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Physiology > Lecture 16: Endocrine Pancreas > Flashcards

Lecture 16: Endocrine Pancreas Flashcards

1
Q

What are the four “musketeers” of glycemic control

A

Liver, adipose tissue, pancreas and muscle

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2
Q

Islet of langerhans

A

Endocrine pancreatic cells

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3
Q

What are the two main regulators of glucose- what cell type and hormone

A
  1. Beta cells-insulin
  2. Alpha cells- glucagon
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4
Q

Insulin and glucagon are the dominant hormone regulators that shift the body between ____

A

Anabolism and catabolism/glucose sparing

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5
Q

What cell type is activated during an increase of blood glucose and which is inhibited

A

Activated: Beta cell to release insulin and decrease BG

Inhibited: alpha cell, decrease glucagon

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6
Q

What cell type is activated during a decrease in BG and which is inhibited

A

Activated: alpha cell to release glucagon and increase BG

Inhibited: beta cell, decrease insulin

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7
Q

What two hormones do beta cells secrete

A

Insulin and amylin

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8
Q

What hormone do alpha cells secrete

A

Glucagon

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9
Q

What hormone do delta cells secrete

A

Somatostatin

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10
Q

What hormone do gamma cells secrete

A

Pancreatic polypeptide

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11
Q

What hormone do epsilon cells secrete

A

Ghrelin

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12
Q

What does amylin do

A

Acts on CNS to suppress appetite

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13
Q

Which hormone inhibits digestive function, inhibits alpha and beta cells

A

Somatostatin

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14
Q

What do pancreatic polypeptides do

A

Putatively inhibit gastric juices, appetite and food intake

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15
Q

What does ghrelin do

A

Stimulates Appetite

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16
Q

Describe the flow chart of insulin regulation upon food intake

A
  1. Food intake causes—>
  2. Increase BG, increase GI hormones and increase AA which all act on—>
  3. Activate islet B cells
  4. Insulin secretion
  5. Decrease: BG, FA, and AA
    Increase: protein synthesis and fuel storage
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17
Q

What type of hormone is insulin

A

Peptide

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18
Q

Describe the synthesis of insulin

A
  1. Preproinsulin in mRNA strand
  2. Enters ER with C peptide attached
  3. Enters golgiand trans Golgi to have cleavage of C-peptide from insulin
  4. C peptide and insulin put in secretory granules
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19
Q

What are the secretory products in granules

A

1:1 insulin: C-peptide
5% pro insulin

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20
Q

What is C-peptide a good marker for

A

Insulin production and B cell function

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21
Q

What mechanism allows glucose to stimulate insulin secretion and in what cell type does this occur

A

Excitation-secretion coupling in Beta cells

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22
Q

Describe the steps in how glucose stimulates insulin release

A
  1. Glucose enters via GLUT2
  2. Close K + channels which depolarizes cell
  3. VG Ca2+ channels open and enter Beta cell
  4. Ca2+ triggers exocytosis of insulin vesicles into circulation
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23
Q

What are some other humoral factors that stimulate insulin release besides glucose

A

Sugars, amino acids, hormones, drugs, short chain fatty acids, ketone bodies

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24
Q

How does insulin effect carbohydrate energy stores

A

Decrease BG, increase storage
Increase glucose uptake
Increase glycogenesis
Decrease glycogenolysis
Decrease gluconeogenesis

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25
Q

How does insulin effect lipid energy stores

A

Decrease blood FA, increase storage
Increase glucose uptake by adipocytes
Increase lipogenesis
Increase FA uptake
Decrease lipolysis

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26
Q

How does insulin effect protein energy stores

A

Decrease blood amino acids, increase storage
Increase amino acid uptake
Increase protein-synthesizing machinery
Decrease protein degradation

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27
Q

What is GLUT1 used for

A

Transports glucose across the BBB

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28
Q

What is GLUT2 used for

A

Transports glucose in kidney and intestine

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29
Q

What is GLUT3 used for

A

Transports glucose into neurons

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30
Q

What is GLUT 4 used for

A

Insulin dependent glucose transporter in most other cells of the body: adipose tissue and resting muscle cells

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31
Q

What is the consequence to low levels of insulin secretion

A

Hyperglycemia

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32
Q

What are some MAP kinase pathways that insulin regulates

A
  1. Fuel storage
  2. Alter gene expression pathways
  3. Enhance cell growth and phenotypes
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33
Q

Glucagon is inhibited by___ and ____

A

High glucose
Somatostatin

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34
Q

Glucagon is stimulated by what 4 things

A

Low glucose, epinephrine (beta2), vagal stimulation, amino acids

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35
Q

Where is glucagon expressed

A

Pancreas alpha cells, liver, intestine and brain

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36
Q

Glucagon is produced as pro glucagon and proteolytically processed to yield glucagon and ____

A

Incretin (GLP1)

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37
Q

When/where is GLP1 released

A

Released from intestine in response to high glucose levels in intestinal lumen

38
Q

GLP1 increases ____ release from B cells

A

Insulin

39
Q

What is the main target of glucagon

A

Liver to stimulate hepatic glucose output: increase plasma glucose levels

40
Q

What does glucagon oppose

A

Insulin and GLP1

41
Q

Does glucagon increase or decrease glyconeogenesis and glycogenolysis

A

Increase glycogenolysis and decrease glyconeogenesis

42
Q

What is the main factor that drives release of glucagon

A

Hypoglycemia

43
Q

Does epinephrine, CCK, vagal stimulation, fasting, and exercise increase or decrease circulating glucagon

A

Increase

44
Q

Does hyperglycemia, somatostatin, insulin, fatty acids, and keto acids increase of decrease glucagon

A

Decrease

45
Q

In the absence of carbohydrates, does dietary protein increase or decrease glucagon

A

Increase

*if meal has carbs this doesn’t happen

46
Q

What is glucagons effect on carbohydrate energy stores

A

Increase BG
Increase gluconeogesis and release from liver
Increase glyconeogenesis
Decrease glycogen synthesis

47
Q

How does glucagon effect lipid energy stores

A

Increase blood FA and ketones
Decrease triglyceride synthesis
Increase lipolysis and release of FA
Increase Ketone production

48
Q

What effects does glucagon have on protein energy stores

A

Minimal effect on blood amino acids
Decrease hepatic protein synthesis
Increase hepatic protein degradation and increase gluconeogenesis

49
Q

When carbohydrates are the main fuel source what happens to insulin and glucagon levels

A

Insulin increases
Glucagon decreases

50
Q

What happens to insulin and glucagon when proteins are the main fuel source

A

Insulin increases in response to blood AA

Glucagon increases in response to low blood sugar

51
Q

What hormone is secreted in a high protein diet in order to avoid BG crash

A

Glucagon

52
Q

What type of hormone is somatostain

A

Peptide

53
Q

What stimulates release of somatostatin

A

High fat, carbs and protein rich meals

54
Q

How does somatostatin inhibit release of glucagon and insulin

A

Hyper polarizing alpha and beta cells

55
Q

What does pancreatic polypeptide inhibit

A

Secretion of pancreatic enzymes, hepatic glycogen, and the contraction of the gallbladder

56
Q

What stimulates the release of pancreatic polypeptide

A

Fasting, intestinal hormones (cholecystokinin, secretin and gastrin), stimulation of vagus nerve, and ingestion of protein

57
Q

does glucose and somatostain increase or decrease pancreatic polypeptide

A

decrease

58
Q

What hormone affects weight regulation and obesity based on its rate of release

A

Pancreatic polypeptide

59
Q

What diabetogenic hormones regulate glucose

A

Glucagon, epinephrine, cortisol, growth hormone and IGF-1, pancreatic polypeptide

60
Q

How does the brain regulate glucose

A

Hypothalamic control of fuel management via autonomic control of hormone release

Senses nutrients and hormone levels

61
Q

What hormones are sensed by the brain and drive appetite

A

Insulin, leptin, and GLP-1

62
Q

Where are the receptors for glucose detection in the brain located

A

Arcuate nucleus

63
Q

Neural control for glucose operate to control ___ and ____

A

Energy balance and regulate body composition

64
Q

What disease results in high blood sugar levels over a prolonged period of time

A

Diabetes Mellitus

65
Q

What is problem in type I DM

A

Lack of insulin secretion from pancreas

  • insulin dependent
66
Q

What are some potential causes of Type I DM

A

Autoimmune: T-lymphocytes destroy Beta cells
Idiopathic, environmental
Alloxan and streptozotocin are two drugs that selectively destroy Beta cells

67
Q

What is the problem in type II DM

A

Tissue resistance to insulin

Non-insulin dependent

68
Q

What type of DM is usually a result of diet/activity

A

Type II

69
Q

What are the acute symptoms of DM

A

Elevated BG

70
Q

What are some chronic effects of DM

A

Retinopathy (dogs)
Pancreatic amyloidiosis (cats)
Neuropathy
Nephropathy
CVD
Ketoacidosis

71
Q

Type I is common in what species

A

Dogs

72
Q

Type II is common in what species

A

II

73
Q

Insulin deficiency results in hyperglycemia as a result of what 2 things

A
  1. Decrease glucose uptake into cells
  2. Increase hepatic output of glucose
74
Q

How does hyperglycemia cause glucosuria, dehydration, and PD

A

Hyperglycemia overwhelms tubular system so can’t reabsorb all of it, results in it being excreted in urine

Osmotic effect of glucose draws water out into filtrate resulting in excess fluid loss=dehydration and then PD

75
Q

Dehydration results in decreased blood volume and therefore circulatory failure to several vital organs, what happens to brain

A

Brain function declines due to failure to oxygenate resulting in death

76
Q

What happens to shape of cells in chronic DM

A

Cells shrink due to osmotic shift of water into ECF and blood

77
Q

What is the effect of chronic DM on nerve cells

A

Lose their ability to maintain correct membrane potential and form AP

78
Q

Due to decreased insulin and therefore decreased uptake of glucose into tissues what happens to pH

A

FA are mobilizes and used by liver resulting in ketosis, ketone bodies cause metabolic acidosis

79
Q

What happens to respiratory ventilation in response to metabolic acidosis in DM

A

Respiratory ventilation increases to vent off CO2 and shift pH up

80
Q

Does lack of insulin cause protein catabolism or anabolism

A

Catabolism

81
Q

Protein catabolism causes muscles to atrophy and cause amino acids to do what

A

Amino acids shift towards greater glucogenesis and contribute to existing hyperglycemia

82
Q

Clinical case: 9yr, SF, DLH presents with 5 months progressive weight loss, muscle weakness, matted fur and moderate periodontal disease. Note plantigrade stance on exam. Owner mentions low energy, occasional tremors and PU. USG=1.034. What is most probable diagnosis

A

Type II DM

83
Q

Clinical case: suspect type II DM cat, what additional tests can be run

A

Serum fructosamine

84
Q

What can insulin excess cause

A

Hypoglycemia

85
Q

What are some dangerous effects/symptoms of hypoglycemia

A

Loss of consciousness, depressed brain function, weakness, fatigue, ataxia

86
Q

What is insulin overdose and what can be given to alleviate

A

Injection of too much insulin, resulting in shock (decrease BG)

Give carbs to alleviate

87
Q

What is reactive hypoglycemia and what can be done to alleviate it

A

Extreme response to glucose, beta cells release too much insulin

Limit carb diet to alleviate

88
Q

What can cause reactive hyperglycemia

A

Islet hyperplasia or lack of somatostatin counterbalance

89
Q

What do islet tumors in dogs cause and what can help alleviate insulin excess

A

Excessive insulin release give carbs to alleviate

90
Q

What is the most common cause of hypoglycemia in dogs

A

Islet tumors

Physiology (10 decks)

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