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GI > Physiology of Stomach > Flashcards

Physiology of Stomach Flashcards

1
Q

Fundus + superior part of body

A

orad

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2
Q

Antrum + lower part of body

A

caudad

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3
Q

What stimulates the basal electric rhythm/gastric slow wave?

A

Interstitial cells of cajal/ pacemaker cells

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4
Q

Where is the highest Basal Electric Rhythm frequency and the lowest frequency ?

A

duodenum
stomach

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5
Q

What is basal electrical rhythm ?

A

Oscillating membrane potentials

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6
Q

What does MMC stand for, what hormone secrets it and what cells does it form from?

A

Migratory motor complex, motilin hormone, and Mo cells of gastric mucosa

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7
Q

When is MMC activated and when does it appear?

A

Fasting condition/ no food in stomach
every 90 minutes

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8
Q

Where are MMC located?

A

From stomach to ileum

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9
Q

What are MMC also called and why?

A

Interdigestive housekeppers of gut because they take away all left over food in stomach and intestine

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10
Q

What happens if the MMC are destroyed?

A

If destroyed, normal flora could collect over the left over food causing infection

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11
Q

What are the three phases of MMC?

A

Phase 1: Resting phase
Phase 2: small contractions
Phase 3: large contractions

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12
Q

When are MMC’s abolished?

A

When we eat

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13
Q

What inreases motility?

A

Parasympathetic

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14
Q

What are the 2 types of parasympathetic ns?

A

cholinergic ( pregang and post gang secreting ACH) and peptidergic (VIP and NO)

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15
Q

How does food enter stomach?

A

You consume food-> mastication in the oral cavity
 Food enters the pharynx-> esophagus
 Peristalsis occurs in the esophagus to push the food towards the stomach
 The LES opens up to allow food to enter the stomach

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16
Q

What is receptive relaxation?

A

relaxation of orad region to accommodate more food

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17
Q

Which neurotransmitters are helping with receptive relaxation ? (direct question)

A

VIP and NO

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18
Q

What neurotransmitter helps with contraction of stomach?

A

Cholinergic fibers —> ACH

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19
Q

What reflex is stimulated by swallowing of food ?

A

Deglutition reflex

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20
Q

When we swallow what happens to the LES and proximal stomach and what happens in the graph?

A

It relaxes (tone decreases) so food can enter from esophagus to stomach and graph would go down

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21
Q

When the mechanoreceptors in stomach stimulates the vagus nerve what happens?

A

Vaso vagal reflex

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22
Q

What is stimulated when there is undigested fats in duodenum and what does it stimulate?

A

CCK from I cells and then CCK stimulates the orad region

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23
Q

Where does peristalsis start?

A

Mid-stomach

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24
Q

What stimulates gastric emptying?

A

Fluidity of chyme, gastrin, small volume of chyme is emptied faster, anger and aggression

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25
Q

If the vagus nerve is cut/inhibited what happens to gastric emptying?

A

gastric emptying would not happen

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26
Q

When does enterogastric reflex occur and which cells are stimulated and what do they secrete?

A

When food reaches duodenum
-I cells—> CCK
-K cells—> GIP
-S cells—> Secretin

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27
Q

What does parietal cells secrete?

A

Intrinsic factor and HCL (also called gastric acid)

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28
Q

What stimulates release of HCL and intrinsic factor?
(H.A.G)

A

gastrin, histamine, and ACH

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29
Q

What does secretin help to secrete?

A

Pepsinogen and gastric lipase

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30
Q

Gastrin helps in the growth of ____ cells

A

Parietal

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31
Q

Undigested proteins and amino acids stimulate what cells ?

A

G-cells—-> gastrin

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32
Q

When is gastrin secreted?

A

When ph is greater than 3

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33
Q

When is somatostatin secreted?

A

When pH is less than 3

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34
Q

What is secreted from mucous neck cells and function of mucus neck cells?

A

mucus and bicarbonate
buffers gastric acid

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35
Q

What is secreted from enterochromaffin-like cells (ECL) and what stimulates the release ?

A

histamine
ACH and gastrin

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36
Q

What is secreted from chief cells and what stimulates the release?

A

pepsinogen and gastric lipase
ACH and secretin

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37
Q

What is secreted from D cells and what stimulates the release?

A

Somatostatin
Acid in stomach (too much)

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38
Q

What is secreted from G cells and what stimulates the release?

A

gastrin
ACH, peptides and amino acids

39
Q

Importance of mucus

A

For protection against acid

40
Q

What does HCL convert?

A

pepsinogin to pepsin

41
Q

What does the parietal cells have a lot of and why?

A

mitochondria because it needs a certain type of ATPase (hydrogen-potassium)

42
Q

Function of parietal cells :

A

To stimulate Hydrogen-potassium ATPase to release H+ to go into the gastric lumen (along with Cl—-> HCL)

43
Q

During acid secretion which ions go into the blood?

A

bicarbonate and sodium

44
Q

During acid secretion which ions go into the lumen?

A

H+, Cl-, and K+

45
Q

What is post-prandial alkaline tide?

A

When bicarb enters the blood

46
Q

Which drugs inhibit H+/K+ pump and what are the effects?

A

omeprazole/pantaprazole and they can completely inhibit the production of acid

47
Q

Explain the vaso-vagal reflex

A

The mechanoreceptors of stomach stimulate afferent fibers of vagus nerve (CN 10) —> dorsal vagus nucleus of medulla—> efferent fibers stimulated—-> synapses onto myentric plexus—> releases ACH and peptidergic fibers release VIP and NO at fundus to relax it

48
Q

How would the graph look for the esophagus when we swallow food ?

A

During swallowing the graph would be at zero because it is at a resting state and after swallowing there’s a peak due to peristalsis

49
Q

What inhibits gastric emptying?

A

Vagotomy, depression, enterogastric reflex

50
Q

How would receptive relaxation be impacted by the loss of
the vagus nerve?

A

Vagus is EXTREMELY important for receptive relxation.
Without vagus, receptive relaxation would be lost.

51
Q

Which cells inhibit gastric emptying?

A

-I cells—> CCK
-K cells—> GIP
-S cells—> Secretin

52
Q

From fastest to slowest, state the rate of gastric emptying
protein, fluid, fat, and carbs

A

Fluid>carbs>protein>fat

53
Q

What are the factors stimulating HCL secretion?

A

1.Neural – Vagal stimulation
2.Hormonal - Acetylcholine
- Gastrin
- Histamine
3.Distension of stomach
4.Products of protein digestion

54
Q

What are the factors inhibiting HCL secretion?

A

1.Ph of gastric luminal content
2.Hormonal – Somatostatin
3.Chyme in the duodenum
4.Secretin,GIP
5.Prostaglandins,Epidermal growth factor,
Transforming growth factor

55
Q

What are hunger pains?

A

More intense MMCs

56
Q

Describe the direct pathway for the stimulation of H+ secretion:

A

Vagus-> Ach-> Muscaneric receptor (M3)-> Gq pathway activated -> pkC-> Ca2+ and IP3 -> H+K+ ATPase

57
Q

Describe the indirect pathway for the stimulation of H+ secretion:

A

Ach-> ECL-> Histamine-> H2 receptors-> Gs pathway-> cAMP-> H+K+ATPase

58
Q

Describe the direct pathway for the stimulation of gastrin secretion:

A

Vagus-> G cells->Gastrin-> CCK beta receptors-> which goes on to stimulate H+K+ ATPase through Gq pathway

59
Q

Describe the indirect pathway for the stimulation of H+ secretion:

A

Ach-> ECL-> Histamine-> H+K+ ATPase

60
Q

Why is atropine not as effective as omeprazole?

A

Because although ACH is stopped, gastrin and histamine can still stimulate gastric acid production

61
Q

Describe the direct pathway for the inhibition of gastrin by somatostatin:

A

D cells-> Somatostatin-> Gi-> H+K+ ATPase inhibited

62
Q

Describe the indirect pathway for the inhibition of gastrin by somatostatin:

A

Somatostatin-> enterochromaffin cells inhibited-> Histamine not released

63
Q

What differs between Cimetedine and ranitidine from atropine?

A

they are H2 receptor blockers that prevent histamine from acting

64
Q

When does basal acid secretion occur?

A

During resting conditions when there’s no food

65
Q

How does Prostaglandin directly inhibit the H+K+ ATPase?

A

Via the Gi pathway

66
Q

What are the three phases of gastric secretion?

A

Cephalic, gastric, intestinal

67
Q

How does Prostaglandin indirectly inhibit the H+K+ ATPase?

A

By inhibiting Histamine release via ECL cells

68
Q

When is gastric phase stimulated?

A

When you have food in your stomach

69
Q

What happens to the stomach when this occurs?

A

When food enters the stomach, the stomach becomes extended/ stretched which activates mechanoreceptors that activate the vagus

70
Q

After the vagus is activated during gastric phase, what happens?

A

Vagus stimulates-> submucosal plexus via Ach-> postganglion releases Ach-> parietal cells-> H+ relased

Another outflow of vagus stimulates Ach which the postganglion fibers causes parietal cells to release more H+
Distention and amino acids and peptides stimulate g cells to release gastrin
When food enters the stomach, it buffers the acid presentthere, raising the pH, causing gastrin secretion and inhibiting somatostatin.

71
Q

What happens during the cephalic phase?

A

1) Vagus stimulates submucosal plexus via ACH—> postganglionic fibers secrets ACh at parietal cells—> H+ secretion
2) Outflow acts on submucosal plexus via ACH—> postganglionic fibers secrete Gastrin releasing peptide (GRP) —> G cells stimulated—> gastrin secreted—-> stimulates parietal cells—> stimulates H+

72
Q

___ phase is stimulated by vagus when you see/smell/think of food

A

Cephalic

73
Q

What is inhitied during Intestinal phase?

A

Gastric secretion and gastric motility is inhibited. Vagus and Ach is inhibited

74
Q

What induces somastatin to be released in the intestinal phase?

A

the low ph of the stomach due to the HCL

75
Q

What kind of anemia is caused if Vit B12 can’t be absorbed?

A

Pernicious anemia

76
Q

In pernicious anemia, why are there high levels of gastrin but low acid secretion?

A

 Because of absence of parietal cells
 Low Hb= anemia
 Macrocytes=big RBCs

77
Q

What prevents prostaglandin production by inhibiting COX-1&2 to inhibit inflammation?

A

NSAIDS

78
Q

The stomach is VERY acidic. How does H pylori colonize the mucosa of the stomach?

A

H pylori produce urease which converts urea into ammonia. Ammonia buffers the gastric acid

79
Q

What can occur as a result of chronic use of NSAIDs.?

A

Erosive gastritis

80
Q

When H. pylori buffers the environment what occurs?

A

More bacteria inhibit the area and burrow into the mucosa

81
Q

What are peptic ulcers?

A

sores that occur due to the breakdown of the barrier that prevents
irritation, autodigestion of the mucosa

82
Q

gastric + duodenal ulcers= ?

A

Peptic ulcers

83
Q

What do gastric ulcers cause and what are causes these ulcers?

A

epigastric pain, right after eating
NSAIDS and H. Pylori

84
Q

What do duodenal ulcers cause what are causes these ulcers?

A

epigastric pain, 2-3 hours after eating
H. Pylori

85
Q

What is Zollinger-Ellison syndrome?

A

Causes a build up of gastrin that leads to gastrinoma (gastrin producing tumor in the pancreas) due to the lack of somatostatin

86
Q

What is the basal acid output for pernicious anemia?

A

0

87
Q

What is the basal acid output for Gastrin secreting tumor?

A

10-30

88
Q

What is the basal acid output for duodenal ulcer?

A

0-3

89
Q

What is the basal acid output for gastric ulcer?

A

0-3

90
Q

Acid secreiton is decreased in gastric ulcers
but increased in duodenal ulcers. Why?

A

In gastric ulcers, acid leaks out of the
gastric ulcers, therefore the total acid is
reduced in the stomach.

91
Q

Why is duodenal ulcers higher than gastric ulcers?

A

In duodenal ulcers, acid secretion is increased because the most common cause of duodenal ulcers is H pylori. H pylori inhibits D cells, which inhibits somatostatin,
so somatostatin can no longer inhibit gastrin secretion, which stimulates acid secretion

92
Q

Why is the output 0 in pernicious cells?

A

In pernicious anemia- loss of parietal
cells- almost no acid secreiton. Some
acid may be released upon eating food

93
Q

Why is basal acid output 10-30 in zollinger-ellison syndrome?

A

Gastrin stimulates acid secretion, so there is increased acid production. Excess gastrin is being released

94
Q

Which hormone is the ONLY hormone released that can inhibit gastric emptying under normal physiological conditions?

A

CCK

GI (12 decks)

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