Disorders of Bone Flashcards

1
Q

Osteoporosis is:

A

*The most common metabolic bone disease in the US
* Is a chronic and progressive disease
* Becomes clinically apparent once a fracture occurs

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2
Q

Osteoporosis

A

The imbalance of new bone formation and old bone resorption. For some they may not make enough new bone, for others have too
much reabsorption of old bone, and for others both may occur

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3
Q

Osteopenia

A

A condition of low bone density with a T-score below normal range from -1.0 to -2.5

Normal bone is defined by a T-score higher than -1.0

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4
Q

Osteoporosis T score & FRAX score

A

T-score of -2.5 or below in the spine, femoral neck, or total hip
Any fragility fracture
Osteopenia + FRAX score > 3% risk of hip fracture or > 20% risk of major osteoporotic
fracture
Severe Osteoporosis T-score -2.5 with fragility fracture or T-score -3.0
or greater

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5
Q

Who gets osteoporosis?

A
  • Postmenopausal women – most common
  • Men – over 65 or secondary cause
  • Premenopausal women – usually a secondary cause
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6
Q

Pathogenesis of Osteoporosis

A

Menopause
Cellular Senescence of osteoblasts and osteoclasts
Changes to Gut Microbiome
Sex steroid deficiency

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7
Q

Clinical Manifestations of Osteoporosis

A

No clinical manifestations until a fracture is present
Pain? – many with hip or feet pain assume they have osteoporosis, but
osteoporosis is painless until a fracture occurs
Osteomalacia causes bone pain

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8
Q

Common Fractures of Osteoporosis

A

Vertebral are the most common, 2/3 are asymptomatic

Hip Fracture affects up to 15% of women or 5% of men by age 80

Risk of hip fracture increases exponentially with age

Colles fracture (distal radius) most common after menopause

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9
Q

Diagnosis of Osteoporosis

A

Usually occurs in the presence of a fragility fracture

Fragility fractures occur from a fall at a standing height or less, without major trauma

Fragility fractures of the spine can occur spontaneously with minimal or no trauma

Fracture of the skull, cervical spine, hands, feet, and ankles are not associated with
fragility fractures

Stress fractures are not fragility fractures since these are due to repetitive injury

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10
Q

The WHO states that _____ is the standard test to diagnose osteoporosis in the absence of a fragility fracture.

A

BMD assessment by DXA

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11
Q

Dexa Scan

A

DXA gives an accurate and precise estimate of bone mineral density

Usually provides measurements of the spine and hips since these sites have
the greatest impact on patient’s health.

BMD has the highest predictive value for hip fracture

If pharmacologic therapy is initiated – BMD of the spine detects earlier
responses to therapy than hip BMD

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12
Q

T-score is the standard deviation difference between the bone mineral density
of a patient and a ______

A

young-adult reference population.

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13
Q

A T-score of_____ mean is
defined as osteoporosis.

A

2.5 standard deviation or more below the young-adult

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14
Q

A T-score of _____ mean is defined
as osteopenia.

A

1 to 2.4 stand deviation below the young-adult

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15
Q

Z-score is the comparison of _____

A

a patient’s bone mineral density with that of an age-matched population.

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16
Q

A Z-score of _____ should alert one to other coexisting problems that
can contribute to osteoporosis.

A

less than 2

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17
Q

coexisting problems that
can contribute to osteoporosis

A

Glucocorticoid therapy

Alcoholism

Hyperparathyroidism

Cushing’s Syndrome

Celiac Disease

Renal or Liver Disease

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18
Q

When to Screen for Osteoporosis

A

All women aged 65 or older should be screened

Postmenopausal women younger than age 65 with clinical risk factors should
be screened

Males >70 or 50-69 with osteoporosis risk factors

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19
Q

Risk Factors for osteoporosis

A

Low body weight, history of hip fracture/fragility fracture, tobacco use, glucocorticoid therapy, excessive alcohol intake, rheumatoid arthritis, chronic liver disease, inflammatory bowel disease

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20
Q

Laboratory Testing for Osteoporosis

A

Vitamin D, CBC, and BMP

Other tests if secondary causes are a concern:

TSH, PTH, Celiac panel, 24-hour urine for calcium, Cr measurement, urinary cortisol

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21
Q

Treatment for Osteoporosis

A

Oral Bisphosphonates are initial therapy of choice. Bisphosphonates inhibit resorption of bone by osteoclasts. They may have an effect on osteoblasts as well.

For postmenopausal women with osteoporosis (T-score < -2.5) or with a
history of a fragility fracture.

High-risk postmenopausal women with T-score between -1.0 to -2.5

Risk fracture is determined based on Fracture Risk assessment Tool (FRAX)

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22
Q

FRAX score

A

Gives the 10-year probability of developing a hip fracture or other major
osteoporotic fractures given BMD of the femoral neck and assessing for other
clinic risk factors for fracture.
High risk is 10-year probability of > 3% of hip fracture and >20% for major
osteoporotic fracture.

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23
Q

Bisphosphonates

A

Fosamax – alendronate, 70 mg weekly

Actonel – risedronate, 35 mg weekly or 150 mg monthly

Take on an empty stomach and remain upright for 30 to 60 minutes

Reclast – zoledronic acid, 5 mg once a year (tx), 5 mg every two years (prevention)

For those who cannot tolerate oral form or have impaired renal function

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24
Q

Bisphosphonates contraindications

A

Esophageal disorders (oral formulation)

Inability to follow dosing requirements

Chronic kidney disease, GFR <30

Bariatric Surgery – Roux-en-Y gastric bypass (oral formulation)

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25
Q

Bisphosphanate side effects

A

Bone pain

Digestive problems

Flu-like symptoms

Low calcium levels

Change in kidney function

Rash

Osteonecrosis

26
Q

RANKL Inhibitors MOA and indication

A

Prevent the development of osteoclasts. Preventing osteoclasts from breaking
down bone.

This is both a first line and second line agent in the treatment of Osteoporosis.
Used for those who are intolerant of both oral and IV bisphosphonates or
those with severe osteoporosis, T-score -3.5 or lower even in the absence of
fracture.

27
Q

RANKL Inhibitors

A

Prolia – denosumab, 60 mg SQ every 6 months

28
Q

RANKL Inhibitors contraindications

A

hypocalcemia

29
Q

RANKL Inhibitors side effecs

A

Hypocalcemia

Osteonecrosis

Bone fractures

Rash

Bone, joint, or muscle pain

Infections of the bladder, skin, or ear

Endocarditis

30
Q

Hormone Treatment for Osteoporosis

A

Estrogen is no longer considered a treatment due to risk factors of breast
cancer

Evista – raloxifene a Selective estrogen receptor modulator.

Forteo – teriparatide a recombinant parathyroid hormone

Tymlos – abaloparatide a synthetic analog of human parathyroid
hormone-related peptide

31
Q

Raloxifene

A

Primarily used for management of breast cancer. May be used for prevention
of osteoporosis. Inhibits bone resorption. Has shown greatest effects with
prevention of vertebral fractures, not so much with non-vertebral fractures.

32
Q

Forteo/Tymlos

A

Parathyroid hormone causes the body to form new bone and increase the
strength and density of existing bone. This medication actually stimulates
bone formation.

33
Q

Forte/Tymlos side effects

A

Usually associated with hypercalciuria

Pain

Weakness

Dizziness/Vertigo

Depression

Difficulty breathing

Nausea, vomiting, and constipation

Abdominal Pain

34
Q

Romosozumab name and MOA

A

Brand Name Evenity

Recently approved monoclonal antibody that inhibits sclerostin, increasing bone formation
and decreasing bone resorption

35
Q

International Society for Clinical Densitometry (ISCD) recommends retesting with
_____ after initiation of therapy

A

Dexa 1 to 2 years

36
Q

Bisphosphonates

A

Alendronate 15 (Vertebral) 91 (Hip)

Risendronate 20 (vertebral) 91 (Hip)

Zoledronic Acid 14 (vertebral) 91 (Hip)

37
Q

Osteonecrosis

A

A pathologic process that is associated with numerous etiologies and
treatments. When there has been obvious damage to bone vasculature or
injury to the bone or marrow, it is easy to identify a cause for the necrosis.
However, many patients suffer bone necrosis with no known mechanism for
the cause. The process is progressive and leads to joint destruction in months
to two years in most individuals.

38
Q

Osteonecrosis types

A

Avascular necrosis
Aseptic necrosis
Atraumatic necrosis
Ischemic necrosis

39
Q

Etiology of Osteonecrosis

A

Traumatic: Fracture, Dislocation, Minor trauma to the bone

Nontraumatic causes:
Corticosteroid use
Alcohol consumption
SLE
Chronic renal failure or hemodialysis
Pancreatitis
Pregnancy
Tobacco Use
HIV
Hyperuricemia

40
Q

Pathogenesis of Osteonecrosis

A

Most believe it is due to combined effects:

Genetic predisposition

Metabolic factors

Vascular damage

Increased intraosseous pressure

Mechanical stressors

41
Q

Clinical Manifestation of Osteonecrosis

A

Usually occurs in the femoral head

When other joints are involved, shoulder or knee, the hip should also be
evaluated.

Early detection is key to joint collapse and need for replacement

High index of suspicion for those patients on chronic corticosteroid use

Pain is the most common symptom

Groin pain

Pain upon weight-bearing or motion induced pain

Pain at rest (about 2/3) pain at night (1/3)

42
Q

Two main types of osteonecrosis

A

Idiopathic – Legg-Calve-Perthes Disease

Slipped capital femoral epiphysis – usually occurs in adolescents

43
Q

Diagnostic Evaluation of Osteonecrosis

A

Physical findings are usually nonspecific

Begin with plain radiograph of the hip. Anterior-posterior and frog leg lateral
views.

Usual findings are:

Crescent sign (pathognomonic) – evidence of subchondral collapse

Later joint space narrowing and degenerative changes of the acetabulum are visible

44
Q

_____ is the gold standard to diagnosis Osteonecrosis.

A

MRI without contrast agent

45
Q

Three approaches to therapy for osteonecrosis

A

Ultimate goal is to preserve the native joint
Non-operative management
Joint-preserving procedures
Joint Replacement

46
Q

Staging of Osteonecrosis

A

Stage 0 – All diagnostic studies normal and diagnosis by histology only.

Stage 1 – Plain radiographs and CT normal, scintigraph or MRI positive, and biopsy positive

Stage 2 – Radiographs positive but no collapse (no crescent sign)

Early Stage 3 – Crescent sign on the radiograph and/or flattening of articular surface of the
femoral head. No collapse.

Late Stage 3 – Collapse on the radiograph and/or flattening of articular surface of the femoral head.

Stage 4 – Joint space narrowing on plain radiography and acetabular involvement

47
Q

Non-operative Management of Osteonecrosis

A

Has been shown to be ineffective at stopping the progression of the disease
when located in the hip or shoulder

Includes:

Bed rest

Partial weight-bearing with crutches

Analgesics

Pharmacologic agents

48
Q

Pharmacologic Agents for osteonecrosis

A

Bisphosphonates

Statins – thought to reduce differentiation for marrow cells to fat cells

Anticoagulants – when due to thrombophilia

Electrical Stimulation

49
Q

Joint Preserving Procedures for osteonecrosis

A

Core Decompression

Osteotomy

Both have similar efficacy in early disease. But, osteotomy is better when there is collapse of the femoral head on initial diagnosis.

50
Q

Paget’s Disease

A

Also known as osteitis deformans. A focal disorder of bone metabolism
resulting in an accelerated rate of bone remodeling and overgrowth of bone.
May occur at a single site or multiple sites.

Usually affects the skull, spine, pelvis, and long bones of the lower
extremities

A disease of the osteoclast

51
Q

Pagets disease is a disease of the _____

A

osteoclast

52
Q

Pathogenesis of Paget’s Disease of Bone

A

A disease of the osteoclast

The osteoclast has an unusual appearance with too many nucleoli

Osteoclasts show hypersensitivity to vitamin D

Inheritance of Paget’s disease

The possibility of viral involvement in Paget’s disease continues to be investigated

53
Q

Clinical Manifestations of Paget’s Disease

A

Patients are usually asymptomatic

Symptoms occur due to overgrowth or deformity of the bone

Pain may be due to pagetic lesion, arthritis, nerve impingement, or tumor

The two main symptoms are pain and deformity

The pain is often described as a mild to moderate deep ache that persists
throughout the day and at rest. Some have pain at night as well.

54
Q

Clinical Manifestations of Paget’s Disease within the skull

A

Hearing loss, headaches, dizziness, jaw deformity or malocclusion

55
Q

Clinical Manifestations of Paget’s Disease within the spine and pelvis

A

Spinal stenosis, nerve compression, compression fracture

56
Q

Clinical Manifestations of Paget’s Disease in long bones

A

Bowing deformities and increased risk for fracture
Tumors

Primarily osteosarcoma

57
Q

Diagnosis of Paget’s Disease

A

Often found incidentally on lab or radiographs performed for other reasons

Elevated alkaline phosphatase

Normal calcium and phosphorus levels

X-ray will show osteolytic lesions, bone thickening, and enlarged bones
X-ray is the predominant diagnostic factor.

Bone Scintigraphy reveals increased uptake activity at focally active pagetic
sites

58
Q

Goal of treatment pagets disease

A

Ease pain

Decrease rate of bone remodeling towards normal

Slow disease progression

59
Q

Indications for Treatment for Paget’s Disease

A

Symptomatic patients

Asymptomatic patients with one of the following:

Biochemically active disease with increased Alkaline Phosphatase

Alkaline phosphatase 2 to 4 times normal

Normal alkaline phosphatase with abnormal bone scintigraphy at a site where complications
can occur

Planned surgery at an active pagetic site

60
Q

_____ are the drug of choice to treat Paget’s disease.

A

Bisphosphonates