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Physiology II > Endocrine Physiology I > Flashcards

Endocrine Physiology I Flashcards

Insulin, Glucagon, and Diabetes/Hypothalamic-Pituitary Axis

1
Q

What are the two functions of the pancreatic cells?

A
  1. Make enzymes
  2. Make hormones (Endocrine)
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2
Q

What are the main function of Acini (cluster of cells)?

A

Make enzymes that dump into the duodenum via pancreatic duct

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3
Q

Where are the majority of hormones created in the pancreatic cells?

A

Islet of Langerhans
-Glucagon, insulin, and somatostatin

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4
Q

In the pancreas, what do alpha cells (20%) make?

A

Glucagon

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5
Q

In the pancreas, what do beta cells (70%) make?

A

Insulin

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6
Q

In the pancreas, what do δ cells (10%) make?

A

Somatostatin

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7
Q

What is the function of somatostatin?

A

Inhibits Insulin, Glucagon and GH

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8
Q

What is the normal range of glucose (mg/dl)?

A

~80-100 mg/dL

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9
Q

How does insulin and glucagon balance each other?

A
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10
Q

What effect does amino acids have on glucagon and insulin?

A

Same, slightly positive effect

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11
Q

What has the greatest effect on the release of insulin?

A

Hyperglycemia

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12
Q

What has the second greatest effect on insulin release?

A

Incretins (GIP/GLP)

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13
Q

What has a moderate postive effect on insulin release? (2)

A

Glucagon, Sulfonylurea drugs

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14
Q

What has an inhibitory effect on insulin? (3)

A

NE/Epi & Cortisol, Somatostatin, Fasting/excersize

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15
Q

What has the greatest effect of the release of glucagon? (1)

A

Hypoglycemia

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16
Q

What has a moderate positive effect on the release of glucagon? (3)

A

Amino acids, NE/Epi & Cortisol, Excersize/fasting

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17
Q

What has a moderete negative effect on the release of glucagon? (3)

A

Incretins (GIP/GLP), Insulin, Somatostatin

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18
Q

What do sulfonylurea drugs do? (3)

A

They stimulate insulin release

  • Treat T2D
  • Block B-Cell KATP
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19
Q

B-Cells release what? (2)

A

Insulin and C-peptide (Connecting-peptide)

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20
Q

What do incretins do?

A

Incretins stimulate the B-cells and inhibit the alpha cells to increase insulin and lower glucagon.

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21
Q

What does the enzyme dipeptidyl pedptidase-4 (DPP4) do?

A

Inactivate GLP-1 and GIP

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22
Q

What do antagonists of DPP-4 do?

A

Antagonists of DPP-4 improve endogenous insulin secretion!

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23
Q

Is insulin release higher when glucose is given orally or through IV?

A

Orally

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24
Q

What function does insulin have on glucose and AA uptake in skeletal muscle?

A

Anabolic

  • Increases glucose and AA uptake in skeletal muscle
  • Supresses hepatic glucose production
  • Inhibits lipolysis​
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25
Q

What effect does glucagon have in liver, adipocytes and skeletal muscle? (4)

A

Catabolic

  • Increases hepatic glycogenolysis
  • Increeases hepatic gluconeogenesis
  • Increases hepatic ketone formation
  • Stimulates lipolysis
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26
Q

What is the largest storage site of glucose, and the tissue responsible for T2D?

A

Skeletal muscle

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27
Q

What receptor does insulin act on in myocytes/adipocytes?

A

GLUT4

28
Q

What pathway mediates most of insulin’s metabolic effects? The phosphorylation of what proteins mediates this pathway?

A

Akt pathway

IRS-1, Akt, PKCz, AS160

29
Q

What is insulitis?

A
30
Q

What is the cause of type 1 diabetes?

A

Loss of beta cells by autoimmune destruction, usually genetic and triggered from environmental factors. This ultimately leads to low insulin levels and decreased glucose uptake that leads to hyperglycemia

31
Q

In T1D, as beta cell mass decreases, what happens to insulin release over time?

A
32
Q

What leads to the development of type 2 diabetes (T2D)?

A

Insulin resistance from inactivity and genetics precedes obesity.
Obesity leads to B-cell hyperplasia where glucose is normal and insulin is elevated.
In early B-cell fatigue, glucose and insulin are elevated.
In late B-cell failure, glucose is elevated and insulin is decreased.

33
Q

What causes insulin resistance?

A

Excess glucose intake leads to oxidative stress where a JNK protein phosphorylates a serine residue on IRS-1, inactivating the Akt pathway that normally brings GLUT4 receptors to the membrane to uptake glucose

34
Q

If you wanted to transport glucose at the same rate of an insulin sensitive person, and you were insulin resistant how would you achieve normoglycemia?

A

You would have to produce more insulin, which is what happens in early stages of type 2 diabetes

35
Q

What effect does T2D’s have on endogenous glucose production and glucose disposal rate? (2)

A
36
Q

Preoperative elevated HBA1C is a predictor of what?

A
37
Q

What clinical implications does diabetes have regarding anesthesic management?

A
38
Q

Low insulin/glucagon can lead too? (Primarily in T1D)

A

Ketogenesis, elevated sugar, dehydration, and coma

39
Q

What is the best clinical indicator that a patient has insulin resistance?

A

Obesity

40
Q

High fructose corn syrup ultimately leads to increase of?

A

VLDL

41
Q

What functions as a glucose sensor in the process of insulin release?

A

Pancreatic B-cell

42
Q

The IRS-PI3K pathway is essential for glucose uptake by ________ and _________?

A

insulin and exercise

43
Q

What are the principle metabolic effects of insulin? (3)

A
  1. Increase glucose utilization in skeletal muscle
  2. Supress hepatic glucose production
  3. Inhibit lipolysis
44
Q

What do incretins do?

A

Amplify glucose-induced insulin release

45
Q

How does glucagon antagonize insulin’s effects?

A

Stimulating hepatic glucose release

46
Q

What does a disruption in the balance of insulin and glucagon lead too? (2)

A
  1. Ketogenesis
  2. Hyperosmolar coma
47
Q

T or F. Your body metabolizes fructose much differently than glucose?

A

True

48
Q

What is the main function of the hypothalamus?

A
49
Q

What is the main function of the pituitary?

A
50
Q

Where are the magnocellular neurons located in the pituitary? What are there function?

A

Posterior

Produces OT, AVP and stores

51
Q

Where are the parvicellular neurons stored? What are their function?

A

Anterior

Produces releasing/inhibiting hormones

52
Q

What are the neurohormones (releasing hormones)?

A
53
Q

What are the tropic hormones?

A
54
Q

What are the non-tropic hormones?

A
55
Q

How is GH (Somatotropin) release regulated?

A
56
Q

What are the normal biological actions of GH-IGF-1?

A

Decrease glucose uptake
Increase lipolysis
Increase hepatic gluconeogenesis
Decrease skeletal muscle glucose uptake
Increase lean body mass
Increase organ size
Increase linear growth

57
Q

Why is GH release pulsatile, rather than sustained?

A
58
Q

Why is GH surge at night significant?

A

Growth and repair during rest

59
Q

What effect would a high carbohydrate meal before bed have?

A
60
Q

How does thyroid hormone, growth hormone, androgens and estrogens vary over time in a normal person?

A
61
Q

What are the net effects of GH/IGF-1 on growth?

A
62
Q

What disease is GH overexpression before puberty?

A
63
Q

What disease is GH deficiency before puberty?

A
64
Q

What is achondroplasia?

A

Mutation in gene 3 (FGFR3); not related to GH

65
Q

What is acromegaly?

A

GH overexpression that starts at puberty and sustains through adulthood

66
Q

What is Laron’s syndrome?

A

GHR insensitivity; no IGF1

Physiology II (10 decks)

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