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Week 10: Abdominal Pain > Gastric Acid Secretion > Flashcards

Gastric Acid Secretion Flashcards

1
Q

Components of gastric juice

A

Water
Organic compounds (intrinsic factor, pepsinogen, lipase, mucus)
Ions (Na, K, H, Cl, HCO3)

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2
Q

6 types of cells you can find in the gastric mucosa

A 
Superficial epithelial cells
Mucus neck cells
Stem/regenerative cells
Parietal (oxyntic) cell
Chief cell
Paracrine or endocrine cell
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3
Q 
Gastric glands in fundus and body:
What does
1. Parietal cell
2. Chief cell
3. Mucus neck cell
4. Paracrine cell
release?
A
  1. HCl, intrinsic factor
  2. Pepsinogen, lipase
  3. Mucus
  4. Histamine, somatostatin
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4
Q 
Pyloric glands in antrum
What does
1. Mucus neck cells
2. Endocrine cells
3. Paracrine cells
Release?
A
  1. Mucus, bicarb
  2. Gastrin
  3. Somatostatin
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5
Q

Intrinsic factor

A

Released from parietal cells into canaliculi

Facilitates vitamin B12 absorption in the small intestine

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6
Q

Activating of the parietal cell causes…

A

Tubulovesicles (with the proton pumps and intrinsic factor) fuse with invaginated areas of the apical membrane
Leads to the formation of many microvilli
Generates canaliculi (tunnels continuous with lumen)
H/K proton pump facilitates HCl production
Bicarb is pumped into the interstitial space, enters bloodstream and buffers

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7
Q

Proton pump

A

Transports H out of the cell, and K into the cell

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8
Q

3 major ion transport pathways in an active parietal cell

A
  1. Proton pump (H out, K in)
  2. NaCl uptake drive by Na/H (basally - Na in, H out) and HCO3/Cl (HCO3 out, Cl in) - gradients driven by Na/K pump
  3. K and Cl move out of the cell apically down a [ ] gradient
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9
Q

4 functions of gastric acid

A

Bacteriostatic
Activates pepsinogen and lipase
Initiates protein denaturation
Facilitates absorption of iron, Ca, and vitamin B12

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10
Q

Chief cells

A

Secretes pepsinogens and gastric lipases via exocytosis
Pepsinogens are inactive (zymogens), need to be activated by acid hydrolysis and autocatalysis
Gastric lipase activity is increased at low pH

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11
Q

Apical mucus layer functions

A

Protects the lumenal epithelium from acid and pepsin-based hydrolysis as well as microorganisms
Barrier contains protective glycoproteins/mucins and pH neutralizing bicarb ions

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12
Q

How is secreted mucus held in place?

A

By apically-targeted ‘surface active phospholipids’

Located in the lumenal membrane of mucus epithelial cells

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13
Q

How is bicarb taken up into the basal surface of the mucus cells?

A

Via a Na/HCO3- co-transporter

Released into the lumen, and neutralizes acid in the mucus

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14
Q

3 major secretagogues that stimulate both pepsinogen and acid production

A

Can act on chief and parietal cells
Gastrin
Histamine
Acetylcholine

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15
Q

G cells

A

Secrete gastrin
Found at the base of pyloric glands
Secretory vesicles are found basally

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16
Q

Gastrin

A

Polypeptide hormone released from G cells
Can act locally or travel through the blood
Binds to gastrin receptors (CCK 2/B)
Activates parietal and chief cells
Production of gastrin is stimulated by GRP from enteric neurons, and by digested protein in the gastric lumen

17
Q

Enterochromaffin-like cells

A 
Found at the base of gastric glands
Produce histamine (paracrine factor)
Histamine production is stimulated by ACh from intrinsic enteric neurons, or gastrin from G-cells
18
Q

Receptors on parietal cells for

  1. ACh
  2. Histamine
  3. Gastrin
A
  1. M3 receptors
  2. H2 receptors
  3. CCK2/B receptors
19
Q

Cephalic stimulatory phase of acid secretion

A

Taste, smell, sight, or thought of food activates your hypothalamus
Sends signals to dorsal vagal motor nucleus
Vagus nerve travels to stomach and can act on G cells or parietal cells to increase acid secretion in prep for a meal

20
Q

Acid secretion from the stomach can be ___ or ___

A

Neuronal

Non-Neuronal

21
Q

Gastric stimulatory phase of acid secretion: neuronal

A

Hypothalamus activates dorsal vagal motor nucleus, vagus travels to stomach, activates G cells and parietal cells
Activation of stretch receptors can stimulate G cells, and can travel via the vagus to the nodose ganglion, which connects into the above path at the dorsal vagal motor nucleus

22
Q

Nodose ganglion

A

Inferior ganglion of vagus nerve

Receives visceral sensory/afferent nerves

23
Q

Gastric stimulatory phase of acid secretion: non-neuronal

A

Food enters the stomach
As its broken down you get buffering of the intragastric pH and the production of peptones and amino acids
Peptones and amino acids stimulate G cells
Food and buffering stimulate parietal cells

24
Q

Intestinal phase of acid production

A

When peptones in the chyme reach the duodenum, G cells there are stimulated to produce more gastrin that acts on the parietal and chief cells in the gastric glands
(via gastrin’s hormonal action)

25
Q

Cephalic inhibitory phase of acid secretion

A

Hypothalamic satiety and feeding nuclei are activated, activate the dorsal vagal motor nucleus
Through vagus sends inhibitory signals to parietal cells

26
Q

Gastric inhibitory phase of secretion

A

Acid in the pyloric antrum stimulates somatostatin release to inhibit meal-stimulated gastrin secretion
Somatostatin works in paracrine way

27
Q

Intestinal inhibitory phase of secretion

A

Chyme into the duodenum stimulates a neuronal enterogastric reflex arc through the sympathetic celiac ganglion
Also stimulates the production of enterogastrones
These inhibit he G cell, parietal cell, and chief cell activity, as well as smooth muscle contraction in the stomach

28
Q

Enterogastrones

A

Hormones that feedback to inhibit the G cell, parietal cell, and chief cell activity, as well as smooth muscle contraction in the stomach
Include: secretin, CCK, GIP, and GLP-1

29
Q

5 functions of prostaglandins

A

Inhibit acid secretion
Prevent surface epithelial cell exfoliation
Increase mucosal blood flow
Stimulate mucus and bicarb secretion
Enhance synthesis of surface-active phospholipids
Prostaglandins are anti-secretory and protective

30
Q

Do you want to inhibit COX1 or COX2

A

COX2! Its the pain pathway

Chronic use of COX1/2 inhibitors is problematic in the gastric mucosa

31
Q

H. pylori

A

Gram negative flagellated bacterium
Produces urease (converts urea to ammonia and CO2 to protect from acid)
Requires special media for growth

32
Q

H. pylori negative ulcers are usually due to…

A

NSAIDs

33
Q

6 survival factors for H. pylori

A 
High mutation rate
Motility (chemotactic - away from acid)
Ability to attach to epithelial cells of the gastric mucosa (adhesions bind surface receptors on epithelial cells)
Virulence factors (cagA, VacA)
Urease activity
Evasion of the adaptive immune response
34
Q

Action of H pylori’s virulence factors

A

Injected into epithelial cells
Cause the cells to release nutrients and urea that are used by the bacteria
Also damage epithelial cells and disrupt tight junctional barrier between cells. facilitated local inflammation
Inflammation results in local production of cytokines that stimulate G cells and inhibit D cells = increased acid production and further local tissue injury inflammation

35
Q

Urease

A

Converts urea into NH3 and CO2
Neutralizes acid which allows for further protection of bacteria attached to epithelial cells
Facilitates further gastrin secretion

36
Q

Treatment for H pylori

A

Most often its a combined proton pump inhibitors and antibiotics

Week 10: Abdominal Pain (9 decks)

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