Bone Clinical Conditions Flashcards

1
Q

osteoporosis - defined

A

*decrease in bone mineral density or mass, resulting in decrease in bone strength and increased risk of fractures
*1 in 2 postmenopausal women will have a fracture; mortality 1 year after hip fracture ~20%

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2
Q

osteoporotic (fragility) fracture - defined

A

*fractures occurring in a setting of low-level or low-energy trauma, defined as falling from standing height or less
*hip, vertebral, forearm are most common
*pts with hip and vertebral fractures often never regain the same level of function, can lose independence, and can experience chronic pain (esp. with vertebral fractures)

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3
Q

pathogenesis of osteoporosis

A

*most common factor contributing to osteoporosis = estrogen deficiency
*other factors include: medications (STEROIDS), hyperparathyroidism, hyperthyroidism, tobacco/alcohol, no weight-bearing activity

note - peak bone mass is achieved around age 30 (due to nutrition, exercise, environment, and lifestyle factors)

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4
Q

osteoporosis - diagnosis/screening

A

*dx can be made based on imaging or clinical presentation (pt sustaining a fragility fracture)
*screening recommended for postmenopausal women > 65yo, or if postmenopausal with other risk factors
*DEXA scan is best imaging modality for diagnosis/screening

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5
Q

screening for osteoporosis: DEXA scan

A

*DEXA = dual energy x-ray absorptiometry, aka “bone density scan”
*reports T-scores at the lumbar spine, total hip, and femoral neck
*T-score: where you lie within the standard deviation of bone density for young, healthy patients of same gender
*Z-score: where you lie within the standard deviation of age-matched patients of the same gender
*osteopenia (low bone density) = T score: -1.0 to -2.5
*osteoporosis (porous bone that can lead to fractures) = T score: < -2.5

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6
Q

osteoporosis - treatment (general)

A

*goal = not to fracture
1. lifestyle modifications:
-vitamin D and calcium through diet/supplements
-weight bearing exercise: causes microfractures that then repair stronger
-balance training: PT trained in fall prevention/osteoporosis
-safe practices: remove slippery rugs, avoid high pile carpet, hand rails, nightlights, walker or cane if necessary, no dogs
2. pharmacotherapy

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7
Q

osteoporosis - pharmacotherapy (general)

A
  1. anti-resorptives: stop bone loss, freeze bones where they’re at
    ex: bisphosphonates, RANK ligand inhibitors
  2. anabolics: promote bone building
    ex: PTH analogues
  3. other: estrogen replacement, selective estrogen receptor modifiers
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8
Q

bisphosphonates - drug class, MOA, examples, uses

A

*drug class: anti-resorptive (prevent bone loss)
*MOA: bind to hydroxyapatite in the bone; inhibit osteoclasts from attaching to bone and from secreting protons; ultimately leads to apoptosis
*ex: aledronate, risedronate, zoledronate
*used for treatment of osteoporosis

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9
Q

RANK ligand inhibitor: denosumab - drug class, MOA, examples, uses

A

*drug class: anti-resorptive (prevent bone loss)
*MOA: binds to RANK-L (mimics osteoprotegerin)
*ex: denosumab
*used for treatment of osteoporosis

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10
Q

anti-resorptives for osteoporosis - ADEs

A

*prolonged use can result in ADEs:
-osteonecrosis of the jaw following dental procedures
-atypical femur fractures
-esophagitis (oral bisphosphonates)

recall: bisphosphonates (“-dronates”) and RANK-L inhibitors are examples of anti-resorptives

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11
Q

PTH analogues - drug class, MOA, examples, uses, ADEs

A

*drug class: anabolic agents (promote bone building)
*MOA: when bone is exposed to PTH in a pulsatile fashion, it can increase osteoblast activity
*ex: teriparatide, abaloparatide
*used for treatment of osteoporosis
*ADEs: orthostatic hypotension, transient hypercalcemia

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12
Q

osteoporosis vs. osteomalacia/rickets

A

1. osteoporosis = not enough bone; matrix and mass are lost but there is still mineralization
2. osteomalacia = undermineralized bone matrix; matrix is maintained but there is not enough mineralization
*both have low bone mineral density on DEXA but underlying cause (and treatment) differs

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13
Q

osteomalacia/rickets - defined

A

*defective mineralization of osteoid (osteomalacia) or cartilaginous growth plates (rickets, only in children)
*most commonly due to vitamin D deficiency; other causes include:
-X linked hypophosphatemia
-hypophosphatasia

note - osteomalacia is referred to as rickets in children; it is more severe; associated with bone deformity

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14
Q

rickets - physical exam findings

A

*pathologic bow legs (genu varum)
*beadlike costochondral junctions / swelling of rib cage at costochondral junctions (rachitic rosary)
*craniotabes (soft skull)

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15
Q

risk factors for vitamin D deficiency

A

*lack of sun exposure - dark skin, climate
*premature baby - not enough Vit D from mother
*mother with severe Vit D deficiency during pregnancy
*exclusive breastfeeding without supplementation (breast milk does not contain enough Vit D)

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16
Q

X-linked hypophosphatemia

A

*mutation of PHEX gene on X chromosome
*kidneys unable to reabsorb phosphorous → loss of phosphorous in urine
*often presents in childhood with features of rickets, but does not improve with Vit D (aka Vit D-resistant rickets)
*also DENTAL ISSUES: get recurrent dental abscesses and have poor enamel
*phosphorus is very low on lab work

17
Q

hypophosphatasia

A

*mutation resulting in dysfunction of Tissue Non-Specific Alkaline Phosphatase
*unable to combine calcium & phosphorous into hydroxyapatite crystals
*often present later in life with recurrent stress fractures and foot pain
*characteristic early loss of adult teeth, alveolar bone loss, poor enamel/dentin
*low Alk Phos on CMP

18
Q

osteopetrosis - overview

A

*petro = rock
*group of inherited disorders affecting osteoclast differentiation or function
*not enough bone resorption occurs, and as a result, too much bone is deposited, resulting in overly dense bones on X-ray / DEXA
*many defects involve osteoclasts’ ability to acidify the bones
*bones in osteopetrosis are paradoxically weak and prone to fracture
*can range from severe syndromes in infants/children, to incidentally discovered dense bones as an adult
*in most severe forms, bone marrow transplant can help

19
Q

osteogenesis imperfecta

A

*“brittle bone disease”
*defect in type 1 collagen production (COL1A1 or COL1A2)
*can vary from severe (numerous fractures from birth) to mild (stress fractures and osteoporosis on DEXA as an adult)
*classic findings: blue sclera, triangular facies

20
Q

Paget’s Disease / Osteitis Deformans - overview

A

*localized areas of excessive bone resorption and accelerated bone formation
*the formed bone is disorganized and weak as a result
*abnormal overactive osteoclasts, with osteoblasts trying to keep up
*occurs in older individuals, ALWAYS over age 50, most often Caucasians
*preference for axial skeleton, but can affect long bones as well

21
Q

Paget’s Disease / Osteitis Deformans - clinical findings & histology

A

*pelvis is most common site; other affected sites include skull, spine, limbs
*most are detected by elevated alkaline phosphatase on CMP
*histology: mosaic pattern of bone matrix
*can have increase in hat size due to skull growth
*diagnosed on X-ray or bone scintigraphy (Tc99m)

22
Q

Paget’s Disease / Osteitis Deformans - complications

A

*pain: arthritis, neuropathic
*hearing loss: loss of bone mineral density in cochlear capsule
*osteosarcoma
*high-output heart failure (lesions are very vascular)

23
Q

Paget’s Disease / Osteitis Deformans - treatment

A

*bisphosphonates - specifically, Zolendronate

24
Q

avascular necrosis (AVN) - overview

A

*blood flow disruption causes necrosis of bone
*most commonly occurs at the femoral head (MEDIAL femoral circumflex artery / watershed zone)
*as the femoral head necrotizes/fractures, osteoclasts begin resorption, but the femoral head becomes deformed, leading to mobility issues

25
Q

avascular necrosis (AVN) - causes

A

*long list of possible causes of blood flow disruption leading to AVN:
-TRAUMA
-systemic CORTICOSTEROIDS
-alcohol use
-SLE
-sickle cell
-Legg-Calve-Perthes disease (idiopathic pediatric AVN)

26
Q

avascular necrosis (AVN) - clinical presentation

A

*presents with significant pain, and often the pain is out of proportion to radiologic findings (which often leads to a delay in dx)
*deep, throbbing pain in groin
*may correlate with movement and weight bearing
*initially pain improves with rest, may eventually develop pain at rest

27
Q

avascular necrosis (AVN) - radiographic evaluation: CT

A

*findings: reactive sclerosis, subchondral collapse
*time to dx: months
*comments: poor sensitivity, OK specificity

28
Q

avascular necrosis (AVN) - radiographic evaluation: radionuclide imaging

A

*findings: decreased uptake early, increased uptake late
*time to dx: weeks
*comments: sensitivity good, specificity poor

29
Q

avascular necrosis (AVN) - radiographic evaluation: MRI

A

*findings: decreased signal in a segmental pattern
*time to dx: DAYS TO WEEKS (best test for dx)
*comments: sensitivity excellent, specificity good

30
Q

avascular necrosis (AVN) - best test for diagnosis

A

*MRI is the best

31
Q

avascular necrosis (AVN) - treatment

A
  1. conservative therapy:
    -weight bearing restrictions
    -treat underlying cause
    -pain management
  2. surgical therapy:
    -can try to prevent collapse: bone grafting, osteotomy
    -total hip arthroplasty (hip replacement)