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Physiology 2 test 1 > Chapter 78 > Flashcards

Chapter 78 Flashcards

1
Q

What two important hormones does the pancreas secrete?

A
  • insulin, Beta cell

- glucagon, alpha cell

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2
Q

What minor hormones does the pancreas secrete?

A
  • amylin: Beta cell
  • somatostatin
  • pancreatic polypeptide
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3
Q

What does somatostatin do?

A

inhibits insulin and glucagon

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4
Q

What does pancreatic polypeptide do?

A

inhibits pancreatic endocrines and exocrines

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5
Q

When is energy abundance hormone elevated? (insulin)

A

when energy is high

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6
Q

What does energy storage hormone increase? (insulin)

A

storage of energy

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7
Q

What do hypoglycemic hormone do? (insulin)

A

acts to reduce blood sugar

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8
Q

What is the dominant hormone in the regulation of blood sugar?

A

Insulin

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9
Q

How is insulin synthesized?

A

as a preprohormone after translation of insulin RNA by ribosomes in ER

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10
Q

How quickly is insulin cleared once its circulating in the blood?

A

10-15 ,

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11
Q

What is insulin degrade into to allow a rapid “turn off”?

A

insulinase

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12
Q

What is the result of a lack of C peptide?

A

Type 1 diabetes

  • neuropathy
  • CVD
  • promotes GFR
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13
Q

How does C peptide affect neuropathy?

A

C peptide promotes axonal repair. With a lack of c peptide axonal repair is impaired.

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14
Q

How does C peptide affect CVD?

A

C peptide promotes microvascular blood flow by stimulating Na+/K+ pump and the release of NO

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15
Q

Which disease is associated with too much C peptide?

A

Type 2 diabetes

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16
Q

What happens with too much C peptide?

A

it deposits on endothelia and causes inflammation

  • macrophage to foam cell
  • T cell mediated inflammation
  • smooth muscle proliferation
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17
Q

What is GLUT-2? and what cells do you find it in?

A
  • it is a concentration dependent glucose transporter

- found in Beta cells

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18
Q

What is glucose influx proportional to?

A

blood glucose concentration

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19
Q

What is the primary factor in Beta cell stimulation?

A

increased blood glucose.

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20
Q

How is glucose phosphorylated?

A

by glucokinase to glucose-6-phosphate

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21
Q

What is the process of insulin secretion?

A

1) GLUT-2 on pancreatic B cells take up glucose
2) Glucokinase –> G6P
3) NADPH and ATP (from glycolysis) close K+ channel
4) Ca2+ channels open
5) vesicles bind Ca2+ and release insulin to blood

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22
Q

What kind of feedback does glucagon provide to insulin?

A

negative

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23
Q

What does glucagon stimulate?

A

Gluconeogenesis

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24
Q

What are some factors in B cell stimulation?

A 
glucagon
arginine and lysine
GI hormones
acetylcholine
Sulfonurea drugs
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25
Q

What are the effects of insulin on carbohydrates?

A
  • increased glucose uptake
  • increased glycogenesis
  • decreased gluconeogenesis
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26
Q

What are the effects of insulin on fat?

A
  • increased triglyceride synthesis

- decreased trigylceride breakdown

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27
Q

What are the effects of insulin on protein?

A
  • increased synthesis

- decreased breakdown

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28
Q

what are the end effects of insulin?

A
  • 80% of cells increase glucose uptake by mobilizing GLUT-4

- Phosphorylation of glucose then allows it to be a substrate for CHO metabolic functions

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29
Q

How does Metformin work?

A

stimulates AKT pathway to increase GLUT-4 in skeletal muscles to treat hyperglycemia in type 2 diabetes

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30
Q

Why is it important to have low serum insulin level in between meals?

A

so glucose can go preferentially to brain.

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31
Q

What does insulin stimulate in the liver?

A

glycogen synthetase and inhibits glycogen phosphorylase in the liver

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32
Q

How is most glucose after a meal stored?

A

Immediately in liver as glycogen

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33
Q

What does inactivation of glycogen phosphorylase prevent?

A

breakdown of glycogen

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34
Q

What does insulin decrease?

A

gluconeogenesis by inhibiting required enzyme action

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35
Q

What does insulin activate?

A

glucose storage/utilization enzymes (+)

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36
Q

What does insulin inactivate?

A

glucose mobilization/synthesis enzymes (-)

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37
Q

What are two conditions where muscle uses glucose?

A
  • exercise

- after meal when blood glucose is high and insulin is high.

38
Q

How much does insulin increase glucose transport to muscle by?

A

15 times

39
Q

What happens when liver glucose storage reaches its limit?

A

insulin causes conversion of excess sugar into fatty acid by the liver. (pyruvate to acetyl CoA)

40
Q

What does insulin inhibit in regards to adipose?

A

insulin inhibits hydrolysis of TG, preventing FFA to blood.

41
Q

Insulin promotes utilization of CHO for energy, but what happens when insulin is low?

A

FAT is preferentially used (except brain)

42
Q

What is the signal for switching between CHO and FAT?

A

blood glucose

43
Q

Which is used when blood glucose is low and insulin is low? FAT or CHO?

A

FAT is used

44
Q

Which is used when blood glucose is high and insulin is high? CHO or FAT?

A

CHO

45
Q

How does insulin promote K uptake to decrease serum [K+] ?

A

1) increase Na+/K+ ATPase
2) increase intracellular Na+ sensitivity
3) Inhibit K+ efflux

46
Q

What can patients with hyperkalemia be treated with to decrease serum [K+]?

A

insulin

47
Q

How does insulin promote phosphate uptake?

A

kidney has immediate response to phosphate conservation upon insulin stimulated phosphate uptake

48
Q

What do the beta cells of the pancreas produce? QUICK CHECK

A

amylin

not somatostatin, insulin, or glucagon and amylin

49
Q

What are insulins actions on CHO in the liver? QUICK CHECK

A

glycogen synthesis

50
Q

Why do insulin and growth hormones make you grow?

A

each promotes cellular uptake of AAs required for growth.

51
Q

Which hormones does insulin stimulate the uptake of?

A

leucine, valine, isoleucine, tyrosine, and phenylalanine

52
Q

What type of cells secrete glucagon and when?

A

alpha cells when blood glucose falls.

53
Q

What are the actions of glucagon?

A
  • increase blood glucose
  • hyperglycemic effect (corrects hypoglycemia)
  • typically opposes the actions of insulin*
54
Q

What are glucagons effects on glucose metabolism?

A

glycogenolysis

-gluconeogenesis

55
Q

What increases the secretion of glucagon?

A
  • low blood glucose
  • exercise
  • high serum AAs (same effect as on insulin, but glucagon makes glucose, insulin makes protein)
56
Q

Why does exercise increase secretion of glucagon?

A

increased circulating AAs
increased beta-adrenergic stimulation
prevents fall in blood glucose

57
Q

What is secretion of Glucagon decreased by?

A
  • high blood glucose

- somatostatin

58
Q

What is amylin secreted by?

A

pancreatic B cells

59
Q

What happens if amylin is insoluble?

A

it forms fibrils and induces apoptosis of pancreatic B cells, thus inhibiting insulin secretion

60
Q

What happens if amylin is soluble?

A

it decreases blood glucose –> synergize with insulin, decrease glucagon

61
Q

What is somatostatin secreted by?

A

Delta cells of Langerhans

62
Q

What does somatostatin do?

A

inhibits glucagon and insulin

63
Q

What is somatostatin increased by?

A

ingestion of food –> increase blood glucose, increased AA, increase FA, increased GI hormones

64
Q

What is the main goal of somatostatin?

A
  • extend period of time over which food/nutrients are assimilated
  • decreases use of absorbed nutrients by tissues, making food available over longer periods of time.
65
Q

What is the critical level for insulin?

A

< 20-50 mg/100ml

66
Q

What happens when the critical level of insulin is reached?

A

hypoglycemic shock
coma
death

67
Q

What processes slow down dramatically with a lack of insulin?

A
  • Protein storage and synthesis

- increased catabolism of protein —> protein wasting leading to weakness and organ dysfunction

68
Q

What does increased use of fat for energy by all tissues cause?

A

(except brain) lipolysis

69
Q

What does excess use of fat lead to?

A

oxidation of FA in liver and generation of ketone bodies.

70
Q

What is diabets mellitus?

A

syndrome of impaired CHO, PRO, and FAT metabolism

71
Q

What is DM caused by?

A
  • lack of insulin secretion (DM type 1, IDDM insulin dependent)
  • decreased insulin sensitivity of tissues (insulin resistance, type 2 DM, NIDDM non-insulin dependent)
72
Q

What is type 1 DM?

A

overt B cell failure –> destruction of B-cell

73
Q

What is type 2 DM?

A

loss of insulin sensitivity –> later loss of B-cell u, decreased capacity to secrete insulin

74
Q

What are some causes of Type 1 DM?

A
  • viral infection
  • auto-immune disease
  • genetics
75
Q

When is the typical onset of Type 1 DM?

A

childhood-early adolescence

76
Q

What are some clinical findings of type 1?

A

increased blood glucose - 300-1200 mg/100ml
increased use of fats for energy, cholesterol synthesis
depletion of proteins

77
Q

How does high blood glucose cause dehydration?

A

-loss in urine = osmotic diuresis (causes decreased electrolytes in addition to water)

78
Q

What is the polyol pathway?

A

glycated protein, loss of normal function, precipitation on tissue “sugar coated proteins”

79
Q

What does chronic high blood glucose lead to in Type 1 DM?

A

tissue damage.

1) vascular
2) nerves
3) HTN and atherosclerosis

80
Q

What are effects of fat metabolism in Type 1 DM?

A
  • hyperventillation increased for expiration of CO2
  • increased cholesterol in circulation causes arteriosclerosis
  • depletion of protein stores causes weight loss, fatigue, polyphagia, severe wasting, DEATH
81
Q

When is the typical onset of Type 2 DM?

A

> 30, usually 50-60

82
Q

What is type 2 DM associated with?

A

increased insulin

83
Q

What are warning signs for type 2 DM?

A
  • obesity, abdominal fat (oh no, SANTA!!!!)
  • reactive hypoglycemia
  • insulin resistance
  • fasting hyperglycemia
  • lipid abnormalities
  • HTN
84
Q

What are causes of insulin resistance?

A
  • chronic insulin exposure
  • obesity
  • excess cortisol
  • Excess GH
  • Pregnancy
  • polycystic ovarian syndrome
  • hemochromatosis
  • genetic causes of obesity
85
Q

What are reasons for progression to IDDM from type 2?

A

hyperglycemia and hyperlipidemia provide constant influx of nutrients into pancreatic B cells. –> nutrient toxicity impairs b cell secretion over time

86
Q

What is a normal sign for the oral glucose/insulin tolerance test?

A

2 ours post-prandial level should be back to normal

87
Q

what is the result for DM on the oral glucose/insulin tolerance test?

A

glucose does not return to normal for 4-6 hours

88
Q

what is the result for DMI on the oral glucose/insulin tolerance test?

A

insulin low or undetectable

89
Q

what is the result for DMII on the oral glucose/insulin tolerance test?

A

insulin high in early stage or low in late stage

90
Q

What is an insulinoma?

A

hypersecretion of insulin from tumor of beta cells

-10-15% malignant

91
Q

What can an untreated insulinoma lead to?

A

insulin shock due to hypoglycemia

Physiology 2 test 1 (3 decks)

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