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Physiology > endocrine 6 - pancreas > Flashcards

endocrine 6 - pancreas Flashcards

1
Q

is the pancreas exo or endo crine

A

both

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2
Q

what do alpha cells release

A

glucagon

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3
Q

what do beta cells release

A

insulin and amylin

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4
Q

what do delta cells release

A

somatostatin

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5
Q

what does amylin do

A

give satisfaction after eating

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6
Q

which cells secrete amylin

A

beta

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7
Q

which cells secrete glucagon

A

alpha

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8
Q

which cells secrete insulin

A

beta

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9
Q

what % of islet cells are alpha

A

15-20%

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10
Q

what % of islet cells are beta

A

55-90%

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11
Q

what % of islet cells are delta

A

3-10%

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12
Q

which hormone is the hormone of feasting

A

insulin

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13
Q

which hormone is the hormone of fasting

A

glucagon

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14
Q

what does insulin do

A

increase uptake and storage of fuels

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15
Q

is insulin cata or ana bolic

A

anabolic

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16
Q

what does glucagon do

A

increases mobilization of fuels when needed

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17
Q

is glucagon cata or ana bolic

A

catabolic

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18
Q

what is the absorptive phase

A

the 4 hours it takes to have food finish stomach digesting after a meal, slowly switches to insulin

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19
Q

what is the predominant hormone after post absorptive phase

A

glucagon

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20
Q

what is the predominant hormone at the start of the absorptive phase

A

insulin

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21
Q

what are 4 catabolic hormones that counter insulin

A

glucagon
Epinephrine
cortisol
growth hormone

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22
Q

which is the only hormone that can promote the stoerage of the major body fuels

A

insulin

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23
Q

what are the roles of the 4 counter regulatory hormones

A 
maintain energy metabolism and cell function
(glucagon
Epinephrine
cortisol
growth hormone)
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24
Q

why are kids with juvenile diabetes so skinny

A

no insulin to store fuels, its all glucagon breaking it down

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25
Q

where does insulin store fuels (3)

A

liver/ hepatocytes
adipose tissue
skeletal muscle

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26
Q

which transporter lets glucose into adipose tissue

A

Glut-4

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27
Q

what does insulin do to glucose in the liver and muscle

A

turn in into glycogen

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28
Q

what does glucose do to amino acids in the liver and muscle

A

turn into proteins

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29
Q

what does insulin do to fatty acids in the liver andadipose tissue

A

turn into triglycerides

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30
Q

what does insulin do to glycogensis

A

increase

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31
Q

what does insulin do to glycogenolysis

A

decrease

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32
Q

what does insulin do to glycolysis

A

increase (so it can become insulin, and also decreasing [glucose] allows more into the cell)

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33
Q

what does insulin do to gluconeogensis

A

decrease

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34
Q

what does insulin do to ketogenesis

A

decrease

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35
Q

what does insulin do to protein and fat breakdown

A

decrease

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36
Q

what kind of hormone is insulin

A

peptide hormone

37
Q

what kind of receptor does insulin bind to

A

receptor tyrosine kinase

no g proteins

38
Q

what is the only insulin sensitive transporter

39
Q

what kind of transport is involved with GLUT 4

A

facilitated transport

40
Q

how is Glu transported into cell

A

uphill Na dependent by SGLTs (symport)

41
Q

how is Glu transported out of cell

A

facilitated Na independent transport (GLUTs)

42
Q

how does insulin affect GLUT4

A

insulin activates transport proteins which move GLUT4 to cell membrane

43
Q

how does exersize affect GLUT4

A

exercise activates transport proteins which move GLUT4 to cell membrane

44
Q

where does glucose come from short term

A

readily available in blood immediately after a meal (absorptive phase, 2-3 hours most active)

45
Q

where does glucose come from long term

A

glycogenolysis in the liver (post absorptive phase)

46
Q

where does glucose come from super long term

A

gluconeogensis from non-carb sources, such as fatty acids or amino acids

47
Q

how is the liver affected by feasting

A

glucose stored as glycogen
acetyl-coa for fatty acid synthesis
amino acids used for protein synthesis

48
Q

how is the adipose tissue affected by feasting

A

triglyceride synthesis

49
Q

how is the muscle affected by feasting

A

amino acids used for protein synthesis

glucose stored as glycogen

50
Q

what happens during insulin deficiency

A

increase gluconeogensis, fat breakdown and muscle breakdown

Catabolic state

51
Q

what happens to GLUT4 during during insulin deficiency

A

glucose uptake into fat and muscle is impaired as 90% of GLUT4 transporters are stuck in vesicles

52
Q

what is the primary goal of glucagon

A

defend against hypoglycemia

53
Q

what is the primary target of glucagon

54
Q

what does glucagon do in the liver

A

promotes breakdown of glycogen and increases glucose using lipolysis

55
Q

how is the adipose tissue affected by fasting

56
Q

how is the liver affected by fasting

A

glucogen breakdown
gluconeogensis (use aa)
glycerol-glucose FFa-ketones

57
Q

how is the muscle affected by fasting

A

glucogen breakdown
fatty acids used for energy
protein catabolism

58
Q

what is the dominant hormone during fasting

59
Q

what does insulin do to blood glucose

60
Q

what does glucagon do to blood glucose

61
Q

what does insulin do to lipolysis

62
Q

what does glucagon do to glycolysis

63
Q

what does glucagon do to glycgluconeogenesis

64
Q

is insulin secretion raised by sympathetic or parasympathetic activity

A

parasympathetic (sym. inhibits)

65
Q

what happens to insulin secretion with high levels of plasma amino acids

66
Q

what is hypoglycemia

A

reduction of blood glucose level

67
Q

what happens when the brain lacks glucose (2 bio ways to fix)

A

increase sympathetic activity, increased production of counter regulatory hormones (glucagon)

68
Q

what causes diabetes mellitus

A

too little insulin

69
Q

what level of insulin creates hyperglycemia

A

too little insulin

70
Q

what level of insulin creates ketoacidosis

A

too little insulin

71
Q

what causes type 1 diabetes mellitus

A

beta cells are destroyed, no insulin made (autoimmune)

72
Q

what causes type 2 diabetes mellitus

A

increased resistance to insulin

73
Q

what is diabetic ketoacidosis caused by

A

insulin deficiency leading to a catabolic state, hyperglycemia, acidosis and ketogenesid

74
Q

what happens when your body breaks down fat

A

ketones are released which makes the blood acidic

75
Q

what happens to insulin in diabetic ketoacidoses

76
Q

what happens to counter regulatory hormones (glucagon, NE/E, cortisol, GH) in diabetic ketoacidoses

A

increase (catabolic)

77
Q

why do you get acetone breath in diabetic ketoacidosis

A

because fat breakdown makes ketones

78
Q

why do you get excess urine in diabetic ketoacidosis

A

high blood glucose makes high urine volume to try to get rid of it

79
Q

why do you get thirsty in diabetic ketoacidosis

A

cause you losing lots of urine trying to get rid of the glucose in blood

80
Q

why do you get hungry in diabetic ketoacidosis

A

no glucose transport into cells

81
Q

why are counter regulatory hormones increased in ketoacidosis

A

no glucose can be used because no insulin, so the body needs to break down fat (these hormones help with this catabolism)

82
Q

what is polyuria

A

increase in urine volume and frequency in urination

83
Q

what is glucosuria

A

glucose in urine

84
Q

what is polyphagia

A

increased hunger

85
Q

what is polydipsia

A

increased thirst

86
Q

what are some chronic complications of diabetes mellitus

A

blindness, renal failure, atherosclerosis, changes in sensation, poor wound healing

87
Q

what are 3 treatments for type 1 diabetes mellitus

A

administration of insulin, islet cell transplant, gene therapy

88
Q

what are 3 treatments for type 2 diabetes mellitus

A

dietary control/ exercise
drugs which increase insulin secretion/ response to insulin
insulin administration

89
Q

how can amylin analogs help with type 1 diabetes mellitus

A

help reduce extreme hunger

Physiology (32 decks)

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