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FHB GI > 49-50 Gastric > Flashcards

49-50 Gastric Flashcards

1
Q

What is the purpose of H+ secretion at the stomach?

A

Killing of microorganisms and conversion of pepsinogen → pepsin

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2
Q

What is the purpose of IF secretion at the stomach?

A

Essential for absorption of vit B12 (occurs at small intestine)

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3
Q

What is the purpose of mucus and HCO3- secretion at the stomach?

A

Protects gastric mucosa

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4
Q

What is the purpose of water secretion at the stomach?

A

Lubricates bolus + suspension of nutrients in soln

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5
Q

Which of the following are responsible for regulating motor and secretory responses of the stomach? Neural, endocrine, paracrine.

A

Neural, endocrine, paracrine

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6
Q

Is neural regulation of the stomach intrinsic, extrinsic, or both?

A

Both

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7
Q

Histamine is a powerful (endocrine or paracrine?) stimulator of ____ secretion.

A

paracrine

- H+

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8
Q

What are the 2 major endocrine hormones of the stomach that affect secretion?

A
  • Gastrin (stomach and duodenum)- stimulates gastric acid secretion.
  • Somatostatin (stomach, duodenum, and pancreas) - inhibits gastric secretion.
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9
Q

What is secreted from the cardia region of the stomach (+ LES)?

A

Mucus and HCO3-

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10
Q

What is secreted from the fundus and body regions of the stomach?

A

Mucus, HCO3-, HCl, IF, pepsinogens, lipase

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11
Q

What is secreted from the antrum and pylorus regions of the stomach?

A

Mucus and HCO3-

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12
Q

What region(s) of the stomach serve(s) as a reservoir and provide a tonic force during emptying?

A

Fundus and body

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13
Q

What region(s) of the stomach perform(s) the most mixing, grinding, sieving, and regulation of emptying?

A

Antrum and pylorus

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14
Q

What region(s) of the stomach is/are responsible for belching, entry of food, and prevention of reflux?

A

Cardia

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15
Q

Describe the regions of the stomach beginning to end.

A

Start at cardia

  • Above it is fundus
  • Below that is body
  • Then antrum
  • Then pylorus
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16
Q

What type of epithelial lining does the stomach contain? What is this layer folded into?

A
  • Simple columnar epithelium

- Folded into gastric pits

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17
Q

Each gastric pit is the opening where _____ ______ empty.

A

gastric glands

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18
Q

What happens to the muscularis mucosae layer of the mucosa during transition from esophagus to stomach?

A

Becomes less thick in stomach

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19
Q

Name the 3 main parts of the mucosal invaginations in the stomach, apical to basal.

A
  1. Gastric pit
  2. Mucus neck segment
  3. Gastric gland
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20
Q

How is stem cell renewal behavior different in the small intestine vs. the stomach?

A
  • Intestines are unidirectional: sc’s at crypts’ base (paneth cells), move apically and then slough off after 3-6 days
  • Stomach is bidirectional: sc’s at mucus neck segment, can move apically for rapid surface cell renewal (4-7 days til sloughing off) or basally towards slow gland cell renewal (weeks)
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21
Q

What 3 regions can the stomach’s gastric mucosa be divided into based on gland structure?

A
  1. Cardiac glandular region (below LES)
  2. Oxyntic or parietal gland region (fundus)
  3. Pyloric gland region (antrum)
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22
Q

What is primarily secreted from the cardiac glandular region?

A

Mucus and HCO3-, provides mechanical and chemical protection of gastric mucosa

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23
Q

Name the 6 types of secretory cells found at the fundus of the stomach.

A
  1. Parietal or oxyntic cells
  2. Mucus neck cells
  3. Peptic or Chief cells
  4. Enterochromaffin-like cells (ELCs)
  5. D cells
  6. G cells (also found at pyloric region)
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24
Q

*What do parietal/oxyntic cells release, and what do these do?

A
  • HCl: kills bacteria; allows pepsinogen -> pepsin; low pH : effective pepsin action
  • IF: Glycoproteins bind vit B12 so intestines can absorb it (*it’s an essential factor!)
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25
Q

What do mucus neck cells release, and what does this do?

A

Mucus (protection of mucosa)

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26
Q

What do peptic or chief cells release?

A

Pepsinogen, which is a variety of proteases (*require acidic environment for activation)

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27
Q

What do ECL cells release, and what does this do?

A

Histamine, *the most powerful stimulator of HCl secretion

- Paracrine

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28
Q

What do D cells release, and what does this do?

A

Somatostatin: powerful inhibitor of HCl secretion

- Endocrine

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29
Q

What do G cells release, and what does this do?

A

Gastrin: HCl secretagogue

- Endocrine

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30
Q

Collectively, cells of the gastric mucosa secrete a fluid called _____________.

A

Gastric juice

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31
Q

In healthy humans, ___________ is the only essential component of gastric juice. (all others have redundant fcns)

A

IF

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32
Q

Describe the change in the resting parietal cell upon activation. (not sure how important details are)

A
  • Resting parietal cell cytoplasm contains numerous tubules and vesicles (tubulovesicular system), their membranes contain transport proteins needed for secretion of H+ and Cl-. Intracellular secretory canaliculi are present.
  • Once activated, the tubulovesicular membranes fuse with the plasma membrane of the secretory canaliculi – (increases the number of H+-K+ antiporters on the secretory canaliculi membrane) – and opens to the lumen of the gland.
33
Q

How did the H+ of the HCl secreted from parietal cells ever get into that parietal cell?

A

Diffused in as CO2, then carbonic anhydrase…

34
Q

What pumps/channels are present on the luminal side of a parietal cell?

A

Active H+ K+ ATPase

Cl- passive channel

35
Q

What pumps/channels are present on the basolateral side of a parietal cell?

A

NKP
Cl- HCO3- exchanger (secondary)
Also: CO2 diffuses in

36
Q

(Not sure if important) How do increased intracellular Ca2+ and cAMP affect luminal conduction of K+ and Cl- in parietal cells?

A

Increase it

37
Q

What drug inhibits the H+ K+ ATPase (found on the luminal side of parietal cells)?
What is it used to treat?

A

Omeprazole

- Used to treat ulcers thru decreased H+ secretion

38
Q

Regarding the gastric parietal cell, what is the net direction of movement of HCl and HCO3-? (lumen vs. bv)

A

HCl secreted to lumen, HCO3- absorbed to blood

39
Q

Using what we just learned regarding parietal cells, explain why “alkaline tide” occurs after a meal (how does it affect gastric blood pH?)

A

Stimulation of parietal cell leads to HCO3- reabsorption (as Cl- enters cell), therefore high pH in gastric venous blood.

40
Q

The surface epithelial cells of stomach secrete a watery fluid into the lumen that contains what 4 major ions?
Which of the 4 have higher concentrations than the plasma?
What is the name of the layer that this forms?

A

Na+, Cl-, K+, HCO3-
- K+ and HCO3-, because HCO3- is entrapped by the viscous mucus that coats the stomach lumen, forming the *gastric mucosal barrier

41
Q

A layer of ________ protects the relatively alkaline, HCO3-rich barrier from the acidic contents of the gastric lumen.

A

Mucus

42
Q

Describe the structure/texture of mucus (not exactly what it contains).
Which stomach cells secrete it?

A

Secretions containing mucins are viscous and sticky, collectively called mucus. 80% carb
- Secreted by mucus neck cells

43
Q

Describe the molecular structure of mucus protein.

What stomach enzyme can break it down via proteolysis, and why is this important?

A

Tetramers w/di-S center that is sensitive to proteolysis by pepsin
- *Once broken down, gel of protective mucus layer dissolves (which is why we have bicarb to neutralize the acids in that area

44
Q

What is the STRONGEST stimulus of gastric secretion?

A

Parasymp stim (vagus n.)

45
Q

Regarding parasympathetic regulation of gastric secretions, extrinsic efferent fibers terminate on intrinsic neurons that innervate what 3 cell types?

A

Parietal cells, ECL cells, G cells

46
Q

What 3 mechanisms can stimulate H+ secretion by parietal cells?

A

Acetylcholine (neurocrine)
Histamine (paracrine)
Gastrin (endocrine)

47
Q

What general type of receptors does ACh bind to when stimulating parietal cells, and what is the intracellular 2nd messenger?

A
  • Binds to muscarinic (M3) receptors on the parietal cells

- 2nd messengers: IP3/Ca++ (stimulates H+ secretion)

48
Q

What’s the name of a drug we talked about that inhibits muscarinic receptors?

A

Atropine

49
Q

Recall: what types of cells release histamine?

A

ECL cells (have paracrine effect on parietal cells)

50
Q

What type of receptors does histamine bind to when stimulating parietal cells, and what is the intracellular 2nd messenger?

A
  • Binds to H2 receptors on parietal cells

- 2nd messenger: cAMP (stimulates H+ secretion)

51
Q

What’s the name of a drug that blocks H2 receptors?

A

Cimetidine

52
Q

What type of receptors does gastrin bind to when stimulating parietal cells, and what is the intracellular 2nd messenger?

A
  • CCK-B (or CCK-2) receptors

- 2nd messengers: IP3/Ca++

53
Q

Define potentiation as it pertains to ACh, histamine, and gastrin’s affects on parietal cell stimulation.

A

The rate of H+ secretion can be regulated by each of these independently as well as by interactions among the three.
- Unclear how it works

54
Q

Will drugs like atropine and cimetidine block only their targets’ stimulation of parietal cells, or all of the potentiation targets as well?

A

All potentiation targets, I believe

55
Q

What percentages of HCl secretion occur during the cephalic/oral phase?
Gastric phase?
Intestinal phase?

A

30%
60%
10%

56
Q

*Describe the (3) mechanisms that support HCl secretion during the oral/cephalic phase.

A
  • Direct stimulation of parietal cells by vagus via ACh (muscarinic receptors) – neural effect.
  • Indirect stimulation of the G cells by vagus via GRP (Gastrin-releasing peptide) – gastrin-endocrine effect.
  • Indirect stimulation of the ECL cells by vagus (ACh) and gastrin (CCKB receptors) to produce histamine – paracrine effect.
57
Q

*Describe the (5) mechanisms that support HCl secretion during the gastric phase.

A

(3 previous from oral phase:)
- Direct stimulation of parietal cells by vagus via ACh (muscarinic receptors) – neural effect.
- Indirect stimulation of the G cells by vagus via GRP – gastrin-endocrine effect.
- Indirect stimulation of the ECL cells by vagus and gastrin (CCKB receptors) to produce histamine – paracrine effect.
(+ 2 additional)
- Distension of the stomach activates vagovagal reflexes – stimulate gastrin release
- A direct effect of AAs and small peptides on G cells – stimulate gastrin release

58
Q

What chemicals found in beverages also stimulate HCl secretion?

A

Alcohol and caffeine

59
Q

How is the (1) mechanism that supports HCl secretion during the intestinal phase mediated?

A

By protein digestion

60
Q

What 2 chemicals produce feedback inhibition on gastric acid secretion by parietal cells?
How is this negative feedback loop initiated?

A
  • Somatostatin and prostaglandins

- Low pH chyme in antrum

61
Q

During feedback inhibition of gastric acid secretion, how does somatostatin inhibit the direct pw?
Indirect pw?

A
  • Direct: SS binds to receptors in parietal cells to inhibit stimulatory effect of histamine
  • Indirect: SS inhibits histamine release from ECL cells and gastrin release from G cells.
62
Q

During feedback inhibition of gastric acid secretion, how do prostaglandins cause inhibition?

A

Inhibit stimulatory effect of histamine

63
Q

Why do long-term aspirin-users have gastric bleeding?

A

Chronic use of NSAIDs blocks negative feedback normally done by prostaglandins, causing too much HCl release.

64
Q

Some digestion occurs in the stomach, but it’s usually not vital (unless there are other, e.g. pancreatic, disorders). What digestive enzymes might you find in the stomach?

A
  • Pepsins (20% protein digestion)
  • Amylase (inactive at low pH unless substrate carb is bound)
  • Lipases (10% lipid digestion)
65
Q

Which region of the stomach has the thickest muscular wall and why?

A

Caudad region (mixing and propelling food)

66
Q

Define receptive relaxation (w/r/t the stomach).
Describe how it works.
What NT is involved?

A
  • Distension of the lower esophagus by food causes relaxation of LES + relaxation of the orad stomach.
  • Vagovagal reflex: mechanoreceptors detect stomach distension and relay this to CNS via sensory neurons. CNS sends efferent information to smooth muscle of orad stomach to relax
  • NT released from postganglionic peptidergic vagal fibers is VIP.
67
Q

Describe, generally, the mixing and propulsion that occurs in the stomach when food enters.

A
  • Caudad region- waves of strong contraction start in the mid portion of stomach and move distally, increasing in strength towards pylorus.
  • They mix the gastric contents and periodically propel a portion of these in the duodenum through pylorus, followed by closure of pylorus.
68
Q

Define retropulsion w/r/t gastric motility.

A

Because pyloric sphincter is often closed, much of the chyme (not emptied into duodenum) is propelled back to stomach for further mixing and break-down.

69
Q

What types of processes (3) do vagovagal stomach reflexes help regulate?

A

Acid secretion, distension of gastric wall, and gastric motility

70
Q

The rate of antral contractions is set by _________________, but the magnitude of contractions is regulated by __________________.

A
  • a gastric pacemaker

- parasympathetic input

71
Q

How long does emptying into the duodenum from the stomach usually take?
How does a liquid meal (e.g. all glucose) vs. a solid meal (e.g. piece of a liver, mostly ptn) influence gastric emptying?

A

~ 3 hrs

- Liquids empty rapidly, solids more slowly (must be broken down)

72
Q

(might not be that important) Explain the different rates of gastric emptying regarding isotonic, hypotonic, and hypertonic foods.

A

Isotonic faster than both hyper and hypotonic.

73
Q

Describe the general structure of the pylorus.

A

Consists of a two ring-like thickenings of circular smooth muscle cells.

74
Q

*Explain the difference in gastric vs duodenal ulcers w/r/t the pylorus. (peptic ulcer disease–PUD, pertains to stomach and/or duodenum)
Which are more common?

A
  • Gastric ulcers form because stomach is sensitive to high pH of bile that leaks back from intestines
  • Duodenal ulcers form because duodenum is sensitive to low pH of gastric juice leaking into duodenum (more common than gastric because H+ rate is high)
75
Q

What 3 major classes of regulation control the pylorus?

A

Neural, paracrine, endocrine

76
Q

What 2 NTs are associated w/gastric emptying during parasymp stim?

A

NO and VIP (via vagus)

77
Q

Recall: Generally, what is the cause of gastric ulcers?
What’s a gram-neg bacteria that could also do this?
What are some others potential causes of gastric ulcers?

A
  • Defects in mucosal barrier (mucosa digested)
  • H. Pylori (releases cytotoxins). Surprisingly, in these pts, net H+ secretory rates are lower and thus the secretion rate of gastrin is increased (lacking the negative feedback).
  • Stress, smoking, NSAIDs, alcohol
78
Q

What is Zollinger-Ellison Syndrome (gastrinoma)?
Sx?
Tx?

A

Tumor (or gastrinoma) located in the pancreas, secretes high quantities of gastrin.
Effects:
- Increased H+ secretion by parietal cells
- Increased parietal cell mass

Sx: Leads to duodenal ulcers
- Sometimes fatty stool (steatorrhea) because pancreatic lipases inactivated at low pH
(there is also a lack of feedback inhibition)

Treatment includes

  • Inhibitors of H+ secretion, e.g. Cimetidine, Omeprazole
  • Surgical removal of tumor

FHB GI (10 decks)

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