12: Endocrine Pancreas Flashcards

1
Q

Three types of innervation to the endocrine pancreas

A

Adrengergic, cholinergic, peptidergic

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2
Q

Three ways cells in the islets communicate

A
  1. Ion concentrations
  2. Gap junctions between a’s and B’s
  3. Blood supply
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3
Q

How does blood flow through the islets

A

Center receives blood first -> insulin released into blood flows by a and D cells so they can sense how much insulin is in blood

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4
Q

C peptide secretion and function

A

Secreted equally with insulin - used as an endogenous insulin secretion marker

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5
Q

Biphasic release of insulin

A

initial spike within minutes + further increase half hour to an hour later

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6
Q

Exercise on blood sugar

A

Muscle contraction activates AMPK -> causes GLUT4 translocation so more glucose can enter cells

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7
Q

Insulin actions on skeletal muscle

A

Increases: glucose uptake, glycogen synthesis, glycolysis, protein synthesis
Decreases: protein breakdown

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8
Q

Insulin actions on liver cells

A

Increases: glycogen synthesis, glycolysis, hexose monophosphate shunt, pyruvate oxidation, lipid storage, protein synthesis
Decreases: gluconeogenesis, lipid oxidation, protein breakdown

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9
Q

Insulin actions on adipose cells

A

Increases: glucose uptake, glycolysis, uptake of FAs
Decreases: lipolysis

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10
Q

Insulin major effect on cells in general

A

Increase K uptake -> decreases K in ECM

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11
Q

What three metabolic processes does glucagon increase

A

Gluconeogenesis, lipolysis, glycogenolysis

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12
Q

Glucagon and insulin actions on one another

A

Glucagon inhibted by insulin, but glucagon stimulates insulin release

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13
Q

How many cases of DM2 have insulin resistance?

A

95%

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14
Q

Incretin effect

A

normal spike of insulin in healthy patients due to GI hormone release - over time, pts with insulin resistance lose normal incretin effect

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15
Q

Environmental risks for DM 2

A

caloric excess, sedentary, maternal disease and nutrition, rapid post-natal growth, sleep debt, endocrine disrupters, chronic inflammation

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16
Q

What happens when adipose tissue is inflamed in terms of insulin resistance?

A

Recruits M1 macrophages -> release of inflammatory markers (IL-6, TNFa, IFN-y) -> disruption of adipokines + release of FA’s

17
Q

Three types of medications for DM2 treatment

A
  1. Insulin sensitizers
  2. Sulfonylurea receptors
  3. Insulin secretagogues
18
Q

Two types of insulin sensitizers

A

Biguanide drugs (metformin), TZDs

19
Q

What are sulfonylurea receptors associated with?

A

ATP-dependent K channels

20
Q

What causes DM 1?

A

T cell mediated destruction of B cells of pancreas -> inadequate insulin secretion

21
Q

When do sx start to appear with DM 1?

A

When about 80% of B cells are destroyed

22
Q

What causes DKA?

A

Decreased utilization of ketoacids

23
Q

Three major symptoms that occ with DM 1

A

Hyperkalemia, osmotic diuresis, glucosuria

24
Q

What causes hyperkalemia in DM 1?

A

Lack of insulin effect on Na/K ATPase

25
Q

What causes osmotic diuresis and glucosuria in DM 1?

A

Increased blood glucose increases filtered load of glucose, exceed reabsorption capacity of proximal tubule + water and electrolyte reabsorption is blunted

26
Q

What does polyuria cause in DM 1?

A

Increased excretion of Na and K even though urine concentration of electrolytes is relatively low

27
Q

Two major alleles associated with DM 1

A

HLA DQ2 and DQ8

28
Q

Environmental factors with DM 1

A

early exposure to cows milk, vitamin D deficiency, gluten intolerance, childhood infections, obesity

29
Q

Treatment for DM 1

A

Timing insulin doses to meal consumption to mimic physiological response