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Physiology GI > Stomach > Flashcards

Stomach Flashcards

1
Q

3 major functions of the stomach

A
  1. temporal storage
  2. absorption of water soluble and lipid soluble substances (like alcohol and some drugs)
  3. preparation of the chyme for digestion in the SI
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2
Q

most of the protein components of food are what? in the stomach

A

broken down into smaller constituents

uses pepsin (acidic environment needed)

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3
Q

surface mucus cells in stomach

A

located at opening of gastric glands

secrete mucus

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4
Q

mucus neck cells in stomach

A

neck of gastric gland and secrete less viscous mucus than those located at the opening

also secrete HCO3-, and water to protect the lining of the stomach against acid

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5
Q

parietal (Oxyntic) cells

A

secrete HCL and intrinsic factor for B12 absorption

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6
Q

chief (zymogen) cells

A

basal region of glands

secrete pepsinogen via exocytosis

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7
Q

D cells in stomach

A

found in the antrum

secrete somatostatin –> inhibits acid secretion therefore gastrin release

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8
Q

enterochromaffin-like cells (ECLs)

A

scattered throughout the mucus

secrete histamine –> which stimulates acid secretion by the parietal cells

also increases blood flow locally

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9
Q

G cells in stomach

A

enteroendocrine cells that secrete gastrin

found mostly in the pyloric region

secreted into blood (not lumen of stomach) and stimulates gastric juice secretion and gastric/intestinal motility

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10
Q

EtOH and aspirin

A

can break down mucus…which is the protective glycocalyx for the stomach

so excessive uses of these can cause ulcers

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11
Q

pepsin

A

secreted by chief as pepsinogen and activated by acid (HCl)

pepsin = endopeptidase

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12
Q

gastric lipase

A

lipid breakdown

78% homologous to lingual lipase

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13
Q

intrinsic factor

A

vitamin B12-binding protein and considered a ‘essential factor’

loss = achlorhydria –> pernicious anemia

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14
Q

relationships between the concentration of these ions as the rate of secretion increases..

HCl
Na
K

A

H+ = increases rapidly

Cl- = increases but not as much as H+ … but also has a higher absolute value

Na+ = decreases

K+ = low absolute amount, but still see slight increase

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15
Q

maximal acid secretion is when after a meal

A

one hour after

lowest pH = 3 hours after

during this process the food acts a buffer to raise pH

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16
Q

parietal cell

A

distinctive characteristics:

  1. intracellular canalculi
  2. abundance of mitochondria
  3. extensive SER (tubulovesicular membranes)
17
Q

parietal cell in the resting state

A

the tubulovesicles (containing transporters responsible for H+ and Cl- secretion) –> located underneath the plasma membrane

18
Q

tubulovesicular membranes

A

in apical portion of the parietal cell and contain the H/K-ATPase

19
Q

stimulation of parietal cells

A

cyctoskeletal rearrangement occurs leading to the fusion of the tubulovesicles membrane into the canalicular membrane

this increases surface area of apical membrane and the appearance of microvilli

as a consequence –> greatly increases number of H/K-ATPase and K+ and Cl- channels into the plasma membrane and O2 consumption to support acid secretion

20
Q

carbonic anhydrase in parietal cell

A

secreted protons by these cells mostly are derived from the dissociation of water and the CA reaction

water –> H + OH

OH + CO2 –> HCO3- via CA –> goes out blood side membrane

H –> goes out into lumen via K/H-ATPase

21
Q

apical membrane transporters of parietal cells

A
  1. H/K-ATPase –> how H+ is secreted into lumen
  2. K+ channel –> how you secrete (recycle) the K+ back into lumen to continue to use #1
  3. Cl- channel –> Cl - enters cell from blood side –> goes into lumen via this channel down gradient
22
Q

basolateral membrane transporters of parietal cells

A
  1. Na/K-ATPase –> pumps in K+ from blood so can secrete K+ out apical membrane to supply fuel for H/K ATPase
  2. K+ channel
  3. Cl-/HCO3- exchanger –> pumps HCO3- out into blood … and Cl- into cell which will eventually go into lumen
23
Q

receptor for gastrin on parietal cell

A

gastrin-cholecystokinin, CCK-B

24
Q

receptor for Ach on parietal cell

A

muscarinic receptor, M3

25
Q

receptor for histamine on parietal cell

A

H2

26
Q

stimulation of CCK-B and M3 receptors on parietal cell –>

A

increases intracellular Ca2+, which stimulates HCl secretion

gastrin –> CCK-B (secreted by D cells into the blood vessels)

Ach –> M3 (from vagus nerve)

27
Q

stimulation of H2 receptors on parietal cell –>

A

increases intracellular cAMP –> HCl secretion

histamine from ECL cell

28
Q

‘potentiation effect’

A

the effect of 2+ stimulants is greater than just 1

Ex: gastrin + Ach –> larger increase in intracellular Ca2+

29
Q

major humoral effectors (secretagogues) for gastric secretion

A

Gastrin (G)

Histamine (H)

ACh

30
Q

neural effectors for gastric secretion

A

a. distention of stomach –> (+) mechanoreceptors –> (+) parietal cells directly through a short local reflex and by long-vagal reflexes

31
Q

direct and indirect mechanisms for stimulating gastric secretion

A

Direct:
- ACh, H, and G all bind to their respective receptor on the parietal cell

Indirect:
- ACh and gastrin indirectly induce acid gastric secretion as a result of their stimulation of histamine release from ECL cells and possibly from mast cells in the lamina propria

32
Q

H2 receptor blockers

A

block the H2 receptors on parietal cells but also inhibit the acid secretion stimulated by ACh and gastrin

33
Q

where else are CCK-B and M3 receptors found - besides the parietal cell

(most important for gastric secretion regulation)

A

ECL cells

activation of these receptors –> (+) Histamine release –> (+) HCl secretion

34
Q

phases of gastric secretion of acid (general)

A
  1. basal
  2. cephalic
  3. gastric
  4. intestinal
35
Q

basal phase of gastric acid secretion

A

inter-digestive period…

36
Q

cephalic phase of gastric acid secretion

A

shortest period

takes place before food enters the stomach

initiated by though, sight, smell and taste (no mental shit…why called cephalic)

A. Neurogenic influence = parasympathetic vagus nerve causes release of ACh –> (+) parietal cells, G cells, and ECL cells
** also stimulates chief cells –> pepsinogen

B. Endocrine influence = vagal stimulation also causes gastrin release which acts like ACh mostly

37
Q

gastric phase of gastric acid secretion

A

longest phase….triggered by the presence of food in the stomach due to distension and chemical nature

A. Neurogenic influence = stomach distension stimulates mechanoreceptors leading to secretion of ACh due to parasympathetic reflexes

B. Endocrine influence = amino acids and peptides activate G-cells in the antrum
…gastrin therefore released into blood to stimulate further acid secretion and Histamine release
…gastrin secretion falls as pH of stomach falls between 2-3 and somatotstatin is released from D cells

38
Q

intestinal phase of gastric acid secretion

A

presence of chyme in duodenum –> enterogastric reflex in order to (-) gastric secretion

acid in duodenum –> secretin released –> (-) G cells and reduces parietal response to gastrin

also…FAs in the duodenum and jejunum cause release of gastric inhibitory peptide (GIP) and CCK –> inhibit acid secretion and gastrin release

Physiology GI (11 decks)

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