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Endocrinology > Parathyroid and pancreas quiz > Flashcards

Parathyroid and pancreas quiz Flashcards

1
Q

What separates the thyroid and parathyroid

A

Connective tissue capsule

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2
Q

What cells make up the parathyroid

A

Chief cells

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3
Q

Synthesis of PTH

A

Synthesized into a prepropeptide. Cleaved to yield proPTH and then to mature PTH

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4
Q

How many amino acids make up PTH

A

84

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5
Q

How many times is PTH released

A

6-7 times an hour (pulsatile)

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6
Q

Where is PTH degraded

A

Kidney and liver

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7
Q

Aminoterminal fragments

A

10% of circulating PTH fragments. Biologically active but have a short half life of 4-20 minutes

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8
Q

Carboxyterminal fragments

A

80% of circulating PTH fragments. No biologic activity and have a longer half life

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9
Q

How much of the PTH levels does intact PTH account for

A

10%

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10
Q

What increases PTH release

A
  1. Catecholamines
  2. Hypocalcemia
  3. Hyperphosphatemia
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11
Q

What suppresses PTH release

A
  1. Hypercalcemia

2. Vitamin D

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12
Q

What does activation of the parathyroid Ca2+ receptor do

A

Leads to leukotriene production and degredation of performed PTH

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13
Q

What does relaxation of the parathyroid Ca2+ receptor do

A

Unimpeded PTH secretion

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14
Q

How does vitamin D inhibit PTH secretion

A

Decreasing gene expression

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15
Q

What (besides calcium) regulates PTH

A

Phosphate and magnesium levels

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16
Q

What does elevated phosophate levels cause

A

Increased PTH secretion

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17
Q

How does an elevated phosphate level increase PTH secretion

A

Decreasing phospholipase A2 activity and arachidonic acid formation removing the inhibitory effect on PTH

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18
Q

What decreasing PTH mRNA

A

Hypophosphatemia

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19
Q

What regulates PTH in a similar manner to calcium

A

Magnesium

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20
Q

What is magnesium balance linked to

A

Calcium balance

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21
Q

What is magnesium deficiency linked to

A

Hypocalcemia

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22
Q

Primary target organs of PTH

A

Kidney and bone

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23
Q

How does PTH increase plasma levels

A
  1. Increasing renal calcium reabsorption
  2. Calcium mobilization from the bone
  3. Intestinal absorption (due to vitamin D)
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24
Q

How are the effects of PTH mediated

A

By binding to a cell membrane receptor on the target organ

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25
Q

Types of PTH receptors

A
  1. PTHR1
  2. PTHR2
  3. PTHR3
    (GPCR)
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26
Q

PTH effects on kidney

A
  1. Calcium reabsorption
  2. Phosphate excretion
  3. Activity of 1 alpha-hydroxylase (the enzyme responsible for forming the active form of vitamin D) (1,25(OH)2D)
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27
Q

PTH effects on bone

A
  1. Stimulates release of calcium and phosphate by acitvation of bone resorption
  2. Osteoblast activation (produces osteoclast differentiation factor resulting in the stimulation and recruitment of osteoclasts)
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28
Q

How does PTH increase the number of osteoblasts

A

Decreasing their apoptosis and increasing their proliferation

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29
Q

What do chronic elevations of PTH result in

A

Bone resorption

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30
Q

What does administration of PTH result in

A

Bone formation more than bone resorption

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31
Q

How much calcium is in the human body and where

A

1100g. 99% in bones and teeth, some in plasma

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32
Q

Fractions of calcium found in plasma

A
  1. Ionized calcium (50%)
  2. Protein bound calcium (40%)
  3. Calcium complexed to citrate and phosphate forming soluble complexes (10%)
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33
Q

Vitamin D cellular effects

A

Changes gene transcription

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34
Q

Genomic effects of vitamin D

A

Dependent on the interaction of 1,25(OH)2D with cytosolic nuclear receptor protein, followed by the interaction of the steroid receptor complex in the nucleus with selective regions of the promotors of genes that are either activated or repressed

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35
Q

Nongenomic effects of vitamin D

A

Interaction of the vitamin with the cell memrane receptor for 1,25(OH)2D that activates a variety of signal transduction systems, inclusing protein kinase C, phospholipase C, and adenylate cyclase and modulates ion (Ca, Cl) channels

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36
Q

Calcitonin

A

32 amino acid peptide

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37
Q

What is calcitonin derived from

A

Procalcitonin

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38
Q

What is procalcitonin produced by

A

Cells of the neural crest origin (parafollicular or C cells)

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39
Q

What stimulates the release of calcitonin

A

Plasma calcium higher than 9mg/dl

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40
Q

Calcitonin half life

A

5 minutes

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41
Q

What organ metabolizes and clears calcitonin

A

Kidney and liver

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42
Q

What regulates release of calcitonin

A

Plasma calcium levels through Ca2+ receptors on the parafollicular cells

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43
Q

Major physiologic function of calcitonin

A

Decrease plasma calcium and phosphate levels

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44
Q

Target organs of calcitonin

A

Bone and kidney

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45
Q

Calcitonin effects on bone

A

Decreases bone resorption, inhibition of osteoclast motility, differentiation, and ruffled border formation

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46
Q

Calcitonin effects on kidney

A

Increases urinary calcium exretion by inhibition of renal tubular calcium resorption

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47
Q

How much on the pancreas is endocrine

A

1%

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48
Q

How much of the pancreas is exocrine

A

99%

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49
Q

Where is the pancreas located

A

Abdominal cavity (behind the stomach). In the curve of the duodenum

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50
Q

Structure of the pancreas

A

Not encapsulated (no muscular wall)

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51
Q

Hormones of endocrine pancreas

A
  • Insulin
  • glucagon
  • SST
  • pancreatic polypeptide
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52
Q

What does the exocrine pancreas release

A

Salts and enzymes in the duodenum

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53
Q

Exocrine pancreas secretions

A
  1. Biocarbonate to neuralize gastric acid
  2. Amylase for breakdown of starch into smaller carbohydrates
  3. Lipase to break down triglycerides into free fatty acids
  4. Proteolytic enzymes (trypsinogen and chyotrypsinogen)
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54
Q

What is a zymogen

A

Inactive form of an enzyme

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55
Q

What activates a zymogen

A

Enteropeptidase in the duodenum

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56
Q

What does the endocrine pancreas release

A

Hormones into the bloodstream

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57
Q

Islet cells of the endocrine pancreas

A
  1. Alpha
  2. Beta
  3. Delta
  4. Gamma
  5. Epsilon
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58
Q

Alpha islet cells

A

Glucagon (takes glycogen and breaks them down to glucose monomers)

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59
Q

Beta islet cells

A

House and release insulin (causes glucose to be built into glycogen for storage)

60
Q

What cells are responsible for diabetes

A

Beta

61
Q

What diseases are caused by diabetes

A

Eye, nerve and kidney

62
Q

Type 1 diabetes

A

No insulin production

63
Q

Type 2 diabetes

A

Insulin receptors are broken

64
Q

Delta islet cells

A

Release SST, stops all other active hormones

65
Q

What is secreted by aciti

A

Enzymes

66
Q

What is secreted by Langerhans

A

Hormones into the blood

67
Q

Gamma islet cells

A

Pancreatic polypeptide

68
Q

Epsilon islet cells

A

Ghrelin

69
Q

Where does insulin act

A

Liver, skeletal muscle, adipose tissue

70
Q

What promotes insulin secretion

A

GIP

71
Q

What is inactivated by DPP4

A

GIP and GLP-1

72
Q

Where is GLP-1 from

A

L cells in the ilium and colon

73
Q

Incretins

A

Increase insulin without affecting pancreas exocrine function

74
Q

What decreases serum glucose

A

Insulin
Amylin
GIP
GLP-1

75
Q

What cells produce enzymes in the pancreas

A

Acinar cells

76
Q

What do the F cells secrete

A

Pancreatic polypeptide

77
Q

What is the blood supply of the pancreas derived from

A

Splenic artery and the superior and inferior pancreaticduodenal arteries

78
Q

Where does the blood from the pancreas drain into

A

Hepatic portal vein

79
Q

What part of the body has the largest concentration of pancreatic hormones

A

Liver

80
Q

Insulin function

A

Decrease blood glucose

81
Q

Glucagon function

A

Increase blood glucose

82
Q

Somatostatin function

A

Inhibits release of glucagon and insulin and slows the activity of the digestive tract

83
Q

Pancreatic polypeptide function

A

Secretion of pancreatic digestive enzymes and inhibits release of bile from the gallbladder

84
Q

What is insulin synthesized from and how

A

Synthesized from preproinsulin. It is modified in the ER to form proinsulin. Active insulin is formed from the cleavage of the C peptide

85
Q

What is released with insulin

A

C peptide

86
Q

Insulin release

A
  1. Glucose is the principal stimulus for insulin release
  2. Glucose enters the beta cell via transporter protein GLUT 2 and undergoes glycolysis leading to the generation of ATP
  3. ATP is converted to ADP. Leads to depolarization and opening of calcium channels
  4. Increased calcium influx. Secretory vesicles with insulin and C peptide fuse and are released by exocytosis
87
Q

First phase of insulin release

A

Rapid release of insulin that has already been produced. Occurs over a period of minutes

88
Q

Second phase of insulin release

A

A more sustained release of newly synthesized insulin. Occurs over an hour or more

89
Q

Immediate effects of insulin

A

Modulation of K and glucose transport into the cell

90
Q

Early effects of insulin

A

Regulation of metabolic enzyme activity

91
Q

Moderate

A

Modulation of enzyme synthesis

92
Q

Delayed

A

Effects on growth and cellular differentiation

93
Q

What does insulin promote the synthesis of

A

Carbohydrates, protein and fat

94
Q

What modulates the synthesis of these things

A

Binding to the insulin receptor

95
Q

Insulin receptor signaling

A
  1. Insulin binding activates intrinsic kinase activity

2. Results in downstream cellular events mediated through phosphorylation of insulin receptor substrates (IRS)

96
Q

Immediate effects of insulin receptor signaling

A

Recruitment of GLUT 4 stored in intracellular vesicles of the cell surface

97
Q

Insulin effect on glucose uptake

A

Increase

98
Q

Insulin effect on glycolysis

A

Increase

99
Q

Insulin effect on glycogen synthesis

A

Increase

100
Q

Insulin effect on gluconeogenesis

A

Decrease

101
Q

Insulin effect on lipogenesis

A

Increase

102
Q

Insulin effect on lipolysis

A

Decrease

103
Q

Insulin effect on protein synthesis

A

Increase

104
Q

Insulin effect on proteolysis

A

Decrease

105
Q

Where does most glucose disposal occur

A

Skeletal muscle

106
Q

How does glucose move in the cell

A

Glucose transporters

107
Q

What does insulin binding to its receptor increase

A

GLUT 4 translocation

108
Q

How are intermediate effects of insulin mediated

A

Modulation of protein phosphorylation of enzymes involved in metabolic prossesses in muscle, fat and liver

109
Q

What does insulin do in fat

A

Inhibits lipolysis and ketogenesis

110
Q

What does insulin do in the liver

A

Stimulates gene expression of enzymes involved in glucose utilization and lipogenic enzymes, and inhibits gene expression of enzymes involved in glucose production

111
Q

How does insulin stimulate glycogen synthesis

A

Increasing phosphatase activity (dephosphorylation of glycogen synthase)

112
Q

What does insulin do in muscle

A

Stimulates glucose uptake and favors protein synthesis through phosphorylation of a serine/threonine protein kinase known as mTOR

113
Q

What does sustained insulin stimulation enhance

A

Synthesis of lipogenic enzymes and suppression of gluconeogenic enzymes

114
Q

What does the MAPK pathway mediate

A

Growth effects of insulin

115
Q

How many amino acids is glucagon

A

29

116
Q

What are the products of proglucagon

A

GLP-1 and glucagon

117
Q

Where is proglucagon expressed

A

Pancreas, enteroendocrine cells, brain, intestines

118
Q

GLP-1

A

Produced in response to a high concentration of glucose in the intestinal lumen

119
Q

Incretin

A

Amplifies insulin release

120
Q

Glucagon half life

A

5-10 minutes

121
Q

Where s glucagon degraded

A

Liver

122
Q

What inhibits glucagon release

A

High blood glucose, carbohydrate rich meals, SST

123
Q

What increases glucagon release

A

Amino acid rich meals, Epinephrine, vagal (parasympathetic) stimulation

124
Q

Target tissue of glucagon

A

Liver

125
Q

Glucagon’s main effect

A

Increase plasma glucose concentrations by stiulating hepatic glucose production through gluconeogenesis and glycogen breakdown

126
Q

Glucagon effects in cells

A

Binds to GCPR. AC –> cAMP –> PKA (resulting in phosphyrlation of enzymes that control glucose metabolism)

127
Q

How does glucagon stimulate hepatic glucose output

A

Stimulating glycogen breakdown and gluconeogenesis. Decreasing glycolysis

128
Q

Glucagon in the adispocytes

A

Glucagon stimulates PKA mediated phosphorylation of hormonsensitive lipase to break down triglycerides into diacylglycerol and free fatty acids (released into circulation)

129
Q

How many amino acids is SST

A

14

130
Q

What causes SST release

A

High fat, high carbohydrate and protein rich meals

131
Q

What inhibits SST

A

Insulin

132
Q

Job of SST

A

Inhibitory effect on all GI and pancreatic exocrine and endocrine functions

133
Q

What does administration of SST cause

A

Suppresses the release of insulin and glucagon

134
Q

How many amino acids in PP

A

36

135
Q

When is PP released into circulation

A

After a meal, vagal stimulation, and exercise

136
Q

Effects of PP

A

Inhibition of pancreatic exocrine secretion, gallbladder contraction, modulation of HCl secretion, and GI moltility

137
Q

What does PP do when it crosses the blood brain barrier

A

Plays a role in regulating feeding behavior

138
Q

How many amino acids in amylin

A

37

139
Q

What family is amylin part of

A

The calcitonin family

140
Q

Where is amylin stored and released with

A

Beta cells, released with C peptide and insulin

141
Q

When does amylin increase

A

After a meal or glucose infusion

142
Q

Role of amylin

A

Works with insulin to lower blood glucose, prvents secretion of glucose after eating, slowing gastric emptying

143
Q

Amylin in muscle

A

Opposes glycogen synthesis and starts glycolysis (increasing lactate production)

144
Q

What diseases have increased amylin

A

Obesity, hypertension, gestational diabetes

145
Q

What diseases have no amylin

A

Type 1 diabetes mellitus

146
Q

How does amylin cause Type 1 diabetes

A

Destroyes B cells in type 2 diabetes patients

Endocrinology (9 decks)

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