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
If the vagus nerve is cut/inhibited what happens to gastric emptying?
gastric emptying would not happen
26
When does enterogastric reflex occur and which cells are stimulated and what do they secrete?
When food reaches duodenum -I cells---> CCK -K cells---> GIP -S cells---> Secretin
27
What does parietal cells secrete?
Intrinsic factor and HCL (also called gastric acid)
28
What stimulates release of HCL and intrinsic factor? (H.A.G)
gastrin, histamine, and ACH
29
What does secretin help to secrete?
Pepsinogen and gastric lipase
30
Gastrin helps in the growth of ____ cells
Parietal
31
Undigested proteins and amino acids stimulate what cells ?
G-cells----> gastrin
32
When is gastrin secreted?
When ph is greater than 3
33
When is somatostatin secreted?
When pH is less than 3
34
What is secreted from mucous neck cells and function of mucus neck cells?
mucus and bicarbonate buffers gastric acid
35
What is secreted from enterochromaffin-like cells (ECL) and what stimulates the release ?
histamine ACH and gastrin
36
What is secreted from chief cells and what stimulates the release?
pepsinogen and gastric lipase ACH and secretin
37
What is secreted from D cells and what stimulates the release?
Somatostatin Acid in stomach (too much)
38
What is secreted from G cells and what stimulates the release?
gastrin ACH, peptides and amino acids
39
Importance of mucus
For protection against acid
40
What does HCL convert?
pepsinogin to pepsin
41
What does the parietal cells have a lot of and why?
mitochondria because it needs a certain type of ATPase (hydrogen-potassium)
42
Function of parietal cells :
To stimulate Hydrogen-potassium ATPase to release H+ to go into the gastric lumen (along with Cl----> HCL)
43
During acid secretion which ions go into the blood?
bicarbonate and sodium
44
During acid secretion which ions go into the lumen?
H+, Cl-, and K+
45
What is post-prandial alkaline tide?
When bicarb enters the blood
46
Which drugs inhibit H+/K+ pump and what are the effects?
omeprazole/pantaprazole and they can completely inhibit the production of acid
47
Explain the vaso-vagal reflex
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
How would the graph look for the esophagus when we swallow food ?
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
What inhibits gastric emptying?
Vagotomy, depression, enterogastric reflex
50
How would receptive relaxation be impacted by the loss of the vagus nerve?
Vagus is EXTREMELY important for receptive relxation. Without vagus, receptive relaxation would be lost.
51
Which cells inhibit gastric emptying?
-I cells---> CCK -K cells---> GIP -S cells---> Secretin
52
From fastest to slowest, state the rate of gastric emptying protein, fluid, fat, and carbs
Fluid>carbs>protein>fat
53
What are the factors stimulating HCL secretion?
1.Neural – Vagal stimulation 2.Hormonal - Acetylcholine - Gastrin - Histamine 3.Distension of stomach 4.Products of protein digestion
54
What are the factors inhibiting HCL secretion?
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
What are hunger pains?
More intense MMCs
56
Describe the direct pathway for the stimulation of H+ secretion:
Vagus-> Ach-> Muscaneric receptor (M3)-> Gq pathway activated -> pkC-> Ca2+ and IP3 -> H+K+ ATPase
57
Describe the indirect pathway for the stimulation of H+ secretion:
Ach-> ECL-> Histamine-> H2 receptors-> Gs pathway-> cAMP-> H+K+ATPase
58
Describe the direct pathway for the stimulation of gastrin secretion:
Vagus-> G cells->Gastrin-> CCK beta receptors-> which goes on to stimulate H+K+ ATPase through Gq pathway
59
Describe the indirect pathway for the stimulation of H+ secretion:
Ach-> ECL-> Histamine-> H+K+ ATPase
60
Why is atropine not as effective as omeprazole?
Because although ACH is stopped, gastrin and histamine can still stimulate gastric acid production
61
Describe the direct pathway for the inhibition of gastrin by somatostatin:
D cells-> Somatostatin-> Gi-> H+K+ ATPase inhibited
62
Describe the indirect pathway for the inhibition of gastrin by somatostatin:
Somatostatin-> enterochromaffin cells inhibited-> Histamine not released
63
What differs between Cimetedine and ranitidine from atropine?
they are H2 receptor blockers that prevent histamine from acting
64
When does basal acid secretion occur?
During resting conditions when there's no food
65
How does Prostaglandin directly inhibit the H+K+ ATPase?
Via the Gi pathway
66
What are the three phases of gastric secretion?
Cephalic, gastric, intestinal
67
How does Prostaglandin indirectly inhibit the H+K+ ATPase?
By inhibiting Histamine release via ECL cells
68
When is gastric phase stimulated?
When you have food in your stomach
69
What happens to the stomach when this occurs?
When food enters the stomach, the stomach becomes extended/ stretched which activates mechanoreceptors that activate the vagus
70
After the vagus is activated during gastric phase, what happens?
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
What happens during the cephalic phase?
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
___ phase is stimulated by vagus when you see/smell/think of food
Cephalic
73
What is inhitied during Intestinal phase?
Gastric secretion and gastric motility is inhibited. Vagus and Ach is inhibited
74
What induces somastatin to be released in the intestinal phase?
the low ph of the stomach due to the HCL
75
What kind of anemia is caused if Vit B12 can’t be absorbed?
Pernicious anemia
76
In pernicious anemia, why are there high levels of gastrin but low acid secretion?
 Because of absence of parietal cells  Low Hb= anemia  Macrocytes=big RBCs
77
What prevents prostaglandin production by inhibiting COX-1&2 to inhibit inflammation?
NSAIDS
78
The stomach is VERY acidic. How does H pylori colonize the mucosa of the stomach?
H pylori produce urease which converts urea into ammonia. Ammonia buffers the gastric acid
79
What can occur as a result of chronic use of NSAIDs.?
Erosive gastritis
80
When H. pylori buffers the environment what occurs?
More bacteria inhibit the area and burrow into the mucosa
81
What are peptic ulcers?
sores that occur due to the breakdown of the barrier that prevents irritation, autodigestion of the mucosa
82
gastric + duodenal ulcers= ?
Peptic ulcers
83
What do gastric ulcers cause and what are causes these ulcers?
epigastric pain, right after eating NSAIDS and H. Pylori
84
What do duodenal ulcers cause what are causes these ulcers?
epigastric pain, 2-3 hours after eating H. Pylori
85
What is Zollinger-Ellison syndrome?
Causes a build up of gastrin that leads to gastrinoma (gastrin producing tumor in the pancreas) due to the lack of somatostatin
86
What is the basal acid output for pernicious anemia?
0
87
What is the basal acid output for Gastrin secreting tumor?
10-30
88
What is the basal acid output for duodenal ulcer?
0-3
89
What is the basal acid output for gastric ulcer?
0-3
90
Acid secreiton is decreased in gastric ulcers but increased in duodenal ulcers. Why?
In gastric ulcers, acid leaks out of the gastric ulcers, therefore the total acid is reduced in the stomach.
91
Why is duodenal ulcers higher than gastric ulcers?
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
Why is the output 0 in pernicious cells?
In pernicious anemia- loss of parietal cells- almost no acid secreiton. Some acid may be released upon eating food
93
Why is basal acid output 10-30 in zollinger-ellison syndrome?
Gastrin stimulates acid secretion, so there is increased acid production. Excess gastrin is being released
94
Which hormone is the ONLY hormone released that can inhibit gastric emptying under normal physiological conditions?
CCK