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Physiology > Gastric Phase of a Meal > Flashcards

Gastric Phase of a Meal Flashcards

1
Q

What is often the cause of gastric ulcers?

A

Loss of the mucosal barrier

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2
Q

What is often NOT the cause of gastric ulcers?

A

Hypersecretion of acid

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3
Q

What is the function of H+ secretion in the stomach?

A

It kills microorganisms and it converts pepsinogen into pepsin

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4
Q

What is the function of intrinsic factor?

A

It is crucial for the absorption of Vitamin B12

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5
Q

What is a powerful paracrine stimulator of H+ secretion in the stomach?

A

Histamine

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6
Q

What is the strongest regulation of stomach function?

A

Neural regulation - both intrinsic and extrinsic

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7
Q

What are some hormones involved in the endocrine regulation of the stomach?

A

Gastrin

Somatostatin

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8
Q

What is the function of gastrin?

A

Stimulates gastric acid secretion

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9
Q

What is the function of somatostatin?

A

Inhibits gastric secretion

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10
Q

What is secreted in the stomach to protect against the acidity?

A

Mucus and HCO3-

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11
Q

When the stomach is not being emptied, what is the status of the pylorus?

A

Closed

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12
Q

What is the function of the distal stomach (antrum and pylorus)?

A

It is a thick muscular wall that is used for grinding and mixing the contents of the stomach

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13
Q

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

A

Reservoir and also provides a tonic force for emptying

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14
Q

What is the function of the cardia of the stomach?

A

Prevents esophageal reflux

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15
Q

What are the 3 regions of the stomach?

A

Cardia
Fundus/Body
Antrum

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16
Q

What is the orad stomach?

A

It is the proximal part closer to the mouth

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17
Q

What is the caudad stomach?

A

It is the distal part further away from the mouth

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18
Q

What are the gastric pits?

A

They are the openings where the gastric glands empty

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19
Q

What are the primary glands of the cardia?

A

Primarily mucus and HCO3- secreting gland cells, that provide mechanical and chemical protection of the gastric mucosa.

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20
Q

What are the primary glands of the fundus?

A

Oxyntic or parietal gland region

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21
Q

What are the primary glands of the antrum?

A

Pyloric gland region

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22
Q

What do parietal/oxyntic cells secrete?

A

HCl

Intrinsic Factor

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23
Q

What is the function of the HCl secreted by the parietal/oxyntic cells?

A

Kills bacteria, and allows activation of pepsin from pepsinogen, low pH for effective pepsin action.

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24
Q

What is the function of intrinsic factor secreted by the parietal/oxyntic cells?

A

It is an essential factor that allows for the absorption of Vitamin B12

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25
Q

What do mucus neck cells secrete?

A

Mucus

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26
Q

What is the function of mucus secreted by mucus neck cells?

A

Protects the gastric mucosa

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27
Q

What do peptic/chief cells secrete?

A

Pepsinogens, which become active as pepsins in acidic environments

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28
Q

What do enterochromaffin-like cells (ECL) secrete?

A

Histamine - the most powerful stimulant of HCl secretion

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29
Q

What do D cells secrete?

A

Somatostatin - most powerful inhibitor of HCl secretion

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30
Q

Where are G cells located?

A

Pyloric region

31
Q

What do G cells secrete?

A

Gastrin - stimulates HCl secretion

32
Q

What do the cells of the gastric mucosa secrete?

A

Gastric Juice

33
Q

What are the contents of gastric juice?

A

HCl
Pepsinogen
HCO3-
Intrinsic Factor

34
Q

What is the only essential gastric secretion?

A

Intrinsic Factor

35
Q

What is the mechanism for gastric acid secretion?

A

In the parietal cell, carbonic anhydrase converts H2O and CO2 into carbonic acid which dissociates into H+ and HCO3-.

On the lumenal side, H+ is transported through a H/K ATPase and Cl- follows through Cl- channels

36
Q

What process is occurring on the basolateral side of the parietal cell as gastric acid secretion is occurring on the lumenal side?

A

HCO3- is absorbed into the blood and exchanged for Cl- into the parietal cell.

This absorbed HCO3- is the reason for the “alkaline tide” (high pH) in gastric venous blood after a meal. This HCO3- is eventually secreted back in the GI tract by the pancreas.

37
Q

What is the net effect of the parietal cell?

A

It leads to a net secretion of HCl and absorption of HCO3-

38
Q

What is the largest component of mucus?

A

Carbohydrates

39
Q

What is the mucin structure?

A

It is a tetramer linked by disulfide cross bridges

40
Q

What is the strongest neural regulation of gastric secretion?

A

Parasympathetic stimulation via vagus nerve is the strongest stimulant for gastric H+ secretion.

41
Q

What is the neurocrine stimulant of H+ secretion?

A

Acetylcholine

42
Q

What is the paracrine stimulant of H+ secretion?

A

Histamine

43
Q

What is the endocrine stimulant of H+ secretion?

A

Gastrin

44
Q

What receptors does ACh bind to for H+ secretion?

A

Parietal cell muscarinic receptors

45
Q

What receptors does histamine bind to for H+ secretion?

A

H2 receptors

46
Q

What receptors does gastrin bind to for H+ secretion?

A

Cholecystokinin B receptors

47
Q

What are the 2nd messengers of ACh and Gastrin?

A

2nd messengers are – IP3/Ca++ - stimulates H+ secretion

48
Q

What are the 2nd messengers of histamine?

A

2nd messenger cAMP – stimulates H+ secretin by parietal cells

49
Q

What is the effect of atropine?

A

It blocks muscarinic receptors and will blocks Ach effects on parietal cells.

50
Q

What is the effect of cimetidine?

A

It blocks H2 receptors – blocks histamine effect.

51
Q

What is potentiation?

A

The rate of H+ secretion can be regulated by each of these independently as well as by interactions among the three – this is called potentiation – the reason is unclear - might be due to the fact that each agent works via a different receptor and in case of histamine via a different 2nd messenger.

52
Q

What types of drugs have the most complete effect on H+ secretion inhibition?

A

Proton pump inhibitors as H2 receptor inhibitors only block one pathway

53
Q

What are the possible effect points of gastrin?

A

Gastrin can have a direct effect on the parietal

cells or an indirect effect through the ECL cells

54
Q

What are the mechanisms that promote gastric secretion during the cephalic and oral phases?

A

o Direct stimulation of the parietal cells by vagus via Ach (muscarinic receptors) – neural effect.

o Indirect stimulation of the G cells by vagus via GRP (Gastrin-releasing peptide) to produce gastrin- endocrine effect.

o Indirect stimulation of the ECL cells by vagus (Ach) and gastrin (CCKB receptors)- to produce histamine- paracrine effect.

55
Q

What are the mechanisms that promote gastric secretion during the gastric phase?

A

o All the mechanisms that are present in cephalic, oral phase also operate here.

o Two additional mechanisms exist:
– Distension of the stomach activates vagovagal reflexes stimulate gastrin release.
– A direct effect of amino acids and small peptides on G cells stimulate gastrin release.

56
Q

How does the inhibition of gastric secretion occur?

A

Acidic chyme in the distal stomach (antrum) initiates a negative feedback loop – inhibits acid secretion.

57
Q

When is somatostatin released?

A

When the pH drops below 3

58
Q

What is the effect of somatostatin?

A
  • In direct pathway, SS binds to receptors in parietal cells and inhibits stimulatory effect of histamine.
  • In indirect pathway, SS inhibits - histamine release from ECL cells and gastrin release from G cells.
59
Q

What is the function of prostaglandins?

A

Inhibit stimulatory effect of histamine.

60
Q

What happens to the effect of somatostatin in people on omeprazole?

A

The somatostatin effect is absent as there is no drop in pH that occurs

61
Q

What makes prostaglandins?

A

Cyclooxygenase

62
Q

What digestion occurs in the stomach?

A

Little digestion occurs here:

  • Amylase on carbohydrates
  • Pepsin on proteins
  • Gastric lipases on lipids
63
Q

What is the difference between the orad and the caudad regions of the stomach?

A

Orad is thin walled and the caudad is thickly walled

64
Q

What is receptive relaxation?

A

Distension of the lower esophagus by food causes relaxation of LES – also relaxation of the orad stomach

65
Q

What is retropulsion?

A

Much of the chyme (not emptied into duodenum) is propelled back to stomach for further mixing and break-down

66
Q

Describe parasympathetic innervation in the stomach.

A

PS innervation in the stomach is excitatory for distal and inhibitory for the proximal part of the stomach.

Activation of the PS system will increase the gastric motility of the distal stomach.

67
Q

What are the functions of the pylorus?

A

o Filtering large size particles of food
o Emptying gastric content at a rate consistent with duodenum’s ability to digest
chyme
o Prevention of reflux of bolus into stomach

68
Q

What excites the pylorus for constriction?

A

CCK and Gastrin

69
Q

What is the cause of peptic ulcer disease?

A

This is caused by the erosive and digestive action of H+ and pepsin on mucosa

70
Q

What is the primary cause of peptic ulcers?

A

Forms primarily because of defects in the mucosal barrier. which is most often due to the bacteria H. pylori

71
Q

What is the primary cause of duodenal ulcers?

A

Excess H+ delivered to the duodenum overpowers the buffering capacity of pancreatic HCO3-. This excess H+ combined with pepsin damages the duodenal mucosa.

72
Q

What is Zollinger-Ellison Syndrome?

A

It is where a gastrinoma is formed in the pancreas that causes high secretion of gastrin, resulting in:
o Increased H+ secretion by parietal cells
o Increased parietal cell mass

This leads to duodenal ulcers and leads to steatorrhea (fatty stool), since low duodenal pH inactivates pancreatic
lipase.

73
Q

Do gastrinomas undergo feedback inhibition?

A

No, they do not have the receptors. Gastrin secretion by the tumor does not undergo feedback inhibition by H+ (as normal gastrin secretion), so gastrin levels continue to increase.

74
Q

How can gastrinomas be treated?

A

Surgery or H+ secretion inhibitors

Physiology (81 decks)

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