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FHB Exam 3: GI & Metabolism > GI V & VI: Gastric Phase > Flashcards

GI V & VI: Gastric Phase Flashcards

1
Q

Why does the distal part of the stomach have a thicker wall than the proximal part?

A

because it is responsible for pushing the bolus forward, so it requires strong contraction

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2
Q

Regulation of both motor and secretory responses in the stomach are via:

A

1) Neural: extrinsic and intrinsic
2) Paracrine: histamine is a powerful stimulator of H+ secretion
3) Endocrine: gastrin and somatostatin

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3
Q

Why is intrinsic factor (IF) significant? What is it secreted by?

A

It is essential for the absorption of vitamin B12, and it is secreted by the stomach.

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4
Q

Intrinsic factor is a(n) ______ factor.

A

essential

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5
Q

What is the strongest stimulant for gastric H+ secretion?

A

parasympathetic stimulation via vagus nerve (extrinsic efferent fibers terminate on intrinsic neurons that innervate parietal cells, ECL cells, G cells)

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6
Q

Which 3 substances stimulate H+ secretion by parietal cells?

A
  • acetylcholine (neurocrine)
  • histamine (paracrine)
  • gastrin (endocrine)
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7
Q

What blocks the direct affects of ACh?

A

atropine, as it is a muscarinic receptor antagonist

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8
Q

What blocks the direct effects of histamine?

A

cimetidine, as it is an H2 receptor antagonist

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9
Q

What is the receptor that ACh, gastrin, and histamine act on, respectively?

A
  • ACh: M3 receptor
  • Gastrin: CCKb receptor
  • Histamine: H2 receptor
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10
Q

Which materials have a negative feedback effect on gastric acid secretion?

A

somatostatin and prostaglandins

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11
Q

Where does the digestion of lipids begin?

A

in the oral cavity (10%)

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12
Q

Where does the digestion of proteins begin?

A

in the stomach (20%)

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13
Q

The stomach can be divided into 2 regions based on ______________.

A

differences in motility

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14
Q

Is the caudad region of the stomach thick walled or thin walled compared to the orad region? Why?

A

thick walled because a lot of motility happens there (contractions in caudad region generated by strong muscles mix the food and propel it into the small intestine)

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15
Q

What are the best ways to treat Zollinger-Ellison syndrome?

A
  • inhibitors of H+ secretion, like cimetidine and omeprazole

- surgical removal of tumor

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16
Q

What is the function of somatostatin?

A

inhibits gastric secretion and reduces rate of gastric emptying; also suppresses exocrine secretory action of pancreas

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17
Q

What is the function of histamine?

A

it is a powerful stimulator of H+ secretion

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18
Q

Does any carbohydrate digestion take place in the stomach?

A

No, as there is no amylase present in the stomach.

19
Q

Describe the functional anatomy of the stomach.

A

The lining contains columnar epithelium folded into gastric pits. These pits are the openings where the gastric glands empty.

20
Q

In the pylorus of the stomach, there are _____ pits and _____ glands.

A

long; short

21
Q

Are there goblet cells in the stomach? (potential exam question)

A

No! Instead, goblet cells are the main cells of the small and large intestine.

22
Q

The fundus and antrum of the stomach contain 6 types of secretory cells:

A

1) Parietal (oxyntic) cells: secrete HCl and IF
2) Mucous neck cells: secrete mucus
3) Chief (peptic) cells: secrete pepsinogens
4) Enterochromaffin-like (ECL) cells: secrete histamine
5) D cells: secrete somatostatin
6) G cells: secrete gastrin

23
Q

In the GI tract, does histamine have an endocrine, paracrine, or neural effect?

A

paracrine

24
Q

What is the function of gastrin?

A

it is an HCl secretagogue

25
Q

What are the major gastric secretions that form gastric juice?

A
  • HCl
  • Pepsinogen
  • Bicarb+mucous
  • IF
26
Q

Are there serious implications for digestion if the stomach is resected?

A

No, as most digestion occurs in the duodenum.

27
Q

In a healthy human, ______ is the only essential component of gastric juice; the other components serve redundant functions.

A

intrinsic factor (IF)

28
Q

What does omeprazole target?

A

It targets the H+/K+ ATPase on the luminal side of gastric parietal cells, thus reducing H+ secretion.

29
Q

What is the reason for the “alkaline tide” in gastric venous blood after a meal?

A

HCO3- is absorbed into the blood via the Cl-/HCO3- exchanger of gastric parietal cells. This HCO3- is eventually secreted back into the GI tract by the pancreas, which is how pH is restored.

30
Q

What forms the mucosal barrier in the stomach?

A

HCO3- entrapped by viscous mucous coating the stomach
(surface epithelial cells of stomach secrete a watery fluid that contains a high conc. of HCO3-; bicarb is then trapped by the mucous)

31
Q

Carbohydrates compose roughly what percentage of mucous?

A

80%

32
Q

Describe “potentiation” of H+ secretion.

A

The rate of H+ secretion can be regulated by each of the 3 stimulatory substances (gastrin, histamine, ACh) independently, as well as by interactions among the three.

33
Q

What are the second messengers for the 3 substances that stimulate H+ secretion?

A

1) ACh: IP3/Ca2+
2) Histamine: cAMP
3) Gastrin: IP3/Ca2+

34
Q

Describe the feedforward control happening during the cephalic and oral phase.

A

-direct stimulation of parietal cells by vagus via ACh
-indirect stimulation of G cells by vagus via GRP
-indirect stimulation of ECL cells by vagus (via ACh) and gastrin
(all of these promote HCl secretion by the parietal cell; this prepares the GI tract for receiving a meal)

35
Q

When does the majority of HCl secretion happen?

A

gastric phase (60%); 30% happens during oral and cephalic phases, while 10% happens during intestinal phase

36
Q

True or false: the gastric component cannot handle an acid load that’s too high.

A

True- this is why somatostatin is released by endocrine cells when gastric luminal pH drops below 3.

37
Q

What do prostaglandins do?

A

Inhibit stimulatory effect of histamine, thereby decreasing H+ secretion from parietal cells. (prostaglandins help control the acid load in the stomach)

38
Q

How does chronic NSAID use affect the gastric compartment?

A
  • NSAIDs reduce the production of prostaglandins
  • chronic use can block the feedback inhibition pathway for gastric acid secretion
  • this can led to erosion of the stomach lining, causing ulcers and bleeding
39
Q

What are the functions of the gastroduodenal junction?

A
  • filtering large size particles of food
  • emptying gastric content at a rate consistent w/ duodenum’s ability to digest chyme
  • prevention of reflux of bolus into stomach
40
Q

Are gastric or duodenal ulcers more common?

A

duodenal

41
Q

What are gastric vs. duodenal ulcers formed by?

A
  • gastric: primarily a defect in the mucosal barrier

- duodenal: high H+ secretory rates

42
Q

What is a major causative agent of gastric ulcers?

A

gram negative bacteria (like H. pylori), which release cytotoxins that destroy the protective mucosal barrier

43
Q

High gastrin secretion in patients with ZE syndrome produces which 2 direct effects?

A

1) Increased H+ secretion by parietal cells

2) Increased parietal cell mass

FHB Exam 3: GI & Metabolism (17 decks)

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