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Physiology > STOMACH > Flashcards

STOMACH Flashcards

1
Q

Major functions of the stomach

A
  • Temporal storage for food
  • Absorption of water-soluble and lipid-soluble substances
    • E.g. alcohol, some drugs
  • Preparation of the “chyme” (semi-fluid material produced by gastric digestion of food) for digestion in the small intestine
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2
Q

Digestion in the stomach

A
  • Physical - muscles contract and relax
  • Chemical - pepsin breaks down proteins
    • Requires acidic medium
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3
Q

Name the major cells of the gastric (oxyntic) gland and what they secrete

A
  • Surface mucous cells - mucus (more alkaline & viscous), HCO3-, water
  • Mucus neck cells - soluble mucus, HCO3-, water
  • Parietal (oxyntic) cells: HCl & intrinsic factor
  • Chief (zymogen) cells - pepsinogen
  • D cell - somatostatin
  • ​Enterochromaffin-like (ECL) cells: histamine
  • G cell - gastrin
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4
Q

What cells are found in teh basal region of gastric glands?

A

Chief (zymogen) cells

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5
Q

What cells are found in the antrum?

A

D cells

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6
Q

What cells are found in the pyloric region?

A

G cells

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7
Q

Functions of HCl & intrinsic factor from parietal cells

A
  • HCl -
    • Denatures proteins
    • Breaks up cell membranes
    • Activates pepsinogen
    • Antibacterial
    • Solubilizes calcium salts
  • IF - absorption of vitamin B12 in ileum for production of mature RBCs
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8
Q

Pepsin

A

Endopeptidase auto-catalytically activated from chief cells’ inactive pepsinogen

refers to all enzymes activated at a pH below 3 by HCl

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9
Q

Somatostatin from D cells

A

inhibits acid secretion & gastrin release

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10
Q

Histamine from ECL ells

A

Stimulates acid secretion

Increases local blood flow

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11
Q

Gastrin from G cells

A

Secreted into the blood (not stomach lumen) to stimulate gastric juice secretion & gastrin/intestinal motility

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12
Q

Function of gastric acid

A
  • Digestion of proteins via acid & proteolytic enzyme production
  • Absorption, esp vitamin B12
  • Protects mucosa from bacteria & autodigestion from its own acid & proteolytic enzymes
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13
Q

Gastric lipase

A

Homologous to lingual lipase

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14
Q

Loss of intrinsic factor causes

A

achlorhydria & pernicious anemia

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15
Q

Gastric juice:

  • mucous
  • pepsin
  • gastric lipase
  • intrinsic factorHCl
  • Other electrolytes: ___, __, and ___
A

HCO3- from mucous cells

K+ for H,K-ATPase

Na+ from mucous cells

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16
Q

How do [HCl], [K+], and [Na+] change as the rate gastric juice secretion increases?

A

HCl increases sharply (food acts a buffer)

K increases a bit

Na+ falls

17
Q

As the stomach empties, what happens to the rate of H+ secretion?

A

It increases

18
Q

What makes the parietal cell distinct?

A

Intracellular canliculi

Abundance of mitochodnria

Extensive smooth ER (tubulovesicular membranes)

19
Q

Resting state of parietal cell vs Stimulated for acid secretion

A

Resting state: tubulovesicles w H/K-ATPase are underneath the plasma membrane on the apical side.

Stimulation: tubulovesicle membranes fuse into the canalicular membrane to increase the apical membrane’s surface area

  • –> increases the # of H/KATPase, K+ and Cl- channels into the plasma membrane
  • –> increases O2 consumption to support acid secretion
20
Q

Name the transporters in the parietal cell on the apical vs the basoalteral membrane

A
  • Apical:
    • H,K-ATPase
    • K+ channel
    • Cl- channel
  • Basolateral:
    • Na,K-ATPase
    • K+ channel
    • Cl-/HCO3- exchanger
21
Q

Secreted H+ from the parietal cell are derived mostly from ___

During active HCl secretion, the blood coming from the stomach contains a lot of ___.

A

H+ secretion is derived mostly from the dissociation of water & the carbonic anhydrase rxn

The blood coming from the stomach contains a lot of HCO3- (alkaline tide)b

22
Q

Name the parietal cell receptors for gastrin, Ach, and histamine (secretagogues) and hwo they mediate their effects

A

Gastrin: gastrin-cholecystokinin (CCK-B)

Ach: muscarinic receptor, M3

HIstamine: H2 receptor

CCK-B & M3 increase intracellular Ca2+ –> HCl secretion

H2 increases intracellular cAMP –> HCl secretion

23
Q

Potentiation effect

A

The effect of any 2 stimulants is greater than the effect of either stimulant alone.

The effect of gastrin, Ach, and histamine will result in an increase in cAMP & Ca2+ –> greatly enhances H/K-ATPase –> more acid secretion

24
Q

Describe parietal cell activation

A
  1. Stomach distension stimulates mechanoreceptors
  2. Activates parietal directly thru
    1. Short local reflexes
    2. Long vago-vagal reflexes (traveling on vagus n)
25
Q

Direct vs Indirect action of secretagogues

A
  • Direct: Ach, gastrin, and histamine bind directly to their respective receptors on the parietal cell –>stimulate & potentiate gastric acid secretion
    • Ach from vagus n (CN10)
    • Gastrin from D cells
    • Histamine from ECL cells
  • Indirect: ACH & gastrin stimulate histamine release from ECL cells & mast cells (histaminocytes) in the lamina propria
26
Q

Cimetidine & Ranitidine

A

H2 recepto rblockers

The block H2 receptors on parietal cells, thus also blocking Ach & gastrin indirect stimulation

27
Q

Phases of gastric acid secreiton

A
  1. Basal (inter-digestive period)
  2. Cephalic
  3. Gastric
  4. Intestinal
28
Q

Cephalic phase (shortest)

A

Initiated by thought, sight, smell, and taste of food; also influenced by emotion

  • Neuro influence: parasympathetic vagus n releases Ach to stimulate acid secretion by
    • stimulating parietal cells, G cells, and ECL cells
    • stimulating chief cells for pepsinogen
  • Endocrine mechanism: Vagal stimulation also causes gastrin release, which acts like Ach
29
Q

Gastric phase (longest)

A

Triggered by presence of food in stomach due to distension & chemical nature

  • Neuro: stomach distension stimualtes mechanoreceptors –> parasympathetic secretion of Ach
  • Endocrine: Amino acids & peptides activate G cells –> Gastrin –> acid secretion & histamine reslease
    • Gastrin falls when
      • stomach pH falls between 2-3
      • somatostatin is released from D cells
30
Q

Intestinal phase

A

Triggered by chyme in the duodenum –> eneterogastric relfelx

  • Acid in duodenum –> secretin: inhibits G cells & the parietal response to gastrin
  • Fatty acids in duodenum –> gastric inhibitory peptide (GIP) and cholecystokinin (CCK) inhibits acid secretion and suppress gastrin release
31
Q

Gastritis & peptic ulcers are ____ caused by ___

A

Both are inflammation of gastric mucosa cauased by bacterial infection of the mucosa (e.g. h pylori) that stimulates gastric secretion

32
Q

H Pylori

A
  • Survives acid bc it produces urease (hydrolyzes urea to produce ammonia, which neutralizes gastric acid)
  • Adheres to epithelial cells and stimulates adhesins, ammonia, proteases, and immune response
  • Induces G-cells to secrete gastrin –> HCl from parietal cells
    • However, its augmentation occurs at a moderate rate
33
Q

What factors predispose to ulcers?

A
  • Smoking - increased nervous stimulation of stomach secretory glands
  • Alcohol - breaks down mucosal barrier
  • Aspirin & NSAIDs - breaks down mucosal barrier
34
Q

How to differentiate between H pylori infection and Zollinger-Ellison Syndrome (ZES)

A

In ZES, there’s an abnormally high gastric acid secretion rate associated w duodenal ulcers and tumors - whereas, gastric ulcers do not produce excessive gastric secretion.

35
Q

Zollinger-Ellison syndrome

A

Gastrinomas secrete very high amts of gastrin unregulated –> extremely high rates of gastric acid secretion

  • Usually comes w gastric and duodenal ulcers
  • Gastrinomas are typically located in the pancreas
  • Tx:
    • Proton pump inhibitor
    • H2R blocker
    • Surgical removal of gastrinoma
36
Q
A

Physiology (42 decks)

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