Pancreas: Histo and Phys (Nutting) Flashcards

1
Q

What islet cells secrete insulin?

A

beta

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2
Q

What islet cells secrete glucagon?

A

alpha

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3
Q

What islet cells secrete somatostatin?

A

delta

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4
Q

What islet cells secrete peptide polypeptide?

A

F cells

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5
Q

inhibits both glucagon and insulin

A

somatostatin

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6
Q

describe the cellular organization in an islet

A

roughly~ alpha cells on outside with beta cells in middle and delta cells in-between beta cells

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7
Q

proinsulin → insulin + _____

A

C-peptide

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8
Q

Islets are separated from the ______ by a fine fibrous capsule that extends into the islet together with blood vessels

A

exocrine cells

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9
Q

round oval islets vs trabecular, irregular in shape islets

A

beta cell rich are rounder

pancreatic peptide rich are irregular

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10
Q

What part of the pancreas are the trabecular, irregular islets that secrete PP found?

A

posterior part of the pancreatic head

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11
Q

contains secretory acini

A

exocrine cells of pancreas

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12
Q

picks up exocrine secretions, to the islet secretions bc they go to capillaries

A

duct of the exocrine pancreas

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13
Q

____ cells occupy 65-70% of the islet volume!

A

beta

**take away is that beta&raquo_space; alpha volume

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14
Q

function of pancreatic polypeptide

A

self regulates the pancreas secretory activities (endocrine and exocrine)
affects hepatic glycogen levels and GI secretions
**DJ talked about it as being *anorexigenic and ↑ conc after a meal

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15
Q

What decreases PP secretion?

A

somatostatin and IV glc

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16
Q

What increases PP secretion?

A

eating protein meal
fasting
exercise
acute hypoglygemia

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17
Q

describe the structure of proinsulin moleucle

A

a chain and B chain attached via 2 disulfide bonds with C peptide between them

at 2 locations, there are a pair of basic aa that are cleaved to release C-peptide and insulin

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18
Q

Pro insulin is converted into the mature hormone by the combined action of …
Where in the cell does this occur?

A

two endoproteases and a carboxypeptidase E

Secretory vesicles

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19
Q

Why is C-peptide used to measure islet function in pts treated with exogenous insulin?

A

cannot measure insulin bc you do not know how much the pt has made and how much is exogenous. Tells you how many islet cells may be left/have residual function

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20
Q

Describe the process of insulin synthesis

A
  1. signal peptide translocates translated protein into the ER
  2. folding and oxidation (and signal seq cleavege) in ER
  3. ER → golgi → vesicle
  4. in vesicle, proteases cleave/liberate C peptide
  5. carboxypeptidase E produces mature insulin
21
Q

Stimuli for increased and decreased insulin secretion:

A
Inc secretion:
↑ plasma glc
↑ plasma aa
↑ FA, ketones
↑ inc GI hormones, mainly GIP, GLPs)
↑ GH
↑ Cortisol 
↑ Ach (parasympathetics)
↑ glucagon 
*GGGG AAFC

Decreased secration:
↑ Epi, NE (sympathetics)
↑ somatostatin

22
Q

Stimuli for increased and decreased glucagon secretion:

A
Increased secretion:
↑ plasma aa
↑ Ach
↑ epi, NE (sympathetics)
↑ VIP
↑ CCK
*VAACS 
Decreased section:
↑ plasma glc
↑ insulin 
↑ somatastatin
↑ FFA, ketones
*FIGS
23
Q

Why does an ↑ in plasma aa signal glucagon to be released?

A

to prevent sudden hypoglycemia if you eat a high protein meal without carbs

24
Q

where is insulin degraded?

A

liver and kidneys by insulinases

25
Q

Where is glucagon degraded?

A

liver

26
Q

Where in the body does insulin exert the majority of its action?

A

liver, that is where it goes first
muscle
adipose

27
Q

Where in the body does glucagon exert the majority of its action?

A

liver, that is where it goes first and it is then degraded there ∴ periphery has very low [glucagon]

28
Q

what additional action will glucagon have at high conc?

A

lipolytic

→ takes high conc to get to periph to have this effect, usually it is localized to the liver bc it is degraded there

29
Q

how do PERIPHERAL glucagon levels change in response to a meal?

A

peripherally it does NOT change (and is LOW)

levels fluctuate in pancreas in response to food

30
Q

What does insulin stimulate in many tissues?

A

glc uptake and utilization

31
Q

How is glc “utilized” in cells?

A
  • make ATP
  • make glycogen
  • make TAG
32
Q

in what cells/tissue will insulin NOT stimulate glc uptake

A

brain (*except part of hypothalamus)
intestinal mucosa
RBCs
Kidney tubules

33
Q

What is the only part of the brain that insulin will stimulate glc uptake?

A

hypothalamus

34
Q

speed and duration of action of glucagon vs insulin

A

both act fast and decrease in conc quickly after action

35
Q

glucagon complements the effects of what substances? WHY?

A

Epi and NE bc is is best to not be hypoglycemic, we need energy! ∴ they can substitute for each other = redundancy!!

36
Q

how does glucagon maintain normal glc conc

A

promotes glc release from the liver

37
Q

what effects does glucagon have on the liver?

A

↑ glycogenolysis
↑ aa uptake → gluconeogenesis
↑ ketoneogenesis (TAG → KB for energy)

38
Q

What is needed for glucagon to be synthesized in the liver

A

corstiol

39
Q

What enzymes does glucagon effect?

A
↑cAMP and PKA to..
↑ phosphorylase → glycogenolysis 
↓ glycogen synthase
↓ F-2,6,6-BP  = ↑gluconeogenesis and ↓glycolysis
↓ PK activity to ↓pyruvate/AcCosA→TAG
40
Q

____ is the most potent hormone

A

insulin

41
Q

insulin is anabolic or catabolic hormone?

A

anabolic (and anti-catabolic)
*promotes synthesis of storage forms and inhibits breakdown from these stores

= Stimulates building up while inhibiting breakdown!

42
Q

What effects does insulin have in muscle?

A

↑ glc uptake
↑ aa uptake
↑ LPL synthesis (extracts FA from VLDL and CMs for energy)

↓ protein breakdown and aa release
(↑ protein synthesis, may or may not)

43
Q

What effects does insulin have in adipose?

A

↑ glc uptake
↑↑↑ TAG synthesis
↑ FA synthesis (glc → pyruvate→ AcCoA → malonylCoA →LCFA)
↑ LPL activity

↓↓↓ lipolysis

44
Q

What effects does insulin have in liver?

A

↑ TAG synthesis
↑ protein synthesis

↓ VLDL and apoB synthesis
↓ glc release
↓ ketogenesis

45
Q

insuilin ↑ or ↓ activity of hormone sensitive lipase

A

46
Q

What effect will high levels of GH and cortisol have on muscle and fat cells (in terms of insulin activity)

A

they become insulin resistant

47
Q

what increases the sensitivity of the body to hyperglyemia

A

GH, cortisol, and T3 → insulin more readily released

48
Q

In terms of biochem mechs, how does insulin increase glc uptake by muscle and adipose?

A

insulin binds receptor and stimulates translocation of glc transporter proteins from vesicles to surface of PM