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PHGY 210 > Gastro VII > Flashcards

Gastro VII Flashcards

1
Q

What is the only hypotonic secretion in the GIT?

A

Saliva

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2
Q

What is the breakdown between neural and hormonal regulation for salivation?

A

Neural only.

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3
Q

What is the composition and pH of parietal cell secretion?

A

It secretes pure hyrochloric acid with a pH of 0.8. The composition is constant.

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4
Q

How does stimulus type affect parietal cell secretion?

A

It doesn’t. The secretion is independent of stimulus type or magnitude.

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5
Q

Compare the pH of mixed gastric juice to that of parietal cell secretion and explain this.

A

pH of mixed gastric juice: 1-2
pH of parietal secretion: 0.8
This difference is because the gastric juice is modified by non-parietal, alkaline gastric secretions.

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6
Q

What is the major determinant of the pH of mixed gastric juice?

A

Depends on the number of the parietal cells that are active.

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7
Q

What are the 4 main functions of HCl?

A
  1. Precipitates soluble proteins, allowing them to remain longer in the stomach
  2. Denatures proteins, making them more readily digested
  3. Activates pepsin
  4. Provides optimal pH for pepsin activity
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8
Q

Explain the process by which pepsinogen is activated and the effect it has.

A

It is only activated when in contact with HCl in the stomach to avoid damaging the chief cells.
Process of activation:
Pepsinogen -> pepsin in the presence of HCl (pH<6). Pepsin will also autocatalyze pesinogen
Protein -> polypeptides in the presence in pepsin (pH 2-3).

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9
Q

Protein breakdown in the stomach begins with the enzyme […]

A

pepsin

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10
Q

What type of cell secretes intrinsic factor?

A

Parietal cells.

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11
Q

What is the only secretion of the stomach essential to life?

A

Intrinsic factor

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12
Q

What is the function of instrinsic factor? Where is it needed?

A

t is required for the absorption of vitamin B12 in the distal small intestine (ileum).

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13
Q

Intrinsic factor deficiency leads to the condition […]

A

pernicious anemia

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14
Q

Explain how IF works.

A

Vitamin B12 gets coupled with IF to form IF-B12 complex. This gets absorbed at the level of the ileum.

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15
Q

What are the locations of mucin secretion?

A

ALL epithelial cells in the GIT produce mucin.
Most production takes place in the stomach, in the cardiac and pyloric tubular glands, and in the fundus and corpus via mucous neck cells.

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16
Q

What parts of the GIT are protected from acid damage?

A

The stomach only.

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17
Q

What is the main function of mucin in the stomach?

A

To serve as a protective mucus gel layer that sites on top of the epithelial cells, protecting them from acid damage.

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18
Q

What are the 3 elements of protection of the gastric mucosa from acidity?

A
  1. Muci-bicarb layer
  2. Gastric mucosal barrier (GMB)
  3. Rapid cell turnover (“re-epitheliazation”)
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19
Q

What is the pH of the muci-bicarb layer?

A

It is 2 on the apical side (lumen side) and 7 on the epithelial side.

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20
Q

Explain how the muci-bicarb layer works.

A

The epithelial cells below it release bicarbonate (HCO3-). When H+ flows into the layer, it will react with HCO3- to produce CO2 and water, which are hamless.

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21
Q

How does the gastric mucosal barrier work?

A

This is a specialization of surface epithelial apical surfaces and tight junctions that makes them impermeable to H+ ions. This is the more critical component to protecting the stomach as compared to the muci-bicarb layer.

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22
Q

How does rapid cell turnover/re-epitheliazation work?

A

The epithelial cells in the stomach rapidly turn over, so old, damaged ones will not stick around for long.

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23
Q

What are the two main causes of stomach ulcers?

A

Possibility 1: normal HCl output but weak protective barrier in gut
Possibility 2: normal protective barrier in gut, but excessive HCl output.

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24
Q

What are two possible causes of stomach ulcers due to a weak protective barrier?

A
  1. Aspirin and NSAIDs
  2. H. pylori in the stomach, which release a toxin that damages the epithelium.
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25
Q

What is a possible cause of stomach ulcers due to excessive HCl output?

A

Gastrin-producing tumours.

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26
Q

How do secretory cells get regulated neurally?

A

The ENS synapses on secretory cells (just as it does for muscle cells) and activates them by releasing ACh.

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27
Q

How is secretion neurally regulated in the cephalic phase?

A

When food is in the mouth or is seen/smelled/thought about, the vagus nerve will activate excitatory ENS neurones that will begin producing HCl pepsin, and mucin. Also releases gastrin

28
Q

Explain the relative timing of each of the 3 phases of gastric secretion.

A

Cephalic: prepares GIT for meal before it reaches the stomach.
Gastric: once food is in stomach
Intestinal: once food is in intestine

29
Q

Explain how secretion is neurally regulated in the gastric phase.

A

Distension at the level of the stomach activates ENS. This also activates vago-vagal inputs that reinforce secretion at the level of the stomach.

30
Q

Explain how hormonal regulation is activated in the stomach.

A

As the meal gets digested in the stomach, proteins get broken down into secretagogues, which lead to the stimulation of secretion at the level of the stomach.

31
Q

What are secretagogues?

A

Amino acids or partially digested proteins which act on G-cells.

32
Q

What is the first type of cell to be activating in hormonal secretion?

A

G-cells.

33
Q

Describe the action of G-cells once activated.

A

These G cells are activated by the secretagogues and release gastrin, which will go into the bloodstream via the hepatic portal vein. This will come back to the stomach through the blood supply and lead to activation of the parietal cell. So, it’ll increase HCl production.

34
Q

Gastrin can be released by G-cells in response to… (3)

A
  1. Secretagogues (products of protein digestion)
  2. Local enteric reflexes (distension in antrum)
  3. Vagally mediated reflexes (vago-vagal reflexes)
35
Q

When does vagally-mediated release of gastrin occur? Explain how.

A

This can occur during the cephalic phase. Vagal inputs lead to the release of gastrin, which then travel through the hepatic portal veins and through the circulation to increase secretion in parietal cells.

36
Q

Describe the positive feedback loop of gastrin self-regulation.

A

When we have food in the stomach, we produce secretagogues, which stimulate the G-cells.
- That will lead to the release of gastrin into the bloodstream.
- When the gastrin returns to the stomach, it acts on the parietal cell to increase its HCl secretion.
- The HCl will activate pepsinogen into pepsin. It also provides the optimal pH for pepsin action.
- All these things will produce more secretagogues.

This is a positive feedback loop

37
Q

Describe the negative feedback loop of gastrin self-regulation.

A

After the positive feedback has brought down the pH:
- If pH goes below 2, the G-cells sense this acidity and stop producing gastrin. This is a form of negative feedback.
- Another negative feedback is via somatostatin. When pH is low in the stomach, we activate cells that secrete somatostatin, which enters the bloodstream and inhibits the release of HCl and gastrin.

38
Q

What are the 2 roles of gastrin?

A
  1. Stimulates HCl secretion
  2. Trophic effect - proliferation of parietal cells
39
Q

During what phase of secretion is gastrin released?

A

Cephalic phase and gastric phase

40
Q

What the two ways that gatrin release can be stimulated?

A

By stretch in the stomach or by the presence of secretogogues in the stomach.

41
Q

What is the role of histamine in the GIT?

A

There is lots of histamine in the gastric mucosa. It ellicits large volumes of gastric juice with lots of HCl.

42
Q

What is the common mediator hypothesis? Is it correct?

A

Parietal cells only have receptors for histamine, and ACh and Gastrin cause histamine release. Histamine is the final local common chemostimulator.
This is not correct.

43
Q

What types of receptors do parietal cells have?

A

ACh, histamine, and gastrin

44
Q

What is the receptor interaction hypothesis?

A

In parietal cells, there is an interaction between the histamine, ACh, and gastrin receptors. Blockage or stimulation of one receptors changes the properties of one or both of the other 2 receptors.

45
Q

When is histamine released? What is its function?

A

Histamine is constantly released and is presented to Parietal cells as a tonic background, sensitizing them to other stimuli.

46
Q

What happens when the H2 receptor is blocked?

A

This is the histamine receptor on parietal cells. Blocking it using H2-receptor antagonists will inhibit HCl acid secretion in response to ACh and Gastrin.

47
Q

Name 2 ways to decrease the amount of HCl produced by parietal cells.

A
  • H2-receptor antagonists
  • Na+/K+ ATPase blocker
48
Q

Is the intestinal phase of secretion excitatory, inhibitory, or both?

A

Both.

49
Q

Describe the excitatory component of the intestinal phase of secretion.

A

Once the secretagogues make their way into the duodenum, they will also have a positive feedback. They release something like gastrin, entero-oxyntin, that will also stimulate parietal cells to produce HCl. This is a minor component, however, as most of the feedback from the SI on the stomach is inhibitory.

50
Q

Describe the stimuli for the inhibitory components of the intestinal phase of secretion

A

Distension, pH < 3.5, osmolarity, chemical composition, FAT&raquo_space; protein > carbs

51
Q

What are the effects of the inhibitory component of the intestinal phase of secretion?

A

Secretin, CCK, GIP, VIP, and neurotensin will be releasde, which will inhibit gastric secretion.

52
Q

What is the enterogastrone hormone complex?

A

It is the secretion of hormones (neurotensin, GIP, VIP, CCK, secretin) in response to dietary components that serves to inhibit gastric secretion.

53
Q

Name the mediators of the cephalic, gastric, and intestinal secretory phases.

A

Cephalic: vagus, vagally-released gastrin
Gastric: local enteric reflex, vago-vagal reflexes, gastrin release and inhibition
Intestinal: excitatory and inhibitory aspects via enterograstric reflexes and enterogastrone hormonal complex release

54
Q

Describe the consistency, pH, and osmotic pressure of the meal before it reaches the intestine.

A

Consistency: chyme, semi-liquid
pH: Acidified
Osmotic pressure: high

55
Q

What components of the meal have been broken down by the time it reaches the intestine? Include which enzymes have been responsible.

A

Some polysaccharides -> disaccharides (salivary amylase ptyalin)
Some proteins -> polypeptides (gastrin pepsin)
Lipids -> di-, monoglycerides, fatty acids

56
Q

What is the purpose of osmotic equilibration in the upper intestine?

A

So that cells from the SI can absorb the nutrients. If the osmolarity is high in the lumen, it’ll draw water into the lumen, which is the wrong direction.

57
Q

What is the source of the secretions in the small intestine?

A

The accessory secretory organs: liver, gall bladder, and pancreas.

58
Q

What is the name of the duct that secretes into the duodenum? What divides the two structures?

A

Secretory pathways come together at the ampulla of vater, which is controlled by a sphincter called the sphincter of oddi

59
Q

Draw and describe the ducts that bring together the accessory organs that secrete into the duodenum.

A

Right and left hepatic duct -> join to form common bile duct. Offshoot of bile duct -> cystic duct (leads to gallbladder). Further offshoot of pancreatic duct. Common bile duct leads to ampulla of vater and sphincter of oddi.

60
Q

What is the pH, osmolarity and composition of pancreatic juice?

A

Isotonic, alkaline, HCO3- dominant

61
Q

What are the 3 major enzymes produced by the pancreas? What is their purpose?

A

Amylases: break down starches
Proteases: breaks down proteins
Lipases: breaks down fats

62
Q

What is the purpose of amylase?

A

Converts polysaccharides to disaccharides at a pH of 7. Note that these must still be converted into monosaccharies before they can be absorbed

63
Q

What is the difference between the enzymes produced in the pancreas and those that end up in the SI?

A

The pancreas secretes proenzymes, which are inactive. They must be activated into enzymes once in the small intestine so that they don’t damage the pancreas.

64
Q

Describe the process by which pancreatic enzymes get activated.

A

In the small intestine, trypsinogen will get converted into trypsin by enterokinase. The typsin will then go on to activate the other proenzymes, such as chymotrypsinogen into chymotrypsin, proelastase into elastase, and procarboxypeptidase into carboxypeptidase.

65
Q

What is the effect of trypsin inhibitor? Where is it secreted?

A

This is secreted in the pancreas as a protective measure in case trypsin forms in the pancreas by mistake.

PHGY 210 (36 decks)

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