MS: Disorders of Bone Flashcards

(49 cards)

1
Q

What are metabolic bone diseases?

A

osteoporosis and osteomalacia

bone is not strong as it should be

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2
Q

What is an infectious bone disease?

A

osteomyelitis

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3
Q

What is a viability of bone disease?

A

osteonecrosis

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4
Q

What is the definition of osteoporosis?

A

a multifactoral skeletal disorder that leads to decreased bone density and organization, which leads to reduced bone strength

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5
Q

What are osteoporosis and osteopenia based off of?

A

bone mineral density or BMD

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6
Q

What are cut off levels for BMD?

A

normal- within 1 SD

osteopenia- within 1-2.5 SD

osteoporosis- more than 2.5 SD

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7
Q

How many people are affected by osteoporosis?

A

10 million diagnosed, 18 mill undiagnosed

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8
Q

What are the non modifiable risk factors for osteoporosis?

A

age- over 50

female, genetics, caucasian/Northern European

long periods of immobilization

arthropometric- small stature, thin build

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9
Q

What are additional risk factors for osteopo?

A

hormonal- early menopause, absence of menses

dietary- low calcium, excess sodium, high caffine?

lifestyle- sedentary, smoking, alcohol

Concurrent illness- RA, CVA, parkinsons, spinal cord injury

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10
Q

What endocrine disorders can be risk factors?

A

hyperparathyroidism, hyperthyroidism, male hypogonadism

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11
Q

What medications can be risk factors for osteopo?

A

if taken longer than 6 months

corticosteroids- pt feels better but bone weak as it strips bone of Ca+

immunosuppressants, anticoagulants

antacids with aluminum- AL replaces Ca in bone

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12
Q

What organic compound is scaffold for bone?

A

collagen contributes to bones flexibility and tensile strength

resist twisting and stretching

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13
Q

What inorganic compound?

A

calcium phosphate gives bone hardness which resists compression

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14
Q

What two things equal bone strength?

A

bone quality and bone density (BMD)

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15
Q

What are prime years for bone deposition?

A

birth to 30

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16
Q

What two hormones are important in bone health

A

parathyroid hormone and Calcatonin

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17
Q

Why is PTH?

A

in early osteoporosis HYPER-PTH will remove Ca from bone in put into bloodstream

activates osteoclasts to break down bone

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18
Q

Why calcitonin?

A

coming from thyroid gland it will counteract PTH

leads to building of bone

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19
Q

What vitamin is important for bone growth?

A

Vitamin D

allows for reabsorption of Ca through small intestines

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20
Q

Why is Wolff’s law so important to osteoporosis prevention or healing?

A

bone grows and remodels in response

it is important as PT to walk a fine line between good stress and bad stress

21
Q

What two ways can stress be provided?

A

Gravity- weight bearing

muscle pull- activity or exercise

22
Q

So why does osteoporosis occur?

A
  1. low calcium and possibly magnesium intake
  2. decreased estrogen- decreases sensitivity of osteoclasts to PTH
  3. inactivity- wolff’s law
  4. smoking- tobacco has anti estrogen effect leading to bone resorption
  5. Diet high in phosphorus- same affect as AL
23
Q

What are clinical manifestations of osteoporosis?

A

often silent- major problem

usually discovered with fx ( femur, humerus, vertebrae, distal radius)

can cause radicular symptoms due to bone collaspe

24
Q

How to diagnose osteopo?

A

Bone density measures

  1. dual energy xray
  2. ultrasound
  3. CT scan- sees bone better than MRI and Xray
  4. lab tests- calcium levels, phosphate
25
What is an osteoporotic posture?
kyphosis in Thoracic region weight moves to anterior portion of IV discs bc thinner head moves forward to compensate with can shut off blood flow to brain (OTN)
26
How to manage osteoporosis?
reduce risk factors, nutrition is huge (calcium and magnesium)
27
PT management of osteopo?
education exercise- wolffs law balance focus on back extensors for posture
28
What type of medications can be used for osteopo?
1. bisphosphonates 2. hormone replacement therapy 3. calcitonin
29
What is osteomalacia and rickets?
disorder where there is insufficient mineralization of bone matrix, resulting from calcium or phosphate deficiency rickets- bowed femurs
30
Risk factors for osteomalacia and rickets?
lack of vitamin D this leads to hypocalcemia which will then activate increased PTH secretion taking Ca out of bone
31
Clinical Manifestations of osteomalacia and rickets?
bone pain and tenderness, softening of cranium in children, proximal myopathy (waddling gait due to weak glute med and max
32
Management of osteomalacia and rickets?
address cause, increased vitamin D and calcium PT- joint protection, progressive loads, positioning
33
What is osteomyelitis? (OM)
mostly a bacterial infection of bone- Staph aureus most common can be viral, parasitic or fungal but less common
34
What are two types of OM?
exogenous and endogenous (hematogenous)
35
What is exogenous OM?
occurs from outside of body (cut in skin, surgery, open fracture) soft tissue to bone
36
What is endogenous OM?
occurs from inside body and is harder to diagnose from ear infection etc.
37
What is acute OM?
looks very inflammed either exo or endo with infection lasting less than one month
38
What is chronic OM?
low level infection, usually an extension from acute case, last more than 4 weeks
39
Pathophysiology of OM?
if invading pathogen is in bone then there is an inflammation response in bone this can cause part of bone to be cut off from blood supply can lead to necrosis of bone if infection not caught and treated in time
40
Clinical manifestations of OM?
warmth, swelling, tenderness, delayed pain fever present in more endogenous OM infection will go from local to systemic effects as time goes on
41
Diagnosis of OM?
Lab values of WBC count, imagining
42
Treatment of OM?
acute- antibiotics chronic- cut bad part of bone out, hyberbaric chamber to help fight infection
43
PT implications?
universal precautions, clarify WB precautions, use vitals and lab results to guide exercise progression
44
What is osteonecrosis? (ON)
death of bony tissue as result of lack of blood supply common in 20-50 year olds
45
Common sites for ON?
``` femoral head ( Bo jackson) scaphoid, talar dome, lunate, proximal humerus ```
46
Pathogenesis of ON?
compromise of precarious blood supply causes flattening collapse of femoral head, common to be bilateral and with repeated traumas
47
Causes of ON?
idiopathic- genetic trauma- sports? associated with steroid use and high alcohol intake sickle cell anemia- cuts off blood flow to distal areas
48
Clinical manifestations of ON?
pain, loss of motion, painful or antalgic gait, degenerative changes
49
Intervention of ON?
activity modification surgical- create microtraumas or total joint replacement to increase blood flow to joint