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Therapeutics Y2 Sem 2 > Osteoporosis > Flashcards

Osteoporosis Flashcards

1
Q

Which form of calcium is preferred?

A

Dietary

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2
Q

If you exceed more then 2000mg/day what may occur?

A

– Nephrolithiasis
– Cardiovascular disease
– Dyspepsia
– Constipation

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3
Q

What is the RDA of Vitamin D for people under 70

A

600 IU

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4
Q

What is the RDA for vitamin D for people over 70

A

800 IU

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5
Q

TO meet RDA health canada recommends a supplement of?

A

400 IU

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6
Q

Which form of Vitamin D is preferred?

A

D3

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7
Q

What are the sources of D3

A
  • Fatty fish (salmon, rainbow trout)
  • Fortified foods (cow’s milk, plant-based beverages)
  • eggs

Sun exposure

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8
Q

How long after supplementation initiation of D3 should monitoring take place?

A

Usually dont monitor, but 3 months generally

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9
Q

What does Serum 25-Hydroxyvitamin level indicate?

A

Indicates Vitamin D levels

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10
Q

What is the “name” of Vitamin D3

A

Cholecalciferol

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11
Q

What is the name of Vitamin D2?

A

Ergocalciferol

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12
Q

What level of serum 25-hydroxyvitamin indicated high risk of deficiency?

A

<30 nmol/L - high risk of vitamin D deficiency

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13
Q

Is routine monitor essential for vitamin D monitoring?

A

No instead we focus on 400 across the board

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14
Q

What is the average half life of vitamin D?

A

15-20 days, hence the serum levels take a while to adjust (3mo)

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15
Q

What is the range for potential risk of inadequacy for bone health for 25-hydroxyvitamin?

A

30 to <50nmol/L

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16
Q

What is generally considered adequate for bone and overall health
in healthy individuals 25-hydroxyvitamin?

A

≥50 nmol/L

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17
Q

What is the level of 25-hydroxyvitamin level that may be linked to potential adverse effects

A

> 125 nmol/L

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18
Q

What are the antiresorptive classes of drugs with respect to osteoporosis drugs

A

A. Bisphosphonates
B. Denosumab
C. Raloxifene
D. Hormone Therapy

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19
Q

What are the anabolic medication(s) for Osteoporosis?

A

Teriparatide
Romosozumab

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20
Q

When should pharmacotherapy be recommended?

A

Intermediate Risk and High risk

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21
Q

What is the definition of intermediate risk? (10 year fracture risk or T score?)

A
  • 10-year fracture risk 15 – 19.9% OR
  • T-score < -2.5 (and age <70)
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22
Q

What is considered high risk (10 year fracture risk or T score)

A
  • 10-year fracture risk >20% OR
  • T-score < -2.5 (and age >70)
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23
Q

What is considered low risk (10 year fracture or T score)

A
  • 10-year fracture risk <15% OR T-score > -2.5
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24
Q

What are the recommended first line treatments for Intermediate and high risk individuals of osteoporosis?

A

– Bisphosphonates first line, denosumab second line

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25
Q

What is the classification of very high risk?

A

Recent severe vertebral fracture or >1 vertebral fracture
and T-score < -2.5

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26
Q

What are the recommended pharmacotherapies for individuals at very high risk?

A

– Teraparatide or Romosumab should be followed by a
bisphosphonate

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27
Q

What is the 5-10year follow up monitoring parameters?

A
  • 5 – 10 yr if the risk of major osteoporotic fracture is < 10%
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28
Q

What is the 5 year follow up monitoring parameters?

A
  • 5 yr if the risk of major osteoporotic fracture is 10%–15%
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29
Q

What is the 3 year follow up monitoring parameters?

A
  • 3 yr if the risk of major osteoporotic fracture is > 15%.
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30
Q

For those on pharmacotherapy what is the retesting window?

A

3 years

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31
Q

When would an individual require a shorter testing window?

A

for those with
secondary osteoporosis or new clinical risk factors, such as a
fracture

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32
Q

What is the mainstay therapy for osteoporosis?

A

Bisphosphonates

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33
Q

What are the indications of Bisphosphonates?

A

– Postmenopausal osteoporosis treatment and prevention
– Osteoporosis treatment in men
– Treatment and prevention of glucocorticoid-induced
osteoporosis
– Paget’s disease

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34
Q

What drugs are included under the drug class Bisphosphonates?

A

Alendronate
Risedronate
Zoledronic Acid

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35
Q

What is the MOA of Bisphosphonates?

A

Are analogues of pyrophosphate which allows for
incorporation into bone

– Binds strongly to hydroxyapatite undergoing remodeling

***– Inhibits osteoclast activity at site

– 2nd generation bisphosphonates additionally inhibit farnesyl
pyrophosphate synthase → osteoclast apoptosis

May prevent osteoblast apoptosis

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36
Q

What is the general dosing of alendronate?

A
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37
Q

What is the dosing of risedronate?

A
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38
Q

What is the dosing of zoledronic acid?

A
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39
Q

What is the caveate with bisphophonates?

A

– Extremely poor bioavailability – space from all medications

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40
Q

How should bisphosphonates be taken? (Immediate release?)

A

– Immediate-release tablets: empty stomach with 1 cup of
water, >30 minutes before food, drink and other medications.
Remain upright for 30 minutes.

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41
Q

How should the delayed release bisphosphonates be taken?

A

– Delayed-release tablets: take with 1 cup of liquid immediately
after breakfast. Remain upright for 30 minutes.

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42
Q

Why should we remain upright for 30 minutes post dosing?

A

May lead to side effects otherwise in the esophagus

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43
Q

With respect to Zoledronic acid how long should the infusion be?

A

– Zoledronic acid: once yearly IV infusion over 15 minutes

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44
Q

What is the general onset of Bisphosphonates?

A

– Weeks to observe bone changes
– Years to observe clinical benefit

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45
Q

What are the clinical benefits of Bisphosphonates?

A

After 3 years results in major reduction in breaks and fractures, compared to placebo

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46
Q

Are there many harms with the short term usage of bisphosphonates?

A

Not really, More so with long exposure

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47
Q

What are the common SE of bisphosphonates? (8)

A

– GI complaints
- Abdominal pain(7%),
Dyspepsia(2%),
Nausea(4%),
Diarrhea/Constipation (3%)
– Headache (2%)
– Dizziness (4%)
– Musculoskeletal pain (5%)

Hence remaining upright will help with GI side effects

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48
Q

What are the zoledronic acid side effects?

A
  • Infusion reaction – fever, myalgia, headache, flu-like
    symptoms, arthralgia
  • Free from GI issue
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49
Q

How might be avoid the side effects of oral bisphosphonates?

A

We can in some circumstances provide the doses in monthly intervals to only provide side effects once a month

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50
Q

What are the serious side effects of Bisphosphonates?

A

Osteonecrosis of the jaw
Atypical sub-trochanteric fractures
Severe musculoskeletal pain
Acute renal injury
Atrial fibrillation
Esophagitis, reflux and ulcers
Esophageal cancer

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51
Q

What is Osteonecrosis of the jaw?

A

– Complication associated with pain, swelling, exposed bone,
local infection and jaw fracture

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52
Q

How is osteonecrosis of the jaw caused?

A
  • Cancer patients; Immunocompromised; High dose; IV zoledronic acid;
    Invasive dental procedures; Steroid use; Smokers;Diabetes
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53
Q

What are the oral bisphosphonate risk? (Person year)

A

25 per 100 000 person years

Doubles with use >5 years

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54
Q

Which other healthcare provider should be aware of bisphosphonate therapy?

A
  • If invasive dental procedure planned, some would prefer delaying the
    initiation or holding bisphosphonate, but there is a lack of data in this
    area
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55
Q

What is Atypical sub-trochanteric fractures?

A

Changes in bone remodeling may inhibit ability of bone to
heal micro-trauma

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56
Q

What is the onset of atypical sub-trochanteric fractures?

A

Generally occurs 7 years into the treatment

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57
Q

Where does a sub trochanteric fracture occur?

A

Occurs not at the joint but away from it

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58
Q

What leads to an increase to atypical sub-trochanteric fractures?

A

– Risk increases with duration of exposure
– Risk returns to baseline once discontinued

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59
Q

If atypical sub-trochanteric fractures how would it present?

A

– May present as unusual thigh pain or dull ache
– Recommend further evaluation with a bone scan
– If atypical fracture identified: discontinue
bisphosphonate, use alternate therapy

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60
Q

Which drug is more associated with acute renal injury?

A

zoledronic acid

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61
Q

What is important to do prior to recieving a zoledronic acid infusion?

A

Must ensure adequate hydration prior to infusion

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62
Q

What populations should Bisphosphonates be cautioned in?

A

Pregnancy, Crosses the placenta and accumulates in fetal bones

No harms noted though (Only anmimal data)

Generally someone taking Bisphosphonates would not be pregnant

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63
Q

What medication conditions are Bisphosphonates be contraindicated? (5)

A

– Esophageal abnormalities
– Inability to stand/sit up for 30 minutes
– Hypocalcemia
– CrCl <35ml/min?

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64
Q

What is the duration of therapy for Bisphosphonates?

A

– Needs to be highly individualized
* Long bone half-life, less benefit with increased risks with long term use

  • “Drug holiday”= Temporary discontinuation after a certain time period

3-6 years

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65
Q

Why would we have a duration of therapy >6 years?

A

6 if hx of hip, vertebral or multiple nonvertebral fractures OR new or
ongoing risk factors for accelerated loss or fracture

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66
Q

What would be a means of extending therapy of bisphosphonates?

A

If in adequate response or ongoing concern for fracture during
therapy, extend or switch therapy, reassess for secondary causes
and seek referral to specialist

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67
Q

What is defined as an inadequate response of Bisphosphonates?

A

In adequate response should be considered when > 1 fracture or
substantial bone density decline (e.g., > 5%) despite adherence to tx
(typically >1 year)

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68
Q

What are someo f the key counselling points of Bisphosphonates?

A

Explain the benefits?

Importance of proper administration

Discuss importance of other factors for bone heatlh
Exercise, adequate calcium and vitamin D intake, lifestyle factors

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69
Q

What are some common side effects to counsel on with bisphosphonates?

A

mild heartburn/reflux, mild MSK pain

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70
Q

Take a moment to review the next slide about Bisphosphonates

A
71
Q

What is Prolia?

A

Denosumab

72
Q

What is the MOA of Denosumab?

A

Binds to RankL which will prevent the activation of osteoclasts

73
Q

What are the main roles of Denosumab?

A

– Cannot adhere to dosing requirements of oral
bisphosphonates

– Intolerance to oral bisphosphonates

– Severe renal impairment

74
Q

What is the onset of Denosumab?

A

– Markers of bone resorption markedly decreased within 3 d

– Maximal reduction within 1 month

75
Q

What is the duration of therapy with Denosumab?

A

– Indefinite treatment recommended:
* Benefits of denosumab rapidly lost upon discontinuation
* Fracture risk sharply increases

76
Q

What is the dosing administration of denosumab?

A

For all osteoporosis indications: 60mg administered once
every 6 months

77
Q

What is the renal impairment Restrictions of Denosumab?

A
  • Used down to CrCl 30ml/min
  • May be cautiously used between 15-30ml/min
  • Generally not recommended if <15ml/min or dialysis
78
Q

What are the common side effects of Denosumab?

A

– Very well tolerated
– Only a few side effects greater than placebo rates:
* Rash / eczema
* MSK pain

79
Q

What are the serious side effects of Denosumab?

A

Hypocalcemia
Osteonecrosis of Jaw
Atypical fractures
Immune system?
Rebound fracture risk upon discontinuation

80
Q

What populations are we worried about with individuals who use Prolia with respect to calcium

A

– If at risk patient (eg. renal impairment), ensure adequate
calcium levels prior to initiation

81
Q

What is the concern with effect on the immune system with respect to prolia?

A

Concern with increased infection risk, but this drug is not considered an immunosuppressive

May increase severe infection such as Cellulitis requiring
hospitalization, Diverticulitis, Pneumonia, Appendicitis

82
Q

Denosumab Rebound fracture risk upon discontinuation description

A

Just generally increased and any BMD gains are lost within 12-24 months

83
Q

What is important for monitoring when on prolia?

A

– Calcium levels if renal impairment
– Otherwise, as with bisphosphonates

84
Q

When is prolia contraindicated?

A

– Hypocalcemia
– Pregnancy or lactation

85
Q

What is the overall efficacy of denosumab/prolia?

A

– Observational data suggests similar fracture risk reduction vs.
bisphosphonates
– But a/e risk slightly higher

86
Q

What are important counseling points for this drug?

A

Adherence
Indefinite therapy generally
Calcium and Vit D intake

Watch for Severe dental pain, atypical fractures, infections

87
Q

What is the MOA of Raloxifene

A

Selective estrogen receptor modulator

Binds to estrogen receptor and acts as an agonist, Therefore decreasing bone resportion, increasing BMD,

Acts as an estrogen antagonist in breast and uterine tissues

88
Q

What role is raloxifene?

A

– 3rd line prevention option for postmenopausal women

– Patient who cannot tolerate bisphosphonates or denosumab

– Postmenopausal women with increased risk of invasive breast
cancer

89
Q

What is the onset of Raloxifene?

A

– Years to observe maximum BMD changes

– Typically lifelong therapy

– No residual benefit to bone after discontinuation

– BMD decreases similar to placebo upon discontinuation

90
Q

What is the dosing and administration of Raloxifene?

A
  • 60 mg once daily
  • Caution if CrCl <50ml/min
91
Q

What are the common side effects of Raloxifene?

A

– Flushing
– Flu-like symptoms
– Leg cramps
– Peripheral edema
– Increase in triglycerides

92
Q

What are the serious side effects that may occur when on raloxifene”

A

Venous thromboembolism
Stroke

93
Q

When is VTE risk highest when on raloxifene?

A

first 4 months of therapy

94
Q

What are the precautions of raloxifene?

A

– High risk of venous thromboembolism or stroke
– Hypertriglyceridemia
– Moderate-severe renal impairment

95
Q

What are the contraindications of Raloxifene?

A

– Pregnancy
– History of venous thromboembolisms

96
Q

What are the Drug interactions of Raloxifene?

A

– No CYP enzyme interactions
– Bile acid sequesterants decreases absorption of raloxifene
– Raloxifene decrease absorption of levothyroxine

97
Q

What should be monitored with raloxifene therapy?

A

– Lipid profile if at risk of hypertriglyceridemia
– Otherwise, as with bisphosphonates

98
Q

What is the efficacy data in women? (3)

A

– Less BMD increases than bisphosphonates and denosumab
– Does not reduce hip fractures
– Ineffective in premenopausal women

99
Q

What are the Non-bone benefits?

A

Decreases LDL, but does not decrease risk of CVD,
Reduces Breast cancer risk,
Possible higher risk of DVT/stroke
Does not cause endometrial hyperplasia
Lowers mortality if used in proper populaton

Reduces high risk of vertebral fractures and breast cancer (Not huip fractures)

100
Q

What are the counselling points of raloxifene?

A

– Raloxifene is typically longterm therapy
– Emphasize Calcium and Vitamin D intake
– Lifestyle modifications
– Common side effects: flushing, edema, cramps
– Watching for serious side effects:
* Signs and symptoms of a DVT
– Assess and be aware of risk factors for DVT

101
Q

What is the role of hormone therapy for osteoporosis?

A
  • Aimed at preventing menopausal associated bone loss
  • Additional benefit of treating menopausal symptoms
102
Q

What is the role of hormone therapy

A

– Women with persistent menopausal symptoms and cannot
tolerate bisphosphonates or denosumab

– For postmenopausal females aged < 60 yr or within 10 yr of who
prioritize alleviation of substantial menopausal symptoms, HRT can be
an alternative option to bisphosphonate therapy.

103
Q

What is the general duration of treatment of hromone therapy?–

A

– Maximum protection if used longer term and initiated
shortly after menopause

  • But HRT is not used indefinitely and should be reassessed q1-12
    months

– Likely accelerated bone loss after stopping estrogen

104
Q

What is the dosage and administration of hormone therapy?

A

– Lower doses of estrogen may effectively prevent bone loss
* Conjugated estrogen 0.3mg oral daily
* Micronized estradiol 0.5mg oral daily
* Estradiol patch (25ug to 50ug weekly)

105
Q

What are the safety concerns of hormone therapy?

A

– Increased endometrial / breast cancer risk
– Thromboembolism risk
– CHD risk increase
– Stroke risk
– Urinary incontinence

(Low frequencies)

106
Q

What is Teripartide?

A
  • More potent than bisphosphonates and denosumab
  • Expensive, non-formulary drug
107
Q

What is the role of teriparatide?

A

– For use in men or postmenopausal women with the highest
fracture risk:

  • Prior fragility fractures who continue to have fractures
    despite treatment
  • Very low BMD
  • BMD continues to decline on other treatments
108
Q

What is the MOA if Teriparatide?

A

– Is recombinant human parathyroid hormone

– Acts as an anabolic agent, similar to physiologic parathyroid
hormone

– Stimulates osteoblast function, increases calcium uptake

109
Q

What is the onset and duration of Teriparatide?

A

– Maximum approved duration of lifetime was 2 years – cancer
concern; but recently changed by FDA

110
Q

What is the dosage and administration of Teriparatide?

A

– Subcutaneous 20mcg once daily into thigh or abdomen x 24
months
– Available as a multidose, prefilled syringe

111
Q

What are the common side effects of teriparatide?

A

– Nausea
– Dizziness
– Leg cramps
– Orthostatic hypotension / syncope

112
Q

What are the serious side effects of Teriparatide?

A

Hypercalcemia,
Hypercalciuria
Osteosarcoma

113
Q

What is hypercalciuria?

A

Renal stones

114
Q

Who should we seek guidance from with respect to teriparatide?

A

Specialists

115
Q

Why is the duration of terparatide lower?

A

Osteosarcoma potential

116
Q

What should be monitored while on Teriparatide?

A

– Must check Ca, SCr, PO4 and ALP prior to initiation
– Calcium every 3-6 months thereafter

117
Q

What is the efficacy data of teriparatide?

A

– Significant reductions in vertebral and non-vertebral fractures,
Unknown benefit in hip fractures

– Additionally reduces back pain associated with osteoporosis

– May accelerate fracture healing time

118
Q

How do we discontinue teriparatide?

A

Transitioning to a bisphosphonate or denosumab will preserve
BMD gains

119
Q

What is the MOA of Romosozumab?

A

– humanized monoclonal antibody directed against sclerostin (an
osteocyte-derived glycoprotein that inhibits bone formation

– Acts as an anabolic agent and anticatabolic

120
Q

What is the onset and duration of therapy of romosozumab?

A

– Treatment duration is 12 months
– Gains in bone density are lost after stopping unless an
antiremodelling agent is started

121
Q

What is the role of Romosozumab?

A

For use in men or postmenopausal women with the highest
fracture risk: Fractures despite treatment. Very low BMD continues to decline on other treatment

122
Q

What is the dosage and administration of Romosozumab>

A

– Monthly SC injections (210 mg q month)

123
Q

What are the common side effects of Romosozumab?

A

– Musculoskeletal /joint discomfort
– headache
– Injection site pain/erythema

124
Q

What are the serious side effects of Romosozumab>

A

– Osteonecrosis of the Jaw
– Atypical fractures
– MI, stroke

125
Q

What are the precautions one should take before starting Romosozumab

A

– History of MI/stroke within the last year

126
Q

What is Romosozumab contraindicated?

A

– Pre-existing hypocalcemia
– Pregnancy or lactation

127
Q

What are the two different type of bone?

A

Cortical and Cancellous

128
Q

What is Cortical Bone?

A

80% of weight if the adult skeleton that forms the dense outershellWh

129
Q

What is Cancellous?

A

20% of weight of the adult skeleton and it is porous forms interior structures

130
Q

What are osteocalsts?

A
  • Builds bone through synthesis of collagen matrix
  • Groups of osteoblast units (osteoids) create hydroxyapatite
131
Q

What are osteoclasts?

A
  • Reabsorbs bone
  • Necessary for homeostasis of acid-base, calcium & phosphate
132
Q

What are osteocutes?

A

Regulate rate of bone mineralization

133
Q

What is oxidative stress?

A

The process of breakdown and resorption

134
Q

What is Osteoblast senescence?

A

Where we have the slowing down of development of Osteoblast

135
Q

What is autophagy

A

provide quality control of bone cells hence as we age it declines and bone building becomes less robust

136
Q

What occurs in decreases of sex steroid?

A

This is important for osteoclast activity as we see increases with lowered sex hormones

137
Q

What is the role of Calcium and vitamin D in bone formation?

A

Calcium required for mineralization
Vitamin D helps regulate calcium

138
Q

What occurs when we have low serum calcium levels/

A
139
Q

What occurs when have have high serum calcium levels?

A
140
Q

What occurs as we age?

A

Osteocute death accelerates,

141
Q

What does osteocyte death lead to>

A

– Increased surface remodeling
– replacement with weaker mineralized connective tissue
– disruption in repair signaling
– decrease in bone vascularity

142
Q

When does bone mass peak?

A

3rd decade of life and decreases by 0.5% per year

143
Q

Women will lose what % of trabecular and % of cortical bone?

A

Women will lose 50% of trabecular and 35% of cortical bone. Men
will lose 2/3 of these amounts

144
Q

What are the most common fractures?

A

Vertebral fractures most common (50%), followed by hip and
distal forearm

145
Q

How does Race increase risk of osteoporosis?

A

White and asian are at higher risk

146
Q

How does Calcium intake during growth increase risk of osteoporosis?

A

Low calcium means we have low bone growth

147
Q

How does menopause increase risk of osteoporosis?

A

Decrease in estrogen especially women who go through early menopause

148
Q

How does Family history increase risk of osteoporosis?

A

Parenteral hip fractures

149
Q

How does small stature increase risk of osteoporosis?

A

Low body weight and fine bone structure

150
Q

How does weight increase risk of osteoporosis?

A

Low body weight is a risk factor, and weightlessness

151
Q

How does Oophorectomy and hypogonadism increase risk of osteoporosis?

A

Delayed puberty leads to delayed bone formation

152
Q

How does cushings syndrome increase risk of osteoporosis?

A

Increases in steroid

153
Q

How does multiple myeloma increase risk of osteoporosis?

A

Just because it is a cancer

154
Q

How does malabsorption syndromes increase risk of osteoporosis?

A

Unable to absorb calcium

155
Q

How does heparin increase risk of osteoporosis?

A

Long term use 10-15% per year if used long term.

156
Q

what duration of therapy does glucocorticoid
therapy do we need to consider increase risk of osteoporosis?

A

– (>3 months cummul/yr; avg dose 7.5mg/d)

157
Q

What do the antiepileptics do with risk of osteoporosis?

A

They increase the the breakdown of vitamin D

158
Q

Which drugs in excess may lead to osteoporosis?

A

Thyroid supplement and vitamin A/retinoids excess

159
Q

What are some criteria for diagnosis of osteoporosis?

A

Vertebral compression fracture, hip fracture, or >1 fragility
fracture over 50 years of age is diagnostic

160
Q

What score helps us differentiate between osteoporosis and osteopenia?

A

BMD <-2.5, (Osteoporosis)

BMD -1 to -2.5 (Osteopenia)

161
Q

Who should be screened for osteoporosis?

A

Men and women >50 should begin routine assessment of risk
factors for osteoporosis and fracture

162
Q

After screening what are the years of re-screening recommended?

A

– If screened and low risk, reassess in 5 years
– If moderate risk (and not treating), reassess in 1-3 years

163
Q

What may be indicative osteoporosis when performing a physical?

A
164
Q

What are the labs usually ordered for osteoporosis diagnosis?

A
  • Calcium, corrected for albumin
  • Phosphate
  • Creatinine (eGFR)
  • Alkaline phosphatase
  • Thyroid stimulating hormone (TSH)
  • 25-hydroxy vitamin D (25-OH-D)
    – Should be measured after 3-4 months of adequate
    supplementation and should not be repeated if an optimal
    level ≥75 nmol/L is achieved.
  • Serum protein electrophoresis for patients with vertebral
    fractures
165
Q

If under 50 what score do we use?

A

Z-score which is catered for individuals within their age demographic

166
Q

What are the indications for BMD testing in adults?

A

– Age 50 – 64 with a previous osteoporotic-related fracture or > 2
clinical risk factors for fracture
– Age > 65 with 1 clinical risk factor
* See risk factors on next slide
– Age > 70

167
Q

What is secondary osteoporsis?

A

Generally secondary to a medication start

168
Q

What is the Caroc?

A

The one with the graph

169
Q

What is Frax

A

Incorporates more variables

170
Q

When should BMD be repeated?

A
171
Q

How much caffeine may cause increases in lower BMD rate?

A

> 4 cups per day

172
Q

What should be the average calcium intake for men?

A

– Men
* 51-70 years: 1000 mg calcium /day
* > 70 years: 1200 mg calcium /day

173
Q

What should be the average calcium intake for women?

A
  • > 50: 1200 mg calcium /day
174
Q
A

Therapeutics Y2 Sem 2 (17 decks)

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