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Gastrointestinal > Lecture 5 and 6: Integrated Response to a Meal - The Gastric Phase > Flashcards

Lecture 5 and 6: Integrated Response to a Meal - The Gastric Phase Flashcards

1
Q

What are the major functions of the stomach

A

1) Storage
2) Secretion (H+, IF, mucus, HCO3, water)
3) Motor activity (mixing)
4) Coordination of emptying

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2
Q

What does intrinsic factor do?

A

absorbs vitamin B12

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3
Q

What is responsible for regulating motor and secretory functions of the stomach?

A

Neural, endo and paracrine

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4
Q

What is the paracrine signaling to the stomach?

A

Histamine (signals to release H+)

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5
Q

What is the endocrine signaling in the stomach?

A

1) Gastrin (from stomach and duodenum) stimulate gastric acid secretion
2) Somatostatin (stomach, duodenum, pancreas) INHIBITS gastric secretion

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6
Q

What are the 2 secretions at the two ends of the stomach (cardiac and pyloric sphincters)?

A

1) mucus

2) HCO3

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7
Q

Where does mixing and grinding of food in the stomach occur?

A

Antrum and pylorus region

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8
Q

What is the function of the fundus and body of the stomach?

A

reservoir (storage)

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9
Q

The lining of the stomach contains _______ epithelium

A

columnar (folded into gastric pits where glands empty)

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10
Q

What are the 6 types of secretory cells in the stomach?

A

1) Parietal (HCl and IF)
2) Mucous neck cells (mucus)
3) Chief cells (pepsinogen)
4) Enterochromaffin-like cells ECL (histamine –> stimulates HCl)
5) D cells (somatostatin –> inhibits HCl secretion)
6) G cells (Gastrin –> HCl secretion)

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11
Q

Where are G cells found?

A

stomach AND duodenum

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12
Q

What are the 4 major gastric secretions?

A

1) HCl
2) Pepsinogen
3) HCO3 and mucus
4) IF

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13
Q

What secretion is the only ESSENTIAL component of gastric juice? (the others are redundant)

A

Intrinsic factor

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14
Q

What is the hallmark of a resting parietal cell?

A

Tubulovesicular system = cytoplasm with many tubules and vesicles (membranes have transport proteins for secretion of H+ and Cl-)

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15
Q

What happens to the tubulovesicular system in the activated parietal cell?

A

fuses with plasma membrane of secretory canaliculi and opens to lumen of the gland

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16
Q

What is the importance of intracellular carbonic anhydrase?

A

converts H2O and CO2 into H2CO3 which then dissociates into H+ and HCO3

that H+ is needed to be secreted by parietal cells

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17
Q

What transporter carries H+ ions across the luminal membrane in the parietal cells?

A

H+/K+ ATPase (K comes in, H goes out)

ACTIVE PROCESS (ATP driven because both ions are going up their conc gradient)

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18
Q

What does omeprazole do?

A

block the H/K transporter to reduce acid secretion

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19
Q

How does Cl leave the parietal cell to enter the lumen?

A

Cl channels

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20
Q

How does cAMP and intracellular Ca++ levels influence Cl conduction?

A

increased cAMP and int. Ca++ increases Cl and K conduction

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21
Q

On the basolateral membrane, how does HCO3 get into the blood?

A

Cl/HCO3 exchanger (Cl into the cell, HCO3 out of it)

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22
Q

Why is venous blood alkaline after a meal?

A

increased HCO3 absorption due to increased HCl secretion

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23
Q

What else do surface epithelial cells of the stomach secrete to contribute to alkaline blood?

A

watery fluid of Na, Cl, K, and HCO

Na and Cl concentrations are similar to plasma but K and HCO conc are higher

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24
Q

Mucus is 80% what biomolecule?

A

carbohydrates

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25
Q

What is the basic unit of mucus and what is its shape?

A

Mucins; glycoprotein tetramer (which has vulnerable central portion susceptible to proteolytic digestion by pepsins)

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26
Q

What two substances are responsible for protecting the surface of the stomach from H+ and pepsin?

A

1) mucus

2) bicarb

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27
Q

What makes up the gastric mucosal barrier?

A

protective mucus layer and alkaline secretions trapped within it (that bicarb neutralizes the H+ so it cannot hurt the epithelia)

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28
Q

What does heliobacter pylori do the the stomach?

A

pokes holes in the epithelia so it damages the cells (doesn’t affect the secretions, per se, but hurts the cells)

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29
Q

What is the strongest stimulant for gastric H+ secretion?

A

PARASYMP via vagus (stimulates parietal, ECL and G cells)

acetylcholine

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30
Q

What are the 3 things that stimulate H+ secretion by parietal cells?

A

1) Ach (neuro)
2) Histamine (paracrine)
3) Gastrin (endocrine)

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31
Q

Ach acts via _________ receptors on the parietal cells to stimulate H+ release

A

muscarinic

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32
Q

the secondary messengers of Ach H+ stim are_______

A

IP3 and Ca++

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33
Q

Histamine is released from _______ cells

A

ECL

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34
Q

The secondary messengers of histamine H+ stim are _____

A

cAMP

35
Q

Which drug blocks Ach stimulation of parietal cells? Histamine stimulation of parietal cells?

A

Atropine; cimetidine

36
Q

Histamine works via ____ receptors on the parietal cells to elicit H+ release

A

H2

37
Q

Gastrin works via _______ receptors on the parietal cells to stimulate acid release

A

CCKB (aka CCK2)

38
Q

The secondary messengers of gastrin H+ stim are ______

A

IP3 and Ca++

39
Q

Define potentiation

A

The observation that the rate of acid secretion can be regulated by Ach, histamine, and gastrin independently AS WELL AS by interactions among the 3

40
Q

Which two signals on the parietal cells share the same secondary messengers?

A

Ach and gastrin (IP3 and calcium)

41
Q

What ramifications does potentiation have for certain treatments?

A

cannot target just one since it will affect the others (ex: cimetidine doesn’t stop just histamine but also the histamine-potentiated effects of Ach and gastrin)

42
Q

During the cephalic and oral phase, _____ of total HCl is secreted

A

30%

43
Q

During the cephalic and oral phase, HCl secretion is both direct and indirect. What is direct and what is indirect?

A

1) DIRECT: Vagus Ach
2) INDIRECT: G cell stimulation by Vagus via Gastrin-releasing peptide (GRP)
ECL cell stimulation by Vagus (Ach) and gastrin (CCKB) to produce histamine

44
Q

What are the 2 effects of gastrin?

A

1) DIRECT: binds to CCK receptors on parietal cells

2) INDIRECT: stimulates ECL cells

45
Q

During the gastric phase, _____ of total HCl is secreted

A

60%

46
Q

What are the 3 stimuli for HCl secretion in the gastric phase?

A

1) distention of stomach
2) presence of amino acids
3) small peptides

47
Q

What are the 2 new mechanisms present here that are not found during the cephalic and oral phases?

A

1) distention of stomach activating vagovagal reflex (stimulating gastrin release)
2) direct effect of AA and small peptides on G cells (stimulating gastrin release)

48
Q

Alcohol and caffeine ________ (stimulate/inhibit) HCl secretion

A

stimulate

49
Q

During intestinal phase, ____ of total HCl is secreted

A

10%

50
Q

What is the signal responsible for triggering the negative feedback inhibition of acid secretion?

A

acidic chyme in the distal stomach (antrum)

51
Q

What hormone responds to low pH in the distal stomach?

A

somatostatin

52
Q

Which cells produce somatostatin?

A

D cells (somadddddostatin)

53
Q

What are the direct and indirect ways somatostatin inhibits acid release?

A

DIRECT: binds to receptors in parietal cells and inhibits release of histamine
INDIRECT: inhibits histamine release from ECL cells and gastrin release from G cells

54
Q

What happens to the negative feedback loop in patients on proton pump inhibitors?

A

it disappears - no proton pump to make stomach acidic, no signal to turn on negative feedback loop

55
Q

In addition to somatostatins, what else has a negative feedback on acid release?

A

prostaglandins (inhibit stimulatory effect of histamine)

56
Q

Pepsin only digests ____% of proteins

A

20

57
Q

What happens to amylase activity in the stomach?

A

It is inactivated by the low pH unless its active site is occupied by carbs, then it keeps digesting but that work is minimal

58
Q

Where does digestion of lipids start?

A

in the stomach (10%)

normally very negligible but becomes important in patients with pancreatic disorders

59
Q

As the stomach progresses from the orad to the caudad region, the wall _______ (thickens/thins)

A

thickens

60
Q

Receptive relaxation causes the reciprocal relaxation of what in response to relaxation of the LES?

A

Orad stomach

61
Q

receptive relaxation is mediated by what neural input?

A

vagovagal reflex (mecahnoreceptors sense stomach distention, relay that to CNS then CNS sends efferent to relax orad)

62
Q

receptive relaxation is mediated by which neurotransmitter?

A

VIP

63
Q

What is retropulsion?

A

the movement most of the bolus takes back towards the orad region of the stomach to get broken down more

64
Q

What 3 important things does the vagovagal response control?

A

1) acid secretion
2) distention of gastric wall
3) gastric motility

65
Q

Parasympathetic innervation via the vagus is ________ (excitatory/inhibitory) in the lower stomach

A

EXCITATORY

66
Q

Parasymp promotes increased motility via which neurotransmitters?

A

Ach and substance P

67
Q

Does neural input control rate or magnitude of antral contractions?

A

MAGNITUDE (gastric pacemaker controls rate)

68
Q

What is the purpose of antral contractions?

A

to grind food and push it thru the pylorus

69
Q

Which empties from the stomach faster, glucose or proteins?

A

Glucose

70
Q

Isotonic, hypotonic, or hypertonic leave stomach fastest?

A

ISOTONIC

71
Q

What size must solids be reduced to in order to pass on thru to the duodenum?

A

less than 1 cubic mm

72
Q

Antrum contracts while the initial portion of the duodenum _______

A

relaxes

73
Q

What are the 3 functions of the gastroduodenal junction?

A

1) filter large size particles of food
2) empty gastric content at a rate consistent with duodenum’s ability to digest chyme
3) prevent reflux of bolus into stomach

74
Q

Which two neurotransmitters from the vagal inhibitory fibers promote gastric emptying via pyloric relaxation?

A

1) VIP

2) NO

75
Q

Which promote pyloric constriction, slowing emptying?

A

NE and Ach

and CCK, Gastrin, GIP, Secretin

76
Q

What are peptic ulcers?

A

lesions of gastric or duodenal mucosa caused by erosive action of H+ and pepsin (can be gastric or duodenal)

77
Q

In gastric ulcers caused by H. pylori, what is the infectious toxin?

A

cagA (destroys protective barrier)

78
Q

In gastric ulcer patients, is H+ secretion lower or higher?

A

LOWER (damaged cells) so gastrin secretion is higher (dont achieve the low pH necessary to turn on the negative feedback)

79
Q

Duodenal ulcers form because H_ secretion rates are ______ (higher/lower)

A

higher! so excess H+ is delivered to duodenum overpowering the HCO3 buffering

80
Q

What is Zollinger-Ellison Syndrome?

A

gastrinoma in pancreas (secretes lots of gastrin)

81
Q

Why is high gastrin secretion dangerous?

A

increases H+ secretion (causing duodenal ulcers) as well parietal cell mass (by increasing cell number)

82
Q

Why do gastrinomas lead to steatorrhea?

A

low duodenal pH inactivates pancreatic lipase so lipids are not digested properly

83
Q

Why does somatostatin not keep the gastrin release in check?

A

No somatostatin receptors on the tumor in the pancreas

84
Q

Other than surgically removing the tumor, how else are gastrinomas treated?

A

proton pump inhibitors (keep the acid secretion in check)

cimetidine and omeprazole

Gastrointestinal (8 decks)

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