Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PMCOL 343 > Calcium, bone and osteoporosis > Flashcards

Calcium, bone and osteoporosis Flashcards

1
Q

what do osteoclasts do

A

dissolve the bone and release IGF1 and TGFβ (transforming growth factor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what recruits osteoclasts to bone

A

cytokines (ILs) and parathyroid hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what do osteoblasts do

A

lay down new oesteoid which will then become the new bone matrix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are osteocytes

A

bone cells which are osteoblasts that became embedded in the matrix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

at what age does bone loss start occuring

A

age 35-40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what % rate bone loss happens per year in both sexes

A

0.5-1%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

why does bone decrease by 0.5-1% per year in both sexes

A

due to decrease in osteoblast numbers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the rate of loss increase during menopause in women

A

10X increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

why does bone decrease by 10X during menopause in women

A

due to increase in osteoclast activities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what % of the body calcium is contained in bone

A

98%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what % of the body phosphates is contained in bone

A

85%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how is calcium phosphate stores as in bone (name and formula)

A

hydroxyapatite, Ca10(PO4)6(OH)2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the formula for hydroxyapatite

A

Ca10(PO4)6(OH)2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the 3 major hormones involved in bone metabolism and remodeling

A

parathyroid hormone, vitamind D, calcitonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what does high plasma [Ca++] do to PTH release

A

decreases PTH release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what does low plasma [Ca++] do to PTH release

A

increases PTH release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what G proteins are coupled to Ca++ sensing receptors

A

Gq Gi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what does high [PO4-] do to PTH secretion and how

A

indirectly increases

-forms complex with Ca++, so less Ca++ in plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what does low [PO4-] do to PTH secretion and how

A

indirectly decreases

-forms complex with Ca++, so more Ca++ in plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what does calcitriol do to PTH release and why

A

makes less, suppresses PTH gene expression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is calcitriol

A

a vitamin D metabolite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what does high intracellular Ca++ do to PTH secretion

A

inhibit

because that means Gq was activated by Ca++ in plasma and high plasma Ca++ means low PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what does low intracellular cAMP do to PTH secretion

A

inhibit

because that means Gi was activated by Ca++ in plasma and high plasma Ca++ means low PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what does PTH do to the bone

A

induce osteoblasts to express and secrete a protein RANKL (RANK ligand)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are PTH receptors coupled to

A

adenylate cyclase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what does RANKL do

A

activate RANK receptors on osteoclast precursors to cause differentiation and activation of osteoclasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what does RANK receptor activation on osteoclasts do

A

cause differentiation and activation of osteoclasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what bone cell has RANK receptors

A

osteoclasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

which bone cell releases RANKL

A

osteoblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what does an increase in bone resorption lead to

A

bone formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what does intermittent exposure to PTH promote

A

bone formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what does chronic high level exposure to PTH promote

A

bone resorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what does PTH do to GI tract

A

increase in Ca++ and phosphate absorption via an increase in synthesis of calcitrol in the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what does PTH do to Ca++ absorption

A

increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what does PTH do to phosphate absorption

A

increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what does PTH do to calcitriol synthesis (where does this occur)

A

increase, in the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

where does calcitriol synthesis occur

A

in the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what does PTH do to kidney

A
  • increase calcitrol synthesis
  • increase Ca++ reabsorption
  • increase PO4- excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what do kidneys do to Ca++ reabsorption (with PTH)

A

increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q 
what do kidneys do to phosphate excretion
and how  (with PTH)
A

increase excretion by decreasing reabsorption in proximal tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what does PTH do to plasma calcium

A

elevates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what does PTH do to plasma po4-

A

decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is a synthetic PTH used for in osteoporosis

A

PTH 1-34

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what are the 2 major sources of vitamin D called

A

ergocalciferol (D2)

cholecalciferol (D3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

where does ergocalciferol (D2) come from

A

plants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

where does cholecalciferol (D3) come from

A

in the skin, generated by UV light

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

is D2 or D3 more strong in humans

A

same potency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is vitamin D tho and what does it do

A

a prohormone that is converted into a number of biologically active metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what enzyme converts calfidediol into calcitriol

A

25(OH)D1αhydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

where is calcifediol produced

A

in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

where is calcitriol produced

A

in the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what does calcitrol do to PTH production

A

inhibit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what does high calcitrol do to PTH production

A

inhibit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what does low calcitrol do to PTH production

A

enhance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what does calcitrol do to calcitrol production

A

inhibit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what is calceifediol

A

the main storage form of vitamin D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what does calcifediol do to Ca++ (renal)

A

stimulates renal reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what does calcifediol do to PO4-

A

stimulates renal reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what does calcifediol do to Ca++ (muscle)

A

regulates Ca++ inlfux and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

where is excessive vitamine D stored

A

in body fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what does vitamin D binding protein have high affinity to

A

calcifediol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what does vitamin D binding protein have low affinity to

A

calcitriol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what is the most potent vitamin D metabolite

A

calcitriol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what is the vitamin D metabolite with the longer plasma half life

A

calcifediol (23 days) vs calcitriol (hours)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what is calcitriols affinity to vitamin D binding protein

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what is calcifediol affinity to vitamin D binding protein

A

high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what does calcitriol do to osteoblasts and what does this cause

A

induces RANKL secretion from osteoblasts so more recruitment of osteoclast precursor cells and maturation of osteoclasts

this causes production of osteocalcin

68
Q

what does calcitriol do to bone (major effect)

A

bone resorption

69
Q

what is osteocalcin

A

Ca++ binding protein in bOne maTriX

70
Q

what secretes osteocalcin

A

osteoblasts

71
Q

why do osteoblasts secrete osteocalcin

A

to regulate bone mineralization

72
Q

what does calcitriol do to GI tract

A

increased Ca++ and PO4- absorption

73
Q

what does calcitriol do to Ca++ reabsorption

A

increase absorption

74
Q

what does calcitriol do to PO4- absorption

A

increase absorption

75
Q

how does calcitriol increase Ca++ absorption in GI (3)

A

by increasing Ca++ binding proteins. TPV6 Ca++ channels and Ca++ flux across basal lateral membranes

76
Q

what does calcitriol do to plasma Ca++

A

increase

77
Q

what does calcitriol do to plasma PO4-

A

increase

78
Q

what does calcitriol do to kidney

A

decrease ca po4 excretion

79
Q

what does calcitriol do to ca in kidney

A

decrease excretion

80
Q

what does calcitriol do to po4 in kidney

A

decrease excretion

81
Q

what does calcitriol do to parathyroid glands

A

decrease PTH secretion

82
Q

what does calcitriol do to PTH secretion

A

decrease

83
Q

what does calcitriol do to other tissues

A

cell maturation and differentiation

84
Q

what are 4 common therapeutic uses for vitamin D

A
  • hypocalcemia
  • rickets
  • osteomalacia
  • osteoporosis
85
Q

what is hypocalcemia

A

failure to mineralize newly formed bone in children, resulting in bone softening and skeletal deformities

86
Q

what is osteomalacia

A

accumulation of undermineralized bone matrix in adults, associated with bone pain and tenderness

87
Q

what are 5 possible causes of hypocalcemia

A 
hypoparathyroidism
vitamin D deficiency
chronic kidney disease
malabsorption (GI disease)
liver disease
88
Q

why would chronic kidney disease cause hypocalcemia

A

decrease in calcitriol synthesis

89
Q

why would liver disease cause hypocalcemia

A

decrease in calcifediol formation

90
Q

what are 4 manifestations of hypocalcemia

A

tetany (tremor/spasms), paresthesia, muscle cramps, seizures

91
Q

what is the main treatment for hypocalcemia

A

Ca++ supplement in conjunction with calcitriol

92
Q

why is Ca++ supplement given in conjunction with calcitriol

A

cause calcitriol helps it absorb in the GI

93
Q

what can cause rickets and osteomalacia (4)

A

nutritional

hypophosphatemic vitamin D resistant

type 1 vitamin D dependent (pseudovitamin D deficiency)

type 2 vitamin D dependent (hereditary vitamine D resistant)

94
Q

how can you fix nutritional causing rickets and osteomalacia

A

cod liver oil or vit D supplement

95
Q

what is hypophosphatemic vitamin D resistant

A

genetic disorder resulting in reduction in renal PO4- reabsorption and decrease calcitriol production

96
Q

what is phosphate critical for with bones

A

BONE mineralization

97
Q

how do you treat hypophosphatemic vitamin D resistant

A

calcitriol and phosphate supplement

98
Q

what causes type 1 vitamin D dependent (pseudovitamin D deficiency)

A

mutation in 25(OH)D 1 hydroxylase

99
Q

what are you deficient in with type 1 vitamin D dependent (pseudovitamin D

A

calcitriol production

100
Q

how do you treat type 1 vitamin D dependent (pseudovitamin D

A

calcitriol

101
Q

what causes type 2 vitamin D dependent (hereditary vitamin D resistant)

A

mutations in the gene for vitamin D receptors

102
Q

what is serum cortisol levels in type 2 vitamin D dependent (hereditary vitamin D resistant)

A

actually high (but low tissue response)

103
Q

how do you treat type 2 vitamin D dependent (hereditary vitamin D resistant)

A

high dose of calcitriol

104
Q

kind of cell releases calcitonin

A

parafollicular C cell in thyroid gland

105
Q

what triggers calcitonin release from parafollicular C cell in thyroid gland

A

high Ca++ in plasma

106
Q

which G receptors is calcitonin coupled to

A

Gs

107
Q

what does calcitonin do to bone

A

less osteoclast activities

less bone resorption

108
Q

how do the bone effects of vitamin D and calcitonin compare

A

they are opposite

109
Q

what does calcitonin do to GI

A

increase Na+ K+ Cl- H2O secretion

less gastrin and gastric acid secretion

110
Q

what does calcitonin do to kidney

A

less Ca++ and PO4- reabsorption

and other ions (Na+ K+Mg++)

111
Q

what does calcitonin do to plasma Ca++ levels

A

lower

112
Q

what does calcitonin do to plasma PO4- levels

A

lower

113
Q

is calcitonin used for osteoporosis and why

A

no cause it gave tumors

114
Q

what does hypercalcemia manefest as

A

CNS depression
coma
fatigue
muscle weakness

115
Q

what can cause hypercalcemia

A

cancer that stimulates bone resoprtion, hyperparathyroidism

116
Q

what is pagets disease

A

abnormality in bone remodelling: uncontrolled osteoclastic bone resorption, secondary increases in poorly organized bone formation

117
Q

what causes pagets disease

A

unknown, maybe virus

118
Q

how can you treat pagets disease

A

calcitonin

119
Q

how can calcitonin help pagets disease

A

lowers pain and compilation

120
Q

what is osteoperosi (simple)

A

increase in bone resorption relative to bone formation

121
Q

what are 2 common causes of osteoporosis

A

low sex hormone production

low vitamin D level and GI Ca++ absorption

122
Q

what are 4 less common causes of osteoporosis

A

glucocorticoids
thyrotoxicosis (thyroid hormone stimulates osteoclasts)
hyperparathyroidism
alcohol abuse (decrease vit D uptake)

123
Q

what are 6 treatments for osteoporosis

A 
teriparatide (fragment of PTH)
vit D supplement
Ca++ supplement
biphosphonate
estrogen replacement therapy/ receptor modulators
denosumab
124
Q

how many generations of biphosphonates have there been

A

3

125
Q

how do 1st gen biphosphonates work

A

metabolize into a nonhydrolyzable ATP analog that accumulates within osteoclasts and induce apoptosis

126
Q

what happens if given a 1st gen biphosphonate at continuously at high doses

A

osteomalacia (bone minerilzation, softening)

127
Q

are 1st gen biphosphonates given as a first line of treatment

A

no

128
Q

how do 2nd gen biphosphonates work

A

inhibit farnesyl pyrophosphate synthesis, an enzyme that is important for osteoclast function and survival

129
Q

how must 2nd gen biphosphonates be administered

A

first thing in the morning on an empty stomach

130
Q

how much more potent are 2nd gen biphosphonates than 1st gen

A

10-100

131
Q

how do 3rd gen biphosphonates work

A

inhibit farnesyl pyrophosphate synthesis, an enzyme that is important for osteoclast function and survival

132
Q

how much more potent are 3rd gen biphosphonates than 1st gen

A

10 000

133
Q

how can you administer 3rd gen biphosphonates

A

once a year IV

134
Q

what do biphosphonates do to bone remodeling and how

A

decrease by decreasing osteoclast activity

135
Q

what do biphosphonates do to osteoclast activity

A

reduce

136
Q

where is the action of biphosphonates concentrated

A

at the site of active bone remodeling

137
Q

what do biphosphonates do to hydroxyapatite

A

reduce formation and dissolution of hydroxyapatite

138
Q

what are 4 therapeutic uses of biphosphonates

A

pagets disease
prophylaxis + treatment of osteoperosis
hypercalcemia
prevent fracture in patients with bone metastases

139
Q

what is a complication with using biphosphonates

A

osteonecrosis of jaw (more with 3rd gen due to limit of blood supply)

140
Q

what happens to calcium levels in blood when on biphosphonates and why

A

lowers because they inhibit bone resorption

141
Q

how is estrogen good for osteoperosis

A

it opposes the action of PTH on bone resorption

142
Q

how does estrogen oppose the action of PTH on bone resorption

A

there are estrogen receptors on bone

143
Q

is estrogen used in postmenopausal women for osteoporosis and why

A

no because there is an increase risk in breast cancer with long-term use

144
Q

what do SERMs stand for

A

selective estrogen receptor modulators

145
Q

what do SERMs do to bone

A

agonist effects on bone - behaves like estrogen

146
Q

what do SERMs do to lipid metabolism

A

agonist effects on lipid metabolism - behaves like estrogen

147
Q

what do SERMs do to breast tissue

A

antagonist effects on breast cancer - so wont cause cancer

148
Q

what do SERMs do to uterus

A

its inactive

149
Q

when are SERMs used

A

alternative to estrogen replacement therapy

150
Q

what do SERMs do to thromboembolic events

A

increased risk

151
Q

what are the agonist effects of SERMs

A

on bone and lipid metabolism

152
Q

what are the antagonist effects of SERMs

A

on breast tissue

153
Q

what is denosumab

A

a human monoclonal antibody

154
Q

what does denosumab do/cause

A

reduces the stimulatory action of RANKL on osteoclasts formation and activation

155
Q

what is the mechanism of denosumab

A

binds to RANKL to prevent it from binding to RANL receptors on osteoclast precursor cells (so it wont become an osteoclast)

156
Q

which drug can be used for postmenopausal osteoporosis

A

denosumab

157
Q

can denosumab be used for postmenopausal osteoporosis

A

yes

158
Q

what do glucocorticoids do to bone (2)

A

decrease bone formation

decrease activities of osteoblasts

159
Q

what do glucocorticoids do to bone formation

A

decrease

160
Q

what do glucocorticoids do to osteoblasts

A

decrease activity

161
Q

what do glucocorticoids do to GI tract

A

decrease Ca++ and PO4- absorption

162
Q

what do glucocorticoids do to Ca++ absorption

A

decrease

163
Q

what do glucocorticoids do to PO4- absorption

A

decrease

164
Q

what do glucocorticoids do to kidneys

A

increase Ca++ excretion

165
Q

what do glucocorticoids do to Ca++ excretion

A

increase

166
Q

what are 3 things that glucocorticoids in treatment of hypercalcemia are good for / associated with

A
  • vitamin D intoxication
  • sarcoidosis
  • cancers that stimulate osteoclastic bone resorption
167
Q

what is sarcoidosis

A

lung granuloma that causes unregulated ectopic production of vitamin D

PMCOL 343 (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions