Exam #5: Gastric Secretions Flashcards

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1
Q

What are the secretory products of parietal cells? Where are these cells located?

A

Parietal cells secrete HCl & Intrinsic Factor

  • HCl functions in protein digestion, sterilization, nutrient absorption
  • Intrinsic Factor= Vitamin B absorption

**Parietal cells are located in the body of the stomach

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2
Q

What is the secretory product of chief cells? Where are these cells located?

A

Chief cells secrete pepsinogen, which functions in protein digestion

*****Chief cells are located in BOTH the body & antrum of the stomach

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3
Q

What are ECL cells? Where are these cells located? What is their product?

A

ECL, or “enterochromaffin-like” cells produce histamine, which promotes HCl secretion

*****ECL cells are located in the body of the stomach

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4
Q

What is the secretory product of G-cells? Where are these cells located?

A

G-cells produce gastrin, which promotes HCl secretion

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5
Q

What is the secretory product of D-cells? Where are these cells located?

A

D-cells produce somatostatin, which suppress HCl secretion

*****antrum of the stomach

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6
Q

What is the secretory product of superficial epithelial/ neck cells? Where are these cells located?

A

Mucous
Bicarbonate

*****Both are gastroprotective & cells are located throughout the entire stomach

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7
Q

How do neuronal pathways regulate acid secretion in the stomach?

A

ACh secretion

- promotion of mucous, bicarbonate, and HCl secretion

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8
Q

How do paracrine pathways regulate acid secretion in the stomach?

A

Histamine binding to receptors on parietal cells stimulates acid secretion

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9
Q

How do endocrine pathways regulate acid secretion in the stomach?

A

Gastrin binding to receptors on parietal cells stimulate acid secretion

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10
Q

What are the functions of gastric acid?

A

1) Protein digestion & conversion of pepsinogen to pepsin (for protein digestion)
2) Provide sterile environment
3) Prevent bacteria and fungal growth
4) Facilitate absorption
5) Promote bile and enzyme flow

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11
Q

What are the positive and negative regulators of gastric acid secretions?

A

Positive=

  • ACh (neural)
  • Histamine (ECL)
  • Gastrin (G-cells)

Negative=
- Somatostatin (D-cells)

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12
Q

What cells release the positive regulators of gastric acid secretion?

A
Histamine= ECL
Gastrin= G
Neural= ACh
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13
Q

What cells release the negative regulators of gastric acid secretion?

A

D-cell secretion of somatostatin

Prostaglandins

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14
Q

Describe the steps of how pepsinogen is converted in lumen of the stomach to the active protease pepsin.

A
  • Pepsinogen is secreted by chief cells in the body & antrum of the stomach.
  • HCl converts pepsinogen into pepsin (active) i.e. lower pH
  • This is protective and ensure that pepsinogen is activated once it is in the lumen of the stomach
  • Higher pH inactivates the enzyme

*****ACh is a key stimulus in the secretion of pepsinogen

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15
Q

What is the site of intrinsic factor secretion?

A

Parietal cells secrete intrinsic factor in the body of the stomach

I.e. damage to parietal cells & the gastric epithelium will result in an inability to absorb Vitamin B12

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16
Q

What is the physiological role of intrinsic factor?

A
  • Complexes with Vitamin B12 in duodenum
  • IF + Vitamin B12= absorbed in ileum via receptor mediated endocytosis

No IF= No Vitamin B12 absorption

17
Q

What are the two key stimuli for mucus secretion by epithelial and neck cells of the stomach?

A

There are two key regulators

1) ACh (neurocrine)
2) Prostaglandins (paracrine)

**Note that prostaglandins: 1) increase mucus & bicarbonate secretion, 2) suppression of HCl secretion, and 3) increased gastric blood flow

18
Q

What is the the physiological role of mucus in the stomach?

A

Gastroprotection; mucus creates a protective layer over the mucosal epithelium

19
Q

What are the components of mucus?

A
Mucin 
Bicarboante 
Phospholipids 
Electrolytes 
Water
20
Q

Outline the pathophysiology of gastritis.

A

Gastritis= inflammation of gastric mucosa caused by damage to the protective mucosal barrier–this inflammation DOES NOT NECESSARILY produce a break in the mucosal lining. Commonly caused by:

1) H. pylori
2) NSAIDs i.e. ASA

21
Q

Outline the pathophysiology of H. pylori infection.

A
  • Urease creates a buffered microenvironment that is hospitalble to H. pylori colonization
  • Colonization and subsequent immune response cause the mucosal damage that leads to ulceration
22
Q

Outline the pathophysiology of peptic ulcers.

A

Break in the protective lining of the lower esophagus, stomach, or duodenum

23
Q

Outline the pathophysiology of Zollinger-Ellison Syndrome.

A

Gastrin secreting tumor that results in high acid levels

24
Q

What are the four different phases of gastric acid secretion?

A

1) Interdigestive
2) Cephalic= sight or smell of food triggers vagal response to increase acid secretion

3) Gastric= stomach distention & presence of proteins causes vagal response to increase acid secretion
- Most gastric acid secreted in this phase

4) Intestinal= proteins in the duodenum causes acid secretion

25
Q

How are the four phases of gastric acid secretion regulated?

A

1) Interdigestive
2) Cephalic
3) Gastric= if pH falls below 1, feedback on D-cells to secrete somatostatin
4) Intestinal= peptides induce gastrin secretion

26
Q

Outline the mechanism of HCl production. What cells produce HCl?

A

Parietal cells secrete HCl i.e. gastric acid via a H+-K+ ATPase, or “proton pump”
- Located on the apical membrane of parietal cells

27
Q

What regulates the H+-K+ ATPase?

A

Stimulation

  • Gastrin= direct increase or stimulation of histamine for indirect increase in H+/K+ ATPase pump
  • ACh= like Gastrin, direct increase or stimulation of histamine for indirect increase in H+/K+ ATPase pump

Inhibition

  • Prostaglandins= direct inhibition
  • Somatostatin= indirect inhibition by decrease Gastrin & Histamine