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PHS 933 > Block 3 Vitamin D and Osteoporosis > Flashcards

Block 3 Vitamin D and Osteoporosis Flashcards

1
Q

When/where is PTH secreted from

A
    • from parathyroid glands

- - in response to decreased Ca or increased PO4

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2
Q

What are PTH’s effects?

A

1) bone resorption
2) increase Vit. D synthesis
3) suppress calcitonin release
4) decrease renal Ca excretion

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3
Q

When/where is calcitonin secreted?

A
    • from parafollicular C cells of thyroid

- - in response to increased Ca

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4
Q

What are calcitonin’s effects?

A

1) inhibit osteoclast-medited bone resorption
2) increase renal PO4 excretion
3) increase renal Ca excretion

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5
Q

What are calcitriol’s effects?

A

1) increase intestinal Ca absorption

2) increase bone resorption AT HIGH LEVELS

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6
Q

What is the structure of calcitonin?

A

32 aa peptide

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7
Q

When/where is FGF-23 released?

A
    • from osteoclasts

- - in response to increased PO4

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8
Q

What are the effects of FGF-23?

A

1) inhibit renal PO4 reabsorption

2) inhibit vitamin D 1a-hydroxylation

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9
Q

What hormones are involved in Calcium homeostasis?

A

1) PTH
2) Calcitonin
3) Calcitriol
4) FGF-23
5) TH, GH, androgen/estrogens, glucocorticoids

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10
Q

What is the UL for Ca?

A

teens: 3g/day
adults: 2.5g/day
elderly: 2g/day

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11
Q

What are the RDAs for Ca?

A
    • adult: 1 g/day
    • 70+, or 50+ woman: 1.2 g/day
    • teens: 1.3 g/day
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12
Q

What is the average teenager intake of Ca?

A

750 mg/day

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13
Q

Where is most calcium obtained?

A

dairy products

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14
Q

How is Calcium lost?

A

300mg/day from bone turnover, increased by loop diuretics

    • half via urine
    • half via feces
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15
Q

How is Ca absorbed?

A

small bowel

1) active Vit.D-dependent transport in proximal duodenum
- - Vit.D boosts 2-fold
- - max 600 mg/day
2) facilitated transport
- - majority of uptake

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16
Q

How does phosphate circulate?

A

NaH2PO4 or Na2HPO4

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17
Q

How is PO4 excreted?

A

in urine

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18
Q

How is phosphate absorbed?

A

Vit.D facilitated active transport

    • 2/3 of intake absorbed
    • PO4 is abundant in food
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19
Q

What is the formula for hydroxyapatite? How much of body’s PO4 is there?

A

Ca10.P6.OH2

80%

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20
Q

How is Paget’s diagnosed?

A

elevated serum alkaline phosphatase

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21
Q

What are the causes of hypercalcemia?

A

1) primary hyper-PTH
2) familial benign hypercalcemia
3) acute hypercalcemia
4) PTH- or calcitriol-tumors
5) bone resorption tumors
6) granulomatous diseases
7) hypercalcemia of malignancy

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22
Q

How is acute hypercalcemia treated? Chronic?

A

acute
– IV saline + loop diuretic
chronic
– bisphosphonates (pam or zole) + calcitonin

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23
Q

What are the symptoms of primary hyperparathyroidism?

A

1) hypercalcemia, osteoporosis, kidney stones
2) osteitis fibrosa cystica
3) fatigue, weakness, depression/confusion, seizures
4) +/- hypophosphatemia

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24
Q

How is hyperparathyroidism treated?

A

parathyroidectomy

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25
Q

If you have primary hyperthyroidism, you probably also have…

A

low vitamin D

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26
Q

What causes familial benign hypercalcemia and what is the result?

A

defunct calcium sensor

    • low renal Calcium excretion
    • PTH might be slightly high
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27
Q

How is familial benign hypercalcemia treated?

A

not treated; it’s benign

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28
Q

How do granulomatous diseases like TB and sarcoidosis cause hypercalcemia?

A

excess calcitriol synthesis by mononuclear cells

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29
Q

How is granulomatous hyperparathyroidism treated?

A

1) glucocorticoids (decrease ectopic calcitriol)

2) oral phosphate (to bind Ca)

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30
Q

How is hypercalcemia of malignancy treated?

A

1) decrease dietary Ca

2) increase renal excretion and inhibit bone resorption

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31
Q

What are the symptoms of Paget’s?

A

may be asymptomatic

1) bone pain (compressed nerves from vertebral outgrowth)
2) deafness (ossicles)
3) deformed bone

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32
Q

What causes Paget’s?

A

unknown

    • maybe measles (paramyxovirus), since it promotes IL-6 and IL-6 stimulates osteoclasts
    • maybe genetic
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33
Q

Patients with Paget’s are more likely to develop…

A

osteosarcoma

gout

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34
Q

What patients are most likely to get Paget’s?

A

English

– 2-9% of those older than 50

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35
Q

Paget’s is due to…

A

single/multiple foci of bone turnover with 3 stages

    • bone resorption
    • exuberant bone production
    • disorganized, unstable, and deformed bone
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36
Q

What is calcitonin used for?

A

1) Paget’s
- - primarily for relief of bone pain due to fracture (analgesic properties)
- - also reduce bone loss and fracture incidence, but BPs more effective
2) hypercalcemia

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37
Q

How is calcitonin supplied?

A

salmon (Miacalcin, Fortical)

    • SQ or IN (IN is approved for osteoporosis)
    • tablet equally effective but not available
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38
Q

What are the ADRs of calcitonin?

A

1) 2x greater cancer risk when used 5+ years post-menopause
2) rhinitis, erythema, excoriation if 65+
3) Ab development leads to loss of efficacy

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39
Q

What is the MoA of Cinacalcet?

A

Calcium receptor agonist

– once a day

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40
Q

When is Cinacalcet used?

A

primary and secondary hyperparathyroidism

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41
Q

What are the effects of cinacalcet?

A

1) lower [PTH] 15-50%

2) lower Ca and PO4 7%

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42
Q

What are the ADRs of cinacalcet?

A

1) hypocalcemia
2) lower seizure threshold
3) CYP3A4 substrate

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43
Q

What causes hypoparathyroidism?

A

1) removal/injury of parathyroid gland
2) autoimmune
3) genetic deficiency

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44
Q

What are the causes of hypocalcemia?

A

1) hypoparathyroidism (most common)
2) renal osteodystrophy secondary to chronic renal failure
3) dietary insufficiency / malabsorption
4) pseudohypoparathyroidism

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45
Q

What are symptoms of hypoparathyroidism?

A

neuromuscular hyperexcitability

1) tetany
2) anxiety, depression, hallucinations
- - minimal bone effects!

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46
Q

How is primary hypoparathyroidism treated?

A

1) Ca
2) Vit. D
3) synthetic PTH in development

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47
Q

What are symptoms of pseudohypoparathyroidism?

A

1) low calcitriol
2) short stature
3) short metacarpals

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48
Q

How is pseudohypoparathyroidism treated?

A

Ca + Vit D or analogs

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49
Q

What causes pseudohypoparathyroidism and what is the result?

A

1) defects in intracellular PTH signaling = resistance
- - hyperphosphatemia, hypocalcemia
- - low calcitriol level

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50
Q

What is concurrent with dietary insufficiency/malabsorption of calcium?

A

low PO4 and Mg

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51
Q

How is renal osteodystrophy secondary to CRF treated?

A

1) Ca antacids
- - bind PO4
2) low phosphate foods
- - avoid soda, dairy
3) Vit D supplement
- - improve Ca
4) Cinacalcet
- - suppress PTH

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52
Q

What causes renal osteodystrophy in CRF?

A

1) can’t excrete PO4
- - high PO4 activates FGF-23
2) can’t make calcitriol
- - less Ca absorbed
- - bone resorbed, and Ca ends up in kidney
- - hypocalcemia, hyperphosphatemia

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53
Q

half life of D, calcitriol, and 25-hydroxyD

A

D (4-6h in plasma, 2 mos in body);
calcitriol (15h);
25-hydroxy (15 days)

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54
Q

relative affinity for VDBP among D, calcitriol, 25-hydroxy

A

D less than
Calcitriol less than
25-OH

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55
Q

How does Vitamin D enter the circulation?

A

enters lymph via chylomicrons
or, made from skin
– slowly transferred to VDBP

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56
Q

What constitutes Vitamin D deficiency? What is normal?

A

25-OH-D less than

20 ng/mL (normal is 40)

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57
Q

What is the storage form of VitD?

A

25-hydroxy/calcifediol

– transported via VDBP

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58
Q

How is calcitriol inactivated?

A

24-OH in liver by p450

– results in calcitroic acid

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59
Q

What 25OH-D level is associated with hypercalcemia? What is normal?

A

25OH = 750 nmol/L = 300 ng/mL

– normal is 250 nmol/L = 100 ng/mL

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60
Q

How does 25OH level affect calcitriol?

A

normally 1000x lower than calcitriol

– if excessive, can displace to cause excessive Vit. D

61
Q

What constitutes hypervitaminosis D?

A

elevated 25OH and calcitroic acid (no change in calcitriol!)

– but, hypercalcemia symptoms due to protein displacement

62
Q

How is 7-dehydrocholesterol turn into cholecalciferol?

A

UV light

    • stratum basale, spinosum
    • melanin slows formation
63
Q

How much sun is required for enough Vit. D?

A

10-15 mins/day on face/hands/arms

64
Q

What enzyme converts cholecalciferol to 25-OH?

A

CYP27C1, CYP2R1 in the liver

65
Q

How is 25-OH converted to 1,25-OH?

A

CYP27B1 (kidney)

– activated by PTH

66
Q

What diseases are caused by Vit. D deficiency?

A

1) rickets

2) osteomalacia

67
Q

What is rickets and what are sxs?

A

deficient bone mineralization in kids

    • secondary PTH increase
    • bowing of long bones and spine
68
Q

What is osteomalacia and what causes it??

A

deficient bone mineralization in adults
– secondary PTH increase
caused by nutritional deficiency or lack of sun exposure

69
Q

How does osteomalacia differ from osteoporosis?

A

bone formation, not just mineralization, is reduced in osteoporosis

70
Q

What are the clinical features of osteomalacia?

A

1) bone fx
2) bone pain, tenderness
3) muscle pain, weakness (esp. large proximal muscles)
4) 25-OH less than 8 ng/mL

71
Q

What are risk factors for nutritional rickets/osteomalacia?

A

1) dark skin
2) elderly
3) obese
4) low vit. D
5) north of SF/Philly

72
Q

What causes Type I Vit. D dependent rickets?

A

deficiency in 1a-hydroxylase

73
Q

What causes Type II Vit. D dependent rickets?

A

Vitamin D receptor (VDR) mutations

74
Q

How is type I vit. D dependent rickets treated?

A

calcitriol or Vit D ANALOGS (must already be activated)

75
Q

How is type II vit D dependent rickets treated?

A

parenteral Ca and/or hi-dose calcitriol or vit D analogs

76
Q

Vit. D deficiency is linked to these things:

A

1) all-cause and CV mortality
2) asthma and food/air allergy
3) T1DM risk
4) 3.4x more likely to die of heart failure (the more black, the worse off)
5) CV risk indicators: CRP, IL-6, cell adhesion, O2 stress

77
Q

Vit. D deficiency has one good benefit:

A

decreased Crohns risk

78
Q

Who should be tested for Vitamin D deficiency?

A

1) any symptoms or potential causes
2) obese
3) drugs that increase D metabolism
4) drugs that interfere with absorption
5) lots of melaning

79
Q

What drugs increase D metabolism?

A

antiepileptics: phenytoin, phenobarb, carbamazepine

80
Q

What drugs interfere with D absorption?

A
  • cholestyramine
  • orlistat
  • colestipol
81
Q

In what populations is D deficiency more common?

A

1) old men
2) worse with age, BMI, north, inactivity
- - supplements have little impact

82
Q

How does D3 relate to D2?

A

D3 3-10x more potent with longer duration of action

– no difference clinically

83
Q

RDA of Vit. D? What if deficient?

A

600 IU/day (800 if 70+ or overweight

– 4000 IU/day used to raise Vitamin D?

84
Q

Where is Vitamin D found? How much in a cup of milk?

A

1) fatty fish
2) mushrooms if UV exposed
3) eggs
4) yeast
5) fortified foods
- - 100 IU/dup milk

85
Q

What is osteopenia? How prevalent?

A

form of osteoporosis where BMD is 1-2.4 std dev away

– 50% of women over 50

86
Q

What is osteoporosis? how prevalent?

A

form of osteoporosis where BMD is 2.5+ std dev away

– 20% of women over 50

87
Q

What are the clinical findings in osteoporosis?

A

1) alkaline phosphatase slightly elevated

2) normal Ca, PO4, PTH

88
Q

Where are fractures most common in osteoporosis?

A

1) wrist
2) femur/hip
3) vertebra

89
Q

What are risk factors for osteoporosis?

A

1) 40+
2) white
3) thin and sedentary
4) premature postmenopause
5) poor diet, smoke, drink
6) f/h
7) long-term steroid use or low T

90
Q

Describe bone loss in osteoporosis?

A

E loss accelerates loss
– increases osteoclast activity
– decreases # of osteoblasts and osteocytes (the sensors)
lost trabecular and cortical bone

91
Q

Where is trabecular bone found?

A

spine, hip

92
Q

What are the Vit. D analogs?

A

good to go
– paricalcitol, oxacalcitriol
need 25 OH in liver
– alfacalcidiol, doxercalciferol

93
Q

When are Vit. D analogs indicated?

A

to suppress PTH release

to prevent renal osteodystrophy

94
Q

What are symptoms of hypercalcemia from Vit. D overdosing?

A

fatigue, weakness, HA
nausea
soft-tissue calcification
metallic taste

95
Q

How is the interindividual variation in Vit. D analog dosing managed?

A

monitoring
– Ca, PO4
avoid Mg antacids
– lead to hypermagnesia

96
Q

What is the indication for calcipotriene topical cream? What’s the efficacy like?

A

mild-moderate psoriasis

    • 40-50% effective
    • slightly more effective than steroids
    • less likely to relapse
97
Q

Describe the systemic effects of calcipotriene topical?

A

rapid metabolism and high VDR affinity = no systemic effects

98
Q

How is Calcipotriene used? What about pregnancy?

A

2 week onset, avoid face
– QD or BID
Cat C

99
Q

What are the risks associated with HRT?

A

1) thromboembolism + MI
2) slight breast cancer risk
3) uterine bleeding, breast pain
4) kidney stones

100
Q

How does HRT work for osteoporosis?

A

1) increases BMD 2-4% in 2 years

2) suppresses IL-6 to promote osteoclast apoptosis

101
Q

What does IL-6 do?

A

activates osteoclasts

102
Q

Should you recommend HRT for osteoporosis?

A

no;

but don’t D/C, because that leads to hip fx risk regardless of BP use

103
Q

When is Raloxifene indicated?

A

prevention and treatment of osteoporosis

– preferred for f/h of breast cancer

104
Q

What is the black box on raloxifene?

A

increased thromboembolism and stroke risk

105
Q

What are C/I’s of raloxifene?

A

1) concurrent HRT
2) pregnancy
3) f/h of thromboembolism
4) men (safety/efficacy not determined)

106
Q

What is the MoA of Raloxifene?

A

SERM

1) ER antagonist in endometrium, breast (reduced breast cancer risk)
2) ER agonist in bone
- - reduced vertebral fx w/ Ca + D
- - increases BMD 1-3% w/ 500mg Ca
- - decreases bone resorption in 3 months, lasts for 2 years
3) lowers LDL

107
Q

ADRs of raloxifene.

A

no significant

no effect on endometrium or bleeding

108
Q

Describe PK of raloxifene.

A

F= 2% (first pass)
protein-bound, not SHBG tho
t1/2 = 28-32h
hepatic

109
Q

Describe structure of bisphosphonates.

A
    • 2 PO4 with connecting O replaced by C
    • side chain amine can enhance activity
    • ring-incorporated amine is 10000x potent
110
Q

What are the ring-incorporated bisphosphonates?

A

risedronate

zoledrenate

111
Q

What is the MoA of bisphosphonates?

A

1) Ca chelators, incorporated into bone and osteoclasts
2) trigger osteoblast apoptosis
3) decrease hydroxyapatite solubility
4) increase BMD 8% over 2 years
5) anti-cancer effects?
6) reduce colorectal and breast cancer risk

112
Q

What are the simple BPs and what’s their MoA?

A

Etidronate

    • non-hydrolyzable ATP analogs
    • pro-apoptotic
113
Q

What are the amino BPs and what’s their MoA?

A

Alendronate, Risedronate, Zoledronate

    • inhibit isoprenoid synthesis for cholesterol
    • block prenylation of cell signaling
    • block enzymes, esp farnesyl synthase

– SECONDARY apoptosis

114
Q

What BPs are available orally?

A

1) Alendronate
2) Risedronate
3) Ibandronate
4) Etidronate
5) Tiludronate

115
Q

What BPs are available parenterally?

A

1) pamidronate

2) zoledronate

116
Q

What is the indication of BPs?

A

Paget’s & treatment/prevention of osteoporosis:
– alendronate, risedronate, ibandronate

Paget’s only
– Etidronate, Tiludronate

IV hypercalcemia of malignancy and oral-failure for osteoporosis

    • pamidronate (preferred for Paget’s)
    • zoledronate
117
Q

What is the oral BP dosing regimen?

A

1x daily, weekly (some monthly)

    • 30+ min before breakfast
    • 6-8 oz water
    • remain upright until eating
118
Q

What oral BPs can be taken once monthly?

A

ibrandronae

risedronate

119
Q

What are administration concerns with BPs?

A

1) Vit D
- - get to 33+ ng/mL prior
2) renal failure if too fast/too large dose in IV
- - 90+ mg

120
Q

Describe IV dosing BP regimens for the available drugs.

A

IV infusion w/ vigorous saline hydration due to insolubility and poor F

Pamidronate
4-24 hr infusion q3 month

Zoledronate
15 min infusion q 1 year

121
Q

Describe M and E for BPs.

A

Renal, no metabolism

122
Q

What are ADRs of bisphosphonates?

A

1) esophagitis, ulcers, bleeding
2) osteonecrosis of the jaw
3) atypical femur fractures if 5+ yrs use
4) mild-severe bone/joint/muscle pain

123
Q

When do the bone ADRs of bisphosphonates occur?

A

1) osteonecrosis of jaw following dental surgery
2) atypical femur fx after 5+ years
3) bone/joint/muscle pain (2 week onset, varies from day to 1 year)

124
Q

What are C/I’s to BPs?

A

esophageal disease

125
Q

How can esophagitis be avoided with BPs?

A

report dysphagia/heartburn

follow dosing regimen

126
Q

What are the indications for Forteo?

A

severe osteoporosis, including glucocorticoid-induced

127
Q

What is the MoA of Forteo/Terpiaratide?

A

active PTH segment

    • bone anabolic agent increases bone mass
    • INTERMITTENT administration promotes bone FORMATION
128
Q

When is Terpiaratide contraindicated?

A

bone cancer risk (Paget’s or radiation therapy)

129
Q

What are the ADRs of Terpiaratide and how are they managed?

A

1) osteosarcomas in rats
- - hyperPTH levels are lower in rats
2) transient orthostasis following injection

limit use to 2 years

130
Q

How is Terpiaratide administered?

A

SQ inj in thigh/abdomen daily

131
Q

What are the effects of Terpiaratide?

A

12% bone mass increase (lumbar, femoral neck)

    • 2x effective as alendronate
    • reduced fx incidence
    • coadmin with E or BP is advantageous
132
Q

What is the MoA of Denosumab?

A

OPG-mimetic, binds to RANKL of osteoblasts

– inhibits RANK-RANKL binding

133
Q

What are the effects of RANK-RANKL binding?

A

osteoblast precursor becomes activated

134
Q

OPG stands for…

A

osteoprotogerin

135
Q

How is OPG secreted?

A

by osteoblasts

– increased by estrogen

136
Q

What are the indications for Denosumab? MoA?

What are its effects?

A

OPG-mimetic mAb

    • indicated for severe osteoporosis
    • decreases vertebral and hip fx
137
Q

What are ADRs of Denosumab?

A

1) hypocalcemia (20%)
2) infection susceptibility (esp, endocarditis)
3) dermatitis
4) jaw osteonecrosis
5) bone/back/muscle pain

138
Q

How often is Denosumab administered?

A

SQ q6 months

139
Q

What are C/I’s of denosumab?

A

hypocalcemia

140
Q

What is UL of Vit. D supplementatino?

A

4000 IU/day (RDA is 600 IU/day)

141
Q

What was odanacatib’s MoA?

A

cathepsin K inhibitor

– prevented proteolytic activity of ostoclasts

142
Q

What was Ronacaleret’s MoA?

A

Anabolic calcilytic

– Ca receptor antagonists to cause PTH pulse release

143
Q

Describe effectiveness of Ca supplementation?

A

only effective if bottom 20th percentile Ca intake

    • does not reduce hip fx risk
    • might slow BMD loss
    • might slow post-menopausal bone loss if prophylactic admin
144
Q

What are the negative effects of Ca supplementation?

A
    • 20% risk increase of kidney stones

- - 20% risk increase of MI/stroke

145
Q

What is the most readily absorbed form of Ca?

A

Ca citrate

146
Q

What is the Ca supplementation range for post-menopausal women? Why not over 2g?

A

1 - 1.5 g/day

over 2g:

    • hypercalcemia, kidney stones
    • no further benefit
147
Q

What happens when Vit D intake exceeds 4 IU /day?

A

increased cancer risk

hypercalcemia

148
Q

What is the effective dose in osteoporosis for Ca and Vit D combined?

A

800 IU/d + 1 g/day

– Vit. D analogs may be 2x as effective as Vit. D

149
Q

What combo treatments are effective for osteoporosis?

A

1) BP + PTH cyclical therapy
- more effective than either alone

2) BP + PTH concurrent
- no better than PTH alone

PHS 933 (14 decks)

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