff
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2
Q

What are the functions of the body of the stomach?

A
  • Storage

Secretion of:

  • Mucus
  • HCl
  • Pepsinogen
  • Intrinsic factor
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3
Q

What are the functions of the antrum of the stoamach?

A

Mixing / grinding

Gastrin secretion

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4
Q

What cells are in gastric pits and glands in the stomach?

A

Surface mucous cells

Mucous neck cells

Parietal cells

Chief cells

G cells

<em>There are some other spicy types like ECL cells but these are the main ones</em>

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5
Q

What do mucus neck cells do?

A

Mucous and Bicarbonate secreting cells found in gastric glands

They eventually mature, move up to the surface epithelium and become surface mucous cells

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6
Q

What do chief cells do?

A

Secrete Pepsinogen

Found at the bottom of gastric glands

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7
Q

What is pepsinogen?

A

Inactive precursor to pepsin, which is an enzyme that digests proteins

It is converted to active pepsin by gastric acid (ie in acidic conditions pH < 3)

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8
Q

What do parietal cells do?

A

Secrete HCl and intrinsic factor

They also have a bunch of receptors to control their secretion

These cells are found in the gastric glands

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9
Q

What is intrinsic factor?

A

Glycoprotein produced by the parietal cells of the stomach. It is necessary for the absorption of vitamin B12 later on in the ileum of the small intestine

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10
Q

How is Gastric acid (HCl) secreted from parietal cells into the stomach lumen?

A
  1. CO2 and H2O in cytoplasm forms carbonic acid (H2CO3)
  2. Carbonic acid –> Bicarbonate (HCO3-) + H+
  3. Bicarbonate removed to blood by transporter in exchange for Cl- ion
  4. Transporter yeets out the H+ into the lumen in exchange for a K+
  5. Cl- moves into lumen through a Cl- channel
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11
Q

What enzyme allows conversion of Carbonic acid to bicarb and H+?

A

Carbonic anhydrase

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12
Q

What chemicals control the level of HCl secretion?

A

Gastrin - stimulates

Histamine - stimulates

Acetylcholine - stimulates

Prostaglandin - inhibits

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13
Q

How does Gastrin control HCl secretion from parietal cells?

A
  1. Gastrin in blood binds to parietal cell’s membrane receptors
  2. Receptor releases intracellular Ca2+
  3. Ca2+ activates protein kinases
  4. Induces H+K+ATPase initiating HCl secretion
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14
Q

How does Histamine control HCl secretion by parietal cells?

A
  1. Histamine in blood binds to H2 receptor on P cell membrane
  2. Receptor activates G coupled (Gs) protein
  3. Gs protein activates adenylyl cyclase
  4. Adenylyl cyclase converts ATP to cAMP
  5. cAMP activates protein kinases
  6. Protein kinases stimulates H+K+ATPase which starts chucking out H+
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15
Q

How does acetylcholine increase HCl secretion?

A
  1. Binds to receptor on parietal cell
  2. Secretes intracellular Ca2+
  3. Acts on protein kinase
  4. Induces H+K+ATPase

(same as gastrin)

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16
Q

How do prostaglandins increase HCl secretion by Parietal cells?

A

Prankt it decreases it

  1. Binds to receptor on parietal cell
  2. activates Gi coupled protein
  3. inhibits AC converting ATP -> cAMP
  4. Basically disabling the histamine pathway
  5. Reduction in protein kinase activty & so gastric acid secretion
17
Q

Gastrin increases the level of HCl secretion, so increases gastrin = increased HCl.

What mechanism causes this to happen in the cephalic phase and why?

A

The levels of Gastrin secretion rise through parasympathetic stimulation through the vagus nerve.

Vagal stimulation causes G cells to produce more Gastrin. This means more parietal cells receptors are bound to and so on…

Gastrin also does some spicy shit involving Histamine but thats in another card

18
Q

What system controls how much ACh stimulates Parietal cells in the Cephalic phase?

A

ACh route for HCl secretion is controlled by the Parasympathetic system through the Vagus nerve (same as Gastrin)

Vagal stimulation = increased ACh binding to Parietal cells = more HCl secreted into lumen

ACh also does some spicy shit involving Histamine but wait

19
Q

What stimulates histamine mediated control of HCl production?

A

Parasympathetic stimulation through the Vagus nerve causes release of Gastrin and ACh

Gastrin and ACh go to ‘Enterochromaffin-like cells’ (ECL cells) and stimulate them to produce Histamine

Histamine goes to parietal cells = HCl secretion

20
Q

What is meant by the cephalic phase and how does it relate to vagal stimulation?

A

Cephalic phase of gastric secretion occurs before the food enters the stomach

Sight, smell and taste of food cause vagal stimulation as we do the whole ‘rest and digest’ thing

21
Q

What stimulates parietal cells to release HCl into the lumen in the Gastric phase?

A
  • Distension of the stomach causes Vagal stimulation and enteric reflexes to release ACh
  • Peptides in the stomach lumen bind to G cell receptors and cause the release of Gastrin

The Gastrin and ACh produced by this^ bind to ECL cells causing release of Histamine

All these then bind to parietal cells and stimulate HCl release

22
Q

What action inhibits Gastric acid secretion in the Cephalic phase?

A

Stopping eating = Decreased Vagal stimulation

23
Q

What inhibits gastric acid secretion in the gastric phase?

A

Drop in pH (increased [HCl]) - inhibits secretion of gastrin

24
Q

How does acid in the duodenum cause inhibition of gastric acid secretion in the intestinal phase?

A

Acid in duodenum causes 2 seperate mechanisms to start inhibiting Gastric acid secretion

  • Activation of Enterogastric (splanchnic) reflex
  • Secretin release by S cells in duodenum

Both cause Decreased Gastrin secretion and decreased gastrin stimulation of parietal cells

25
Q

How does Fat/CHO in the duodenum inhibit acid secretion in the intestinal phase?

A
  1. Fat and CHO (carbohydrate) in duodenum cause GIP release into blood by K cells
  2. GIP (gastric inhibitory polypep.) decreases Gastrin secretion and parietal cells HCl secretion
26
Q

What is an enterogastrone?

A

Hormones released from gland cells in duodenal mucosa

They work to prevent excessive acid build up in the duodenum

27
Q

What are examples of enterogastrones?

A

Secretin

Cholecystokinin (CCK)

Gastric inhibitory polypeptide (GIP)

28
Q
A
29
Q

What stimulates the release of enterogastrones?

A

acid

hypertonic solutions

fatty acids

monoglycerides

(in duodenum)

30
Q

How do enterogastrones work to inhibit acid build up in the duodenum?

A

Inhibit gastric acid secretion

Reduce gastric emptying (shut the pyloric sphincter)

By reducing gastric emptying - prevent more acid from the stomach getting into the duodenum

31
Q

Why is it important to store pepsinogen in its zymogen form and not as pepsin?

A

Prevents cellular destruction

Pepsin would hydrolyse all the shit in the cell

32
Q

How is pepsinogen secretion by chief cells controlled?

A

Same way as HCl secretion

Negative feedback loop

33
Q

Mucous serves a ‘cytoprotective’ role in the stomach

What does this mean?

A

Protects the surface from mechanical injury

Contains fuck tons of Bicarbonate (HCO3-) which acts as a buffer. This means it neutralises the acid (thus inactivating any pepsin) at the epithelium.

This protects the epithelium from being digested by the lumenal enzymes.

34
Q

Intrinsic factor secretion is described as the only ‘essential’ function of the stomach

What does this mean?

A

Parietal cells always secrete it at a fairly constant rate - there is no stimulation/inhibiton

35
Q

What is intrinsic factor used for?

A

Required for absorption of vitamin B12

The vitamin B12 / intrinsic factor complex is absorbed from the ileum

36
Q

Defect in the secretion of intrinsic factor leads to what?

A

Pernicious anaemia

(failure of erythrocyte maturation)

37
Q

How does the bloods pH change after a meal?

A

Becomes more alkaline

Transient alkalisation from bicarbonate being pumped into the blood from the stomach epithelium in exchange for Cl- ions for HCl secretion

Yr2 GI Joe (28 decks)

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