GI-Physiology Flashcards

(50 cards)

1
Q

What is the source of gastrin?

A

G cells located in the antrum of the stomach and the duodenum

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2
Q

What does gastrin do?

A

increase gastric acid secretion, and promote growth of gastric mucosa and gastric motility

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3
Q

What things promote gastrin production/release? Inhibit?

A

Promote- stomach distension, AAs from protein directly, vagal stimulation via Ach, food (food has buffering capacity leading to alkalization)

Inhibits- pH below 2

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4
Q

What things lead to increased gastrin levels?

A
  • chronic atrophic gastritis (e.g. H. pylori)
  • Zollinger-Ellison syndrome
  • chronic PPI use
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5
Q

Where is somatostatin made?

A

D cells in the stomach antrum, pancreas and the GI mucosa

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6
Q

What does somatostatin do?

A

decrease gastric acid secretion and pepsinogen secretion from chief cells

decrease insulin, GH, and glucagon release

decrease pancreatic and small intestine fluid secretion

decrease gallbladder contraction

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7
Q

What stimulates somatostatin release? Inhibits?

A

Promote- acid

Inhibits- vagal stimulaton via Ach

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8
Q

Where is Cholcystokinin made?

A

I cells in the duodenum and jejunum

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9
Q

What does cholecystokinin do?

A

increase pancreatic secretions and gallbaldder contraction

decreases gastric emptying

relaxes the sphincter of Oddi

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10
Q

What causes cholecystokinin release?

A

fatty acids and AAs

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11
Q

Where is secretin produced?

A

S cells in the duodenum

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12
Q

What does secretin do?

A

increase pancreatic HCO3- and bile secretion

decrease gastric acid secretion

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13
Q

What promotes secretin release?

A

acid and fatty acids in the lumen of the duodenum (the HCO3- produced neutralizes gastric acid in the duodenum to allow pancreatic enzymes to function)

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14
Q

Where is Glucose-dependent insulinotropic peptide (GIP)(aka gastric inhibitory peptide) made?

A

K cells in the duodenum and jejenum

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15
Q

What does GIP do?

A

exocrine: decrease gastric H+ secretion
endocrine: increase insulin release

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16
Q

What promotes GIP release?

A

fatty acids, AAs, and oral glucose (thus oral glucose leads to more insulin release via GIP influence than IV)

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17
Q

Where is motilin made?

A

M cells in the small intestine

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18
Q

What does motilin do?

A

The main function of motilin is to increase the migrating myoelectric complex (MMCs) component of gastrointestinal motility and stimulate the production of pepsin. Motilin is also called “housekeeper of the gut” because it improves peristalsis in the small intestine and clears out the gut to prepare for the next meal.

A high level of motilin secreted between meals into the blood stimulates the contraction of the fundus and antrum and accelerates gastric emptying. It then contracts the gallbladder and increases the squeeze pressure of the lower esophageal sphincter. Other functions of motilin include increasing the release of pancreatic polypeptide and somatostatin

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19
Q

What are some motilin receptor agonists?

A

Erythromycin and related antibiotics act as non-peptide motilin agonists, and are sometimes used for their ability to stimulate gastrointestinal motility.

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20
Q

Where is vasoactive intestinal polypeptide (VIP) made?

A

parasympathetic ganglia in sphincters, gallbladder, and small intestine

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21
Q

What does VIP do?

A

With respect to the digestive system, VIP seems to induce smooth muscle relaxation (lower esophageal sphincter, stomach, gallbladder), stimulate secretion of water into pancreatic juice and bile, and inhibit gastric acid secretion and absorption from the intestinal lumen.

Its role in the intestine is to greatly stimulate secretion of water and electrolytes, as well as relaxation of enteric smooth muscle, dilating peripheral blood vessels, stimulating pancreatic bicarbonate secretion, and inhibiting gastrin-stimulated gastric acid secretion. These effects work together to increase motility.

It also has the function of stimulating pepsinogen secretion by chief cells

22
Q

What are the symptoms of excess VIP production, as in the case of a VIPoma in the pancreas?

A

Copius Watery Diarrhea

Hypokalemia

Achlorhydria

(WDHA syndrome)

23
Q

Where is intrinsic factor made?

A

parietal cells of the stomach

24
Q

What does intrinsic factor do?

A

it is required for vitB12 uptake in the terminal ileum

25
Gastric acid is also made by stomach parietal cells and works to decrease the stomach pH. What things trigger its release/synthesis?
histamine, Ach, and gastrin trigger its production
26
What things inhibit gastric acid production?
somatostatin, GIP, prostaglandins, and secretin
27
Where is pepsin made and what is its function?
In **chief cells** in the **body** of the stomach in order to digest protein NOTE: pepsinogen can only be converted to pepsin via H+
28
Describe how Ach is released briefly
Vagus nerve input can promote several things including: - direct stimulation of acid-secreting parietal cells - gastrin release from G cells which then act on ECL cells to promote histamine release, which then binds to the parietal cells to promote acid secretion
29
What is the MOST important mechanism of acid secretion in the stomach?
via histamine from ECL cells binding to parietal cells
30
What does Ach binding to M3 receptors and gatrin binding to CCK 12 receptors cause?
Gq mediated rise in intracellular calcium, activating the K/H+ ATPase to promote acid secretion
31
What part of acid secretion do PPIs inhibit?
the H+/K+ ATPase
32
Note about pancreatic fluid
It is isotonic fluid with mainly Cl- at low flow and HCO3- at high flow
33
What are some pancreatic enzymes?
- a-amylase - lipases - proteases - trypsinogen
34
What is the role of a-amylase?
starch digestion NOTE: secreted in active form
35
What are the role of pancreatic lipases?
fat digestion
36
What are some pancreatic proteases?
-trypsin, chymotrypsin, elastase, and carboxypeptidases NOTE: These are secreted as zymogens and are resposnible for protein digestion
37
How is trypsinogen converted to trypsin?
enterokinase/enteropeptidase, a brush-border enzyme on the duodenal and jejunal mucosa NOTE: Trypsin then activates the other pancreatic proteases
38
T or F. Only monosaccharides (glucose, galactose, and frutcose) can be absorbed by enterocytes
T.
39
How are glucose, galactose, and fructose absorbed from the GI?
glucose and galactose are absorbed via SGLT1 (Na+ dependent) fructose is absorbed via GLUT5 All are transported to blood by GLUT-2
40
What test can distinguish GI mucosal damage from other causes of malabsorption?
D-xylose absorption test
41
Where is iron absorbed?
Absorbed as Fe2+ in the **duodenum** **I**ron **F**ist, **B**ro
42
Where is folate absorbed?
small bowel
43
Where is B12 absorbed?
terminal **ileum** (requires intrinsic factor), along with **bile salts**
44
What are Peyer's Patches?
Unencapsulated lymphoid tissue found in lamina propria and the submucosa of the ileum. These contain specialized **M cells** that sample and present antigens to underlying immune cells
45
B cell stimulated in germinal centers of Peyer's patches differentiate into _______ plasma cells, which ultimately reside in the the lamina propria
IgA-secreting
46
What is the composition of bile?
bile salts (bile acids conjugated to glycine or taurine, making them water soluble), phospholipids, cholesterol, bilirubin, water, and ions.
47
What enzymes catalyzes the rate-limiting step of bile production?
cholesterol 7a-hydroxylase
48
Where is bilirubin produced?
RBC heme is metabolized by **heme oxygenase** to bilverdin and then reduced to unconjugated (indirect) bilirubin (water insoluble)
49
How is unconjugated bilirubin removed from the body?
it complexes with **albumin** in the bloodstream to form unconjugated bilirubin-alubmin complexes, which then is acted upon by **UDP-glucuronosyl-transferase** to form conjugated (**direct**-water soluble) bilirubin, which is then broken down to urobilinogen by gut bacteria
50
What happens to urobilinogen?
80% is excreted in feces as **stercobilin**, which gives the brown color to stool and of the remaining 20%, 90% enters enterohepatic circulation and 10% is excreted in urine as **urobilin**, which gives the yellow color of urine