Brainscape's Knowledge GenomeTM

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


See full index

FHB Endocrinology > L76: Pancreas > Flashcards

L76: Pancreas Flashcards

1
Q

Describe the sequence of ducts with the gall bladder, liver, and pancreas

A

Cystic duct + common hepatic duct -> common bile duct +pancreatic duct -> greater duodenal papill-> duodenum

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

What is the the exocrine pancreas?

A

Makes up majority of cells in the pancreas

Acinar cells: secrete digestive enzymes into pancreatic duct

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

What is the endocrine pancreas?

A

3 major cell types making up islets of langerhans (alpha, beta, delta)

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

What do the ductal cells in the exocrine pancreas do?

A

secretes mucous and bicarb to the pancreatic enzyme mixture from acinar cells

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

What which cells of the endocrine pancreas regulate glucose metabolism?

A

Alpha: glucagon
Beta: inuslin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What do the PP and delta cells do?

A

produced pancreatic polypeptide and somatostatin

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

What does pancreatic polypeptide do?

A

Inhibit acinar cells via paracrine action

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

What do epsilon cells secrete?

A

ghrelin

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

How is the blood flow arranged in the endocrine pancreas?

A

Blood flow is from arteriole into center of islet outward to the venule

Insulin rich blood flows from the center into the periphery of the islet

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

How are beta and alpha cells organized in the islets?

A

Beta cells clustered in core -> alpha cells surround beta cells in a sandwich formation -> allows paracrine effects between them

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

What does insulin do?

A

Anabolic hormone: energy storage

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

What does glucagon do?

A

Catabolic: energy mobilization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the minor hormones in the pancreas?

A

Somatostatin
Amylin
Pancreatic polypeptide
Ghrelin (hunger hormone)

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

How i insulin synthesized?

A

Insulin+ C peptide released together as proinsulin -> cleavage of C peptide exposes end of insulin chain to interact wiht receptor

Insuline and C peptide are packaged together in storage vesicles

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

Why is the C peptide important for insulin biosynthesis?

A

C peptide is critical for proper folding and formaiton of disulfide bonds between the alpha and beta chain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How can C peptide be used clinically?

A

Can indicate pancreatic function status due to long half life (35 mins) compared to insulin (3-8 minutes)

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

How is insulin released from the pancreatic beta cell?

A

Glucose outside of the beta cell transported in by GLUT-2 (only when glucose is HIGH) -> glucose phosphorylated by glucokinase (glucose sensor) -> G6P-> increased ATP via glucose metabolism -> closes K+ channels w/ SUR subunits -> cell depolarizes -> open Ca2+ channels -> vesicle exocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What do sulfonylurea drugs do?

A

Closes K+ channels to cause depolarization of the cell -> and thus cause insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do FFAs and amino acids modulate insulin release from beta cells?

A

Increase ATP levels via oxidation and thus close K+ channels

20
Q

What do incretins (GLP-1) do?

A

potentiate insulin released

STILL NEEDS GLUCOSE

21
Q

How do catecholeamines affect insulin release?

A

Inhibit it

22
Q

In what behavior is insulin released in response to glucose?

A

Biphasic:
5% of vesicles available for immediate release at membrane
95% stored or newly synthesized insulin

Initial spike-> followed by gradual increase in 2nd phase

23
Q

What kind of receptors does insulin bind?

A

Membrane receptor tyrosine kinases at hte alpha subunit

24
Q

What does insulin binding to its receptor do?

A

Binds at alpha subunit on EC space -> autophosphorylation of intracellular beta subunit (tyrosine kinase domains)

25
Q

What are insulin’s actions on muscle cell?

A

Glucose cannot enter cell without insulin
Insulin binds- > autophosphorylation of receptors -> recruit IRSs -> activate intracellular signaling cascades -> promote GLUT-4 insertion into membrane -> allows glucose to enter cell

26
Q

What is IRS(insulin receptor substrate)?

A

Scaffolding protein that recruits intracellular signaling components like PI3K and MAPK

27
Q

Which GLUT transporters are insulin dependent?

A

GLUT-4 (Skeletal muscle, fat)

28
Q

Which GLUT transporters are insuin INdependent?

A

GLUT-1(brain, vasculature, erythrocytes, skeletal msucle, fat, heart)
GLUT-2(Pancreatic beta cells, liver, intestine, kidney)
GLUT-3(neurons)

29
Q

What effects does insulin have on the liver?

A

promote glycogen and TG produciton

REduce glucose produciton/output

30
Q

What effect does insulin have on muscle?

A

promote glycogen and TG production, and protein synthesis

31
Q

What effect does insulin have on fat?

A

Promote TG production, release FFAs from chylomicrons, glycolysis, inhibit lipolysis

32
Q

How is glucagon synthesized and processed?

A

Preproglucagon (SP-GRPP-GLUC-GLP-1-GLP-2)

Pancreatic Alpha Cells: GRPP cleaved from Glucagon -> secreted as inactive peptide -> GLP-1 and GLP-2 remain linked(inactive) => GRPP(inactive) + GLUC + GLP-1/GLP-2(inative)

Intestinal L Cells: GRPP linked to glucagon (glicentin) -> inactive -> GLP-1 and GLP-2 cleaved -> active INCRETINS
=> Glicentin + GLP-1 + GLP-2

33
Q

What do incretins do?

A

Potentiate insulin release from pancreatic beta cells

Stimulated by carbohydrates in intestines

34
Q

What is the stimulus for glucagon release?

A

low blood glucose
Amino acidss (protein meal)
Catecholeamines/Exercise

35
Q

Does glucagon exhibit biphasic release like insulin?

A

NO

Glucagon levels fall at a constant rate

36
Q

How do insulin and glucagon work together?

A

Insulin: dephosphorylate kinase activity enzyme-> phosphorylation activity -> promotes glycolysis

Glucagon: phosphorylates phosphatase activity enzyme-> desphosphorylation activity -> promote gluconeogenesis

37
Q

What are the main targets of glucagon?

A

Liver and Adipose: promote energy mobilization

Opposite of insulin

38
Q

Where are somatostatins produced and what stimulates their release?

A

Delta Cells
Stimulated by high fat, high carb diets
Inhibited by insulin

39
Q

What does somatostatin do?

A

Inhibit insulin released

Can be used clinically to manage insulin producing tumors

40
Q

What does Amylin do?

A

Released with insulin from beta cell vesicles and works synergistically with insulin

41
Q

What causes an increase in amylin?

A

Obesity, HTN

42
Q

What does amyloid formation lead to in the pancreas?

A

beta cell destruction

43
Q

Where is Ghrelin produced?

A

Stomach (most)

Epsilon cells in islet

44
Q

What does Ghreln do/?

A

Stimulate food intake at hypothalamus
Stimulate GH release
Inhibit insulin release from beta cells by activating K+ channels and decreasing intracellular calcium release

45
Q

How is ghrelin related to obesity?

A

Inversely related: obesity -> lower ghrelin

46
Q

What are counter regulatory hormones to insulin?

A

Glucagon: primary
GH + Cortisol: promote gluconeogenesis and lipolysis
Catecholeamines: increased with exercise and stress; stimulates glucagon release and inhibit insulin release

47
Q

How are insulin and GH related?

A

Absent insulin + GH increased -> cannot stimulate hepatic IGF-1 => direct GH effects on glucose mobilizaiton but no cellular proliferation effects of IGF-1

Also get no neg feedback to GH (NO IGF-1)

FHB Endocrinology (10 decks)

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