Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

STEP 1 (1) > GI-Physiology > Flashcards

GI-Physiology Flashcards

1
Q

What is the source of gastrin?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does gastrin do?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What things lead to increased gastrin levels?

A
  • chronic atrophic gastritis (e.g. H. pylori)
  • Zollinger-Ellison syndrome
  • chronic PPI use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where is somatostatin made?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What stimulates somatostatin release? Inhibits?

A

Promote- acid

Inhibits- vagal stimulaton via Ach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where is Cholcystokinin made?

A

I cells in the duodenum and jejunum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does cholecystokinin do?

A

increase pancreatic secretions and gallbaldder contraction

decreases gastric emptying

relaxes the sphincter of Oddi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What causes cholecystokinin release?

A

fatty acids and AAs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where is secretin produced?

A

S cells in the duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does secretin do?

A

increase pancreatic HCO3- and bile secretion

decrease gastric acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

K cells in the duodenum and jejenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does GIP do?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where is motilin made?

A

M cells in the small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where is vasoactive intestinal polypeptide (VIP) made?

A

parasympathetic ganglia in sphincters, gallbladder, and small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Gastric acid is also made by stomach parietal cells and works to decrease the stomach pH. What things trigger its release/synthesis?

A

histamine, Ach, and gastrin trigger its production

26
Q

What things inhibit gastric acid production?

A

somatostatin, GIP, prostaglandins, and secretin

27
Q

Where is pepsin made and what is its function?

A

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
Q

Describe how Ach is released briefly

A

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
Q

What is the MOST important mechanism of acid secretion in the stomach?

A

via histamine from ECL cells binding to parietal cells

30
Q

What does Ach binding to M3 receptors and gatrin binding to CCK 12 receptors cause?

A

Gq mediated rise in intracellular calcium, activating the K/H+ ATPase to promote acid secretion

31
Q

What part of acid secretion do PPIs inhibit?

A

the H+/K+ ATPase

32
Q

Note about pancreatic fluid

A

It is isotonic fluid with mainly Cl- at low flow and HCO3- at high flow

33
Q

What are some pancreatic enzymes?

A
  • a-amylase
  • lipases
  • proteases
  • trypsinogen
34
Q

What is the role of a-amylase?

A

starch digestion

NOTE: secreted in active form

35
Q

What are the role of pancreatic lipases?

A

fat digestion

36
Q

What are some pancreatic proteases?

A

-trypsin, chymotrypsin, elastase, and carboxypeptidases

NOTE: These are secreted as zymogens and are resposnible for protein digestion

37
Q

How is trypsinogen converted to trypsin?

A

enterokinase/enteropeptidase, a brush-border enzyme on the duodenal and jejunal mucosa

NOTE: Trypsin then activates the other pancreatic proteases

38
Q

T or F. Only monosaccharides (glucose, galactose, and frutcose) can be absorbed by enterocytes

A

T.

39
Q

How are glucose, galactose, and fructose absorbed from the GI?

A

glucose and galactose are absorbed via SGLT1 (Na+ dependent)

fructose is absorbed via GLUT5

All are transported to blood by GLUT-2

40
Q

What test can distinguish GI mucosal damage from other causes of malabsorption?

A

D-xylose absorption test

41
Q

Where is iron absorbed?

A

Absorbed as Fe2+ in the duodenum

Iron Fist, Bro

42
Q

Where is folate absorbed?

A

small bowel

43
Q

Where is B12 absorbed?

A

terminal ileum (requires intrinsic factor), along with bile salts

44
Q

What are Peyer’s Patches?

A

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
Q

B cell stimulated in germinal centers of Peyer’s patches differentiate into _______ plasma cells, which ultimately reside in the the lamina propria

A

IgA-secreting

46
Q

What is the composition of bile?

A

bile salts (bile acids conjugated to glycine or taurine, making them water soluble), phospholipids, cholesterol, bilirubin, water, and ions.

47
Q

What enzymes catalyzes the rate-limiting step of bile production?

A

cholesterol 7a-hydroxylase

48
Q

Where is bilirubin produced?

A

RBC heme is metabolized by heme oxygenase to bilverdin and then reduced to unconjugated (indirect) bilirubin (water insoluble)

49
Q

How is unconjugated bilirubin removed from the body?

A

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
Q

What happens to urobilinogen?

A

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

STEP 1 (1) (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions