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P2 hormones > Pack > Flashcards

Pack Flashcards

1
Q

What are the classic/offical hormones produced by the enteroendocrine APUD cells?

A

Secretin, gastrin, CCK, GIP

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2
Q

What are the neurocrines produced ENS neurons?

A

VIP, GRP, enkephalins

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3
Q

What are the paracrines produced in the GIT by ENS?

A

Somatostatin, histamine

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4
Q

What are the sites where gastrin is produced?

A

Antrum (Most), duo,

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5
Q

What are the sites where CCK is produced?

A

Duo

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6
Q

What are the sites where Secretin is produced?

A

Duo, jejun, illeum

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7
Q

What are the sites where GIP is produced?

A

duo and jejun

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8
Q

What are the sites where motilin is produced?

A

Duo, Jejnum

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9
Q

What is the concentration of serum gastrin that indicates that a person has a Zollinger-Ellison Syndrome (Gastrinoma) after ChiRhoStim is adminstered?

A

Above 110 pg/ml

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10
Q

What is gastrin stimulated by?

A

Secretion is stimulated by protein digestion products
— Nervous impulses, physical distention
— calcium, regular &decaf coffee, and wine

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11
Q

What is gastrin inhibted by?

A

Secretion is inhibited by acidification of antrum

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12
Q

What does gastrin stimulate?

A

Gastrin stimulates pyloric contraction and increases cardiac sphincter tone, preventing
reflux. Gastrin also stimulates acid and pepsinogen secretion and antral motility, thus
facilitating gastric digestion

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13
Q

How does gastrin effect the mucosa?

A

Stimulates growth of oxyntic mucosa of the stomach, the duodenal mucosa, and colonmucosa
Surgical removal ofthe antrum causes atrophy.

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14
Q

What do patients with gastrinomas have in relation to the mucosa?

A

Patients with gastrin-secreting tumors have mucosal hyperplasia and hypertrophy.

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15
Q

What does CCK do in relation to sphinchers and enzymes?

A

Contraction of pyloric
sphincter and inhibition
of gastric emptying

↑ pancreatic
secretion of enzymes

↑ glucagon secretion

Augments the secretin effect
on secretion of bicarbonate
in the pancreas and liver

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16
Q

What kinase does CCK increase the secretion of?

A

Enterokinase

17
Q

In what conditions does cck have maximal effect?

A

Normal vagal tone and the prescence of secretin

18
Q

What does CCK do in relation to the gall bladder?

A

Gallbladder contraction, emptying
of the gallbladder and relaxation of
the sphincter of Oddi

19
Q

What does secretin do in realtion with the spintchers and secretion?

A

May stimulate the contraction of the pyloric spintcher

Inhibts the secretion of HCL and gastric motility

20
Q

What does secretin do in relation with CCK

A

Augments its action on the pancreas and antagonises gastrin

21
Q

What does secretin do in relation with bicarbonate?

A

Stimulates its secretion from the pancreatic duct cells and biliary tract

22
Q

What stimulates secretin secretion?

A

Stimuli for release
- Acid in duodenum and jejunum (pH <4.5)
(small amounts can be released fromileum)
- Fatty acids

23
Q

What does secritin do in relation to pepsin?

A

Stimulates pepsin secretion

24
Q

Where is GIP released from and what stimulates its release?

A
  • Released from K-cells of duodenum and proximal jejunum
  • All major foodstuffs—fat must be hydrolyzed.
  • Oral glucose but not i.v. glucose
25
Q

What does GIP stimulate the release of and what does it inhibit?

A

Stimulates the release of insulin and inhibits gastrin (Enterogasrone)

26
Q

What are PROGLUCAGON-DERIVED PEPTIDES (GLPGLUCAGON-LIKE PEPTIDES) released from and what stimulates their release?

A

L cells

oral ingestion of Carbohydrates or fats

27
Q

What do PROGLUCAGON-DERIVED PEPTIDES (GLPGLUCAGON-LIKE PEPTIDES) do in relation to insulin and glucagon?

A

Secretion, thus called an incretin hormone
- Suppresses glucagon secretion

28
Q

What do PROGLUCAGON-DERIVED PEPTIDES (GLP GLUCAGON-LIKE PEPTIDES) do in relation to gastric emptying, food aptite, and beta cell profilation?

A

Slows gastric emptying
- Reducesfood intake via the reduction of appetite
- Promotes beta cell proliferation.

29
Q

How does GLP help pateints with Type 2 diabetes?

A

In patients with type 2 diabetes mellitus (T2DM), GLP-1 concentrations are
decreased in response to an oral glucose load. Clinical data have demonstrated
that GLP-1 receptor agonists therapies help restore insulin secretory functions, thus improving glycemic control and reducing body weight in patients with T2DM

30
Q

What is the structure of molitin?

A

Linear 22 AA polypeptide - unrelated to other hormones

31
Q

What is molitin released from and what stimualtes its release?

A

Released from M cells

Fasting stimulates it and it is released in 100 min intervals

  • Release is under neural control (acid and fat can also
  • cause small amounts to be released)
32
Q

What does motilin to in relation to motility?

A

Stimulates upper GI motility

Accounts for the migrating motility complexes

33
Q

Where is somatostatin found and what stimulates its release?

A

Found in gastric/duodenal mucosa and pancreas
- Release—stimulated by acid, inhibited by Ach

34
Q

What does somatostatin inhibit?

A

Inhibits release of all gut hormones
- Directly inhibits parietal cell acid secretion
- Mediates acid-induced inhibition of gastrin release

35
Q

What stimulates the release of histamine?

A

Gastrin and Ach cause release from cellsin the stomach

36
Q

What does histamine stimulate?

A

The release of gastric acid

37
Q

What are examples of histamine (H2) receptor blockers and what do they do?

A
    • Cimetidine (Tagamet), Ranitidine (Zantac)

Decrease the release of acid

38
Q

What is the location of the neurocrines: VIP, GRP, Enkephalins?

A

P2 hormones (4 decks)

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