Endocrine Pancreas And Parathyroid Flashcards

1
Q

What is the pancreas an organ of

A

The GI system

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2
Q

What kind of functions do the pancreas have

A

Endocrine and exocrine

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3
Q

What are the endocrine functions of the pancreas

A

Releases hormones involved in blood sugar homeostasis

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4
Q

What are the exocrine functions of the pancreas

A

Releases digestive juices into the small intestine

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5
Q

What are the pancreas cells grouped in

A

Endocrine pancreas cells are in tight groups called islets of langerhans

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6
Q

What are in the islets of langerhans

A

Many different cells release various hormones

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7
Q

What is insulin released by

A

Beta cells

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8
Q

What is glucagon released by

A

A cells

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9
Q

What is somatostatin released by

A

Delta cells

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10
Q

What is pancreatic peptide released by

A

F cells

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11
Q

What is grehlin released from

A

Epsilon cells

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12
Q

What are the different hormones released by the pancreas

A
  • insulin
  • glucagon
  • somatostatin
  • pancreatic polypeptide
  • grehlin
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13
Q

How do the cells of the endocrine pancreas communicate

A

Gap junctions

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14
Q

Type 1 diabetes is an autoimmune disease where the pancreas cannot make insulin. Which type of cell is responsible for insulin production

A

Beta

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15
Q

What does insulin consist of

A

A chain, B chain, and C chain

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16
Q

What happens to insulin during production

A

C chain is removed

-secreted with insulin when its released

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17
Q

What’s a good way to tell the difference between type 1 and type II diabetes

A

C chain levels in the blood

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18
Q

What kind of diabetes would there be no C chain in the blood

A

Type 1

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19
Q

What kind of diabetes would there be high levels of C chains in the blood

A

Diabetes 2

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20
Q

Where is insulin degraded

A

By the liver

-the A and B chains are separated and excreted in the urine

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21
Q

When is insulin released

A

When blood glucose is high

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22
Q

What transports glucose into B cells

A

GLUT2

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23
Q

What happens to glucose when it is transported into the B cells

A

Oxidized to produce ATP

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24
Q

What does high levels of ATP levels during glucose being taken into the cell cause

A

ATP sensitive K+ channels to close, and less K leaving cell causes depolarization, which opens Ca2+ channels

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25
Q

What does the opening of the Ca channels do when the K channels close after glucose being brought into the cell

A

Ca2+ causes exocytosis of insulin into the bloodstream

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26
Q

How does insulin signal through

A

A receptor tyrosine kinase mechanism

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27
Q

What happens through the receptor tyrosine kinase mechanism for insulin

A
  • insulin binds receptor
  • receptors phosphorylate themselves and become active
  • phosphorylate other proteins inside the cell
  • other activated proteins affect cellualr function
  • receptor is then internalized and destroyed
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28
Q

What does insulin cause

A

Storage of excess energy

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29
Q

Insulin dependent glucose transporters

A

GLUT4

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30
Q

How does insulin decrease blood glucose

A
  • causes GLUT4 to be inserted in the cell membranes
  • glocuse is taken up by the cells and stored as glycogen
  • reduces gluconeogensis
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31
Q

How does insulin decrease blood fat levels

A
  • inhibits lipolysis

- reduces ketoacidosis production

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32
Q

How does inclusion decrease blood amino acid levels

A

Increases protein synthesis

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33
Q

Insulin and K+

A

Causes K+ to be taken up in the cells

-pulls K out of blood and into cells, increases K uptake into the cells

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34
Q

What could be a good treatment for hyperkalemia

A

Insulin

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35
Q

How does insulin affect the hypoathalamic satiety

A

Makes you feel less hungry

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36
Q

Action of insulin

A
  • increases glucose uptake into the cells
  • increases glycogen formation
  • decreases glycogenolysis
  • decreases gluconeogensis
  • increases protein synthesis (anabolic)
  • increases fat deposition
  • decreases lipolysis
  • increases K+ uptake into cells
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37
Q

What is the effect of insulin on blood levels

A
  • decreased blood glucose levels
  • decreases AA cxn in blood
  • decreases FA cxn in blood
  • decreases ketoacidosis in blood
  • decreased K+ cxn in blood
38
Q

Uncontrolled blood glucose due to loss of insulin production or function

A

Diabetes Mellitus

39
Q

Uncontrolled blood glucose due to loss insulin production

A

Insulin depend, Type 2, juvenile

40
Q

Uncontrolled blood glucose due to loss of insulin function

A

Non insulin dependent diabetes, type II, adult

41
Q

Type 1 diabetes or juvenile diabetes

A

Insulin dependent diabetes

42
Q

What is insulin dependent diabetes (type I, juvenile)

A
  • autoimmune destruction of B cells
  • no insulin produced
  • increases blood glucose, lipids, and proteins
  • muscle wasting
  • diabetic ketoacidosis due to utilization of fast as energy stores
  • diuresis, acidosis, and hyperkalemia
43
Q

Treatment for insulin dependent diabetes (type I or juvenile)

A

Lifelong insulin therapy

44
Q

What is non-insulin dependent diabetes (type II or adult)

A
  • loss of insulin sensitivity due to chronic high levels of blood glucose (insulin resistance)
  • make insulin, body does not respond to it
  • usually in older, obese, hypertensive individuals
  • retinal problems due to loss of autoregulation of blood flow
45
Q

Treatment for non-insulin dependent diabetes

A
  • lose weight, exercise

- metformin-increase number of insulin receptors

46
Q

What is insulin deficiency the same as

A

Glucagon excess

47
Q

Insulin excess

A

Hypoglycemia crisis

-can occur in diabetics if they over medicate

48
Q

Which of the following would be a consequence of acute hyperinsulinemia in a normal person

A

Hypokalemia

49
Q

What does glucagon function as

A

Opposing force to insulin

50
Q

What does glucagon promote

A

Mobilization and utilization of energy storage

51
Q

Glucagon storage

A

Stored until release is stimulated

52
Q

What stimulates the release of glucagon

A
  • Reduced blood sugar
  • meals rich in protein stimulate its release unless glucose is also ingested
  • prolonged fasting or exercise
53
Q

What inhibits glucagon stimulators factors of glucagon

A
  • fasting
  • decreased glucose concentration
  • increased AA cxn
  • cholecystokinin (CCK)
  • B-adrenergic agonists
  • acetylcholine
54
Q

Inhibitory factors of glucagon

A
  • insulin
  • somatostatin
  • increased FA and ketoacid cxn
55
Q

How does glucagon work

A

Acts through Gs (cAMP) receptor

  • increases blood glucose
  • increases gluconeogenesis
  • increases glyconeogenolysis
  • increases lipolysis
56
Q

Hyperglucagonmia

A
  • rare
  • too much glucagon
  • weight loss
  • high blood glucose
  • can result in T2 diabetes
  • necrolytic migratory erythema-dry crusty, cracked inflamed skin usually around the lips and face
57
Q

What is somatostatin produced by

A

Delta cells

58
Q

What is another name for somatostatin

A

Growth hormone inhibiting hormone

59
Q

What is somatostatin stimulated by

A

Ingestion of any food source

60
Q

What does somatostatin inhibit

A

Secretion of insulin and glucagon

61
Q

What does somatostatin do

A

Modulates response to ingested meal

62
Q

What produces pancreatic polypeptide

A

F cells

63
Q

What does pancreatic polypeptide do

A

Acts to regulate all pancreas functions

64
Q

When is pancreatic polypeptide increased

A

After a protein meal, fasting, exercise

65
Q

What decreases pancreatic polypeptide

A

Somatostatin

66
Q

What is ghrelin produced by

A

Epsilon cells

67
Q

This is the hunger hormone- released when staunch is empty, promotes feelings of hunger

A

Ghrelin

68
Q

What does ghrelin inhibit

A

Secretion of insulin

69
Q

What are the parathyroid glands

A

4 glands under the thyroid gland

70
Q

What hormone does the parathyroid release

A

PTH

71
Q

What is responsible for calcium homeostasis

A

PTH along with calcitonin and vitamin D

72
Q

What must happen to maintain normal calcium blood levels

A

Must balance ingested calcium with excretion to maintain normal calcium blood levels, necessary for bone and cell communication

73
Q

What hormones increase blood calcium levels

A

PTH and vit D

74
Q

What hormone reduces blood calcium levels

A

Calcitonin

75
Q

Where is PTH made and stored

A

Parathyroid

76
Q

When is PTH released

A

When free Ca levels are low

77
Q

What is most calcium bound to

A

Albumin, changing albumin and pH can change Ca2+ levels

78
Q

What does the PTH function on the kidney to do

A

Increase phosphate excretion (PCT) and calcium reabsorption (DCT)
-reduced blood phosphate levels allowing calcium to stay in solution

79
Q

What does PTH do ultimately

A

Dissolve bone and activated vit D to allow for better absorption of dietary calcium

80
Q

What causes hyperparathyroidism

A

Generally from parathyroid tumors

81
Q

Primary hyperparathyroidism

A
  • too much PTH
  • hypercalcemia
  • weakened bones
  • hypophosphatemia
82
Q

Secondary hyperparathyroidism

A
  • usually due to renal failure
  • vit D must be activated in kidney
  • hypocalcemia due to failed dietary absorption
  • weakened bones
83
Q

Hypoparathyroidism

A
  • usually due to thyroid removal
  • hypocalcemia
  • hypophosphatemia
84
Q

Released by the C cells of the thyroid

A

Calcitonin

85
Q

Between PTH, vit D, and calcitonin, which is not necessary for humans

A

Calcitonin

86
Q

What does calcitonin do

A
  • inhibits bone breakdown
  • increases phosphate excretion (PCT)
  • reduced Ca2+ reabsorption (DCT)
87
Q

What is necessary for calcium reabsorption form diet

A

Vit D

88
Q

Lack of vit D

A

Causes weak bones

-Rickets

89
Q

How do you produce active vit D

A

Need exposure to UV light and functioning kidneys

90
Q

What increases the production of vit D

A

PTH