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5 SKEL RAD A > #2 > Flashcards

#2 Flashcards

1
Q

What is TR (time repition) in MRI pulse sequence?

A

Time between each RF pulse, varies from 500msec to 4000msec

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2
Q

What is TE (time echo)?

A

Time each RF to listening for signal generated by patient varies from < 40msec to 100msec>

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3
Q

What determine the type of image created?

A

TR and TE times

Time Repetition

Time Echo

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4
Q

T1 in MRI (Time 1) main characteristics

A
  • Weighted image with short TR (500msec) and short TE (40msec)
  • Water is dark (CSF, edema, synovial fluid - NOT water in fat)
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5
Q

What does the pathology look like on a T1 film?

A

Usually dark on T1 due to edema (most pathologies have edema with water)

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6
Q

T2 MRI main characteristics:`

A

Weighted image - long TR (1500-4000msec)

  • Long TE (80-100msec)
  • Water is BRIGHT
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7
Q

T2 allows what?

A

System to go back to neutral state

  • Listened long enough for echo signal, so now we see water that looks brighter, and can now see edema
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8
Q

what color is bone marrow on T2 MRI?

A

Gray

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9
Q

What does fat look like on MRI?

A

It re-aligns quickly and appears as bright white on MRI

  • Fatty tumors, subcutaneous fat, yellow marrow
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10
Q

Contrast in MRI (signal intensity) is related to ____ ?

A

How tightly bound water is to time

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11
Q

Describe the Hydrogen properties in MRI contrast formation?

A

Hydrogen is more loosely bound in fat than water substance like CSF; re-aligns faster in fat than CSF

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12
Q

Spin-echo flip angle?

A

90 degrees

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13
Q

Gradient echo flip angle:

A

< 90 degrees

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14
Q

SE T1: (Fat color)

A
  • Fat image
    • Structures containing fat appear brighter/whiter (bone marrow, subcutaneous fat);
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15
Q

SE T1: (Water containing) -

A
  • Edema, neoplasm, inflammation, CSF, large amounts of Fe) appears DARK

* long TR, short TE

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16
Q

SE T1 is standard or not?

A

Standard

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17
Q

SE T2 first echo:

A

Proton density, good anatomical detail, has properties of both T1 and T2

  • Not done anymore
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18
Q

SE T2 second echo water image (loosely bound)?

A

Loosely bound water (neoplasms, edema, inflammation, healthy nucleus puposus, CSF) appear bright/white

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19
Q

What is the appearance/what does it detect of tightly bound or low water content on SE T2 second echo?

A

Ligaments, menisci, tendons, calcium, sclerosis, cortical bone or large amounts of Fe appear dark/black

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20
Q

Main charac. of SE T2 second echo?

A
  • Classic Image
  • Standard
  • MRI is the ONLY one that can see water in an IVD
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21
Q

FSE, fast spin echo:

A

Multiple echoes/TR, faster exam time, good in neuroimaging especially spine myelographic images

  • Very sensitive to EDEMA
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22
Q

Gradient Echo:

A

Fast MRI using short TR and TE with (flip angle)

  • >90 degrees
  • Provides a T2 image in less time, but does sacrifice some signal
    • Terms: GRE, GRASS, FLASH, FISP, MPGR, SPGR
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23
Q

Fat Suppression:

A

Technique that suppresses signal from fat, making small areas of pathology (often appearing bright because of edema) more evident and increasing the overall sensitivity of the exam, usually accomplished

(STIR)

  • VERY SENSITIVE TO WATER
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24
Q

Techniques providing function information:

A

Kinematic (kMRI) functional joint movement

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25
Q

MRA is used to ____ ?

A

image VASCULAR flow

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26
Q

Diffusion MRI does what?

A

Reveals disturbances of fluid restriction as seen in stroke

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27
Q

MR spectroscopy can display what?

A

Concentration of biochemical metabolites

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28
Q

Functional MRI (fMRI) does what?

A

Displays changes in oxygen concentration associated with neural activation, and provides high resolution imaging of the brain

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29
Q

What can upright MRI reveal?

A

Weight bearing (kMRI) can reveal pathologies that may be missed (canal stenosis, transitional motion, & disc lesion)

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30
Q

WHat is the most important clinical indication to use an MRI?

A

Suspicion of C, T, or L spine disc disease

*** MRI IS THE GOLD STANDARD OF DISC PATHOLOGY*

  • IS THERE A MASS?
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31
Q

Suspicion of what would be a good reason to send out for an MRI?

A

Central canal, foramina, or lateral recess stenosis

SPinal CORD pathology - MYELOMALACIA

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32
Q

What is a congenital disorder that would be of good use for an MRI?

A

Arnold Chiarimalformation (herniation of cerebellum through foramen magnum) syringomyelia

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33
Q

What would be some good things to evaluate using MRI?

A
  • Bone marrow infiltration
  • Primary bone neoplasms (benign and malignant)
  • Suspected failed back syndrome - Gd DTPA
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34
Q

What is a red flag, and would suggest getting an MRI?

A

FAILURE TO IMPROVE with TREATMENT

Persistent bone pain with malignant history

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35
Q

SHould a patient have painful scoliosis?

A

NO

80% is not painful

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36
Q

What’s the biggest MRI contraindication?

A

1st trimester pregnancy

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37
Q

What is something in the body that would cause a contraindication of MRI?

A

Ferromagnetic artifacts

  • aneurysm clips, intraocular foreign bodies (welders), permanent eyeliner, subcutaneous metal shards and shrapnel
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38
Q

Cardiac Pacemakers/defibrallators/implanted neurotransmitters (TENS) unit would mark a red flag for what?

A

MRI

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39
Q

T1 film

A
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40
Q

T2 film

A
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41
Q

WHen does bone marrow change on bone pathology?

A

FIRST

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42
Q

STIR VS FAT SUPRESSION

A
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43
Q

MRI cervical spine, sagittal T1 and T2

A
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44
Q

pic of herniated discs

A
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45
Q

disc herniations can be:

A

Soft discs, herniation without surrounding osteophytosis, can be acute, subacute or chronic

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46
Q

Herniated disc

A
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47
Q

Contained central protrusion

A
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48
Q

What would Cauda Equina Syndrome present as?

A
  1. _Saddle Parestesia or anesthesia**_
  2. _Bowel and Bladder distrubances**_
  3. Lower extremity motor weakness and sensory deficits
  4. Reduced or absent lower external reflexes
  5. Low back pain
  6. Uni or bi lateral sciatica

_***IMMEDIATE REFERRAL****_

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49
Q

What is this?

A

Synovial Cyst

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50
Q

What are characteristics of synovial cyst?

A

Can have them with no symptoms, no way to see on plain film, and complication of facet DJD

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51
Q

What are the main points of an annular tear?

A
  • POSTERIOR anular fibers
  • clincially significant
  • Pain generator due to nociceptors
  • CAN MANAGE chiropractically
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52
Q

Clinical Significance of Modic Changes:

A

Type 1: Represents marrow edema. Painful! Associated with an acute process. Converts to

Type 2: Represents fatty degneration of subchondral marrow. Associated with a chronic process

Type 3: Correlate with extensive bony sclerosis on plain radiographs

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53
Q

Describe fatty infiltration of spinal musculature:

A
  • Semispinalis cervicis or lumbar multifidus
  • Strongly associated with LBP
  • Is an indicator for spine stabilization exercises
  • Responds favorably to neuromusculoskeletal rehab and therapy exercises
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54
Q

WHat is Tarlov’s Cyst?

A
  • Perineural cyst - fluid filled meningeal dilation of the nerve root sheath
  • up to 9% of pop.
  • Usually asymptomatic
    • 20% do have symptoms –> if it expands
  • May need drainage
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55
Q

Levoscoliosis =

A

Wrong way

Convex Left > 15 degrees may indicate interspinal pathology

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56
Q

What is pictured?

A

Arnold Chiari

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57
Q

What is a descriptive term for decreased bone density?

A

Osteopenia

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58
Q

Is, “osteopenia” a precise diagnosis?

A

NO

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59
Q

When does osteopenia occur?

A

When bone resporption exceeds bone formation regardless of specific pathogenesis

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60
Q

What are the major causes of diffuse osteopenia:

A
  • Osteoporosis
  • Osteomalacia/Rickets
  • Hyperparathyroidism
  • Neoplasm
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61
Q

What is an osteoprogenitor cell?

A

Originates from the marrow stem cells, develop into osteoblasts

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62
Q

What is an osteoblast?

A

Produces osteoid (soft material) 90-95% collagen, remainder is ground substance (mucopolysaccharides); numerous and large in growing skeleton

  • Decrease in # and size at maturity
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63
Q

What is an osteocyte?

A

Arise from osteoblasts that become entrapped in their own osteoid, maintain the integrity of the bone around them

MATURE BONE CELLS

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64
Q

What are inactive cells?

A

inacive/dormant osteoblasts

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65
Q

What are osteoclasts?

A

Bone resorptive cells, derived from hematopoetic monocyte lineage

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66
Q

for normal bone density, Osteoblastic activity should =

A

Osteoclastic activity

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67
Q

what is the process in getting to a mature Osteocyte?

A
  1. Marrow stem cell
  2. Osteoblast - produces osteoid
  3. Osteoid is mineralized by Calcium Hydroxyapatite
  4. Osteocyte is formed
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68
Q

bone resorption

A
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69
Q

Water is responsible for _____ % of wet weight of bone?

A

20

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70
Q

Cellular components make up a ____ fraction of bone weight?

A

TINY

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71
Q

What is the remaining organic matrix/osteoid?

A
  • (90% collagen) and 10% mucopolysaccharides account for 30% by dry weight
  • The inorganic material accounts for 70% of osseous tissue by dry weight
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72
Q

Bone quality ratio aka

A

*MATRIX vs. MINERAL RATIO****

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73
Q

Organic matrix/osteoid is _____ , remaining _______ is what?

A
  1. 90% collagen
  2. Remaining 10% is mucopolysaccharide material (ground substance)
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74
Q

Inorganic material exists as what?

A

Calcium Hydroxyapatite

  • It is destributed regularly along the length of collagen fibrils surrounded by ground substance
  • Ca10(PO4)6OH2
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75
Q

What does the skeleton do in relation to calcium?

A

Contains 99% of the body’s calcium and serves as the reservoir for maintenance of serum calcium; normally 10mg/dL ****

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76
Q

70% of plasma calcium is believed to be maintained by?

A

A continuous exchange of calcium ions between bone and extracellular fluid

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77
Q

What is defined as producing an inward flux of calcium from extracellular fluid?

A

Hypocalcemia

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78
Q

if 70% of plasma calcium is an exchange between bone and ECF, whats the remaining 30%?

A

Mediated by the actions of the parathyroid hormone and other hormones

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79
Q

The process of resorption and formation occur ______ ?

A

Continuosuly in normal bone and are related to the function of osteoclasts and osteoblasts, whose function must remain in balance

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80
Q

Osteoclasts exists where?

A

In pits on bone surface called resorption bays or Howship’s lacuae

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81
Q

What are the osteoclasts main function?

A

Secrete acid to breakdown hydroxyapatite, and collagenase to break down osteoid

  • May secrete substances to attract and promote function of osteoblasts
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82
Q

What is the key production of osteoblasts?

A

Produce osteoid/matrix which is then mineralized by calcium hydroxyapatite

  • Scurvy can actually impede the osteoblasts ability to produce osteoid/matrix
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83
Q

What is the substance capable of directly or indirectly stimulating osteoclasts or increasing formation of new osteoclasts?

A

PTH, active metabolites of Vit. D, Prostaglandin E2, Thyroid hormone, Heparin

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84
Q

Is calcitonin inhibiting or excitatory when it comes to osteoclasts?

A

Inhibitory

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85
Q

What is osteoporosis characterized as?

A

Qualitatively normal, but quantitatively deficient bone

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86
Q

What is the MOST FREQUENT BONE DISEASE IN HUMANS?

A

OSTEOPOROSIS

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87
Q

What is associated with decreasing osteoblastic function with age?

A

Osteoporosis

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88
Q

When is osteoporosis radiographically significant?

A

when 30-50% bone loss (spine closer to 50)

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89
Q

Where is osteoporosis predominant?

A

Axial Skeleton

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90
Q

Is osteoporosis bone softening?

A

NO

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91
Q

What is Osteomalacia defined as?

A

Pathology, inadequate mineralization of osteoid

Immature cortical and spongy bone (osteomalacia) and interruption of orderly development and mineralization of physis (rickets)

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92
Q

What is related to the deficiency of calcium, Vit D, or phosphorus?

A

Osteomalacia

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93
Q

Is Osteomalacia a quality or quantity problem?

A

Quality, its bone SOFTENING

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94
Q

pic of Vit D process in body

A
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95
Q

What are the deficiencies of osteomalacia related to?

A
  1. Dietary
  2. Liver Disease
  3. GI disease
  4. RENAL DISEASE*** (with loss of phosphorus)
  5. Sunlight def.
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96
Q

Osteoid is a soft material and gains it’s hardness by adding what?

A

Calcium and minerals

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97
Q

Hyperparathyroidism accelerates what?

A

Osteoclastic activity

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98
Q

Describe primary HPT:

A

Increased production of parathormone by glands, usually benign adenoma = HYPERCALCEMIA

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99
Q

Describe Secondary HPT:

A

Abnormal stimulation of glands by sustained hypocalcemia: Chronic renal disease, GI malsorption,

  • serum calcium - low, low normal and phosphorus is elevated
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100
Q

Describe Tertiary HPT:

A

In long standing HPT, parathyroid function may become autonomous, can be related to ectopic tissue, paraneoplastic syndrome, may have hypercalcemia

  • Can be from external stimulus, ext production of parathyroid hormone via tumor
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101
Q

What is the parathormone function (main):

A

ULTIMATELY INCREASE SERUM CALCIUM

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102
Q

Osteoblastic inhibition would be a characteristic of what?

A

Parathormone function

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103
Q

If serum calcium drops, what does parathormone do?

A

Parathyroid hormone increases serum calcium, it is a positive feedback

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104
Q

What are the 3 features in regards to the function of Parathyroid hormone function?

A
  • Renal Conservation of calcium and inhibiton of phosphate resorption
  • Renal stimulation of 1-alpha-hydroxylase causing increase formation of 1,25 Vit. D
  • Indirect effect on GI absorption of calcium
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105
Q

What is calcitonin secreted by?

A

The human parafollicular or C cells of the the human thyroid gland

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106
Q

What is calcitonin controlled by?

A

Serum calcium levels

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107
Q

What does calcitonin inhibit?

A

Bone calcium resorption by decreasing osteoclastic function and may lead to hypocalcemia and hypophosphatemia

  • also inhibits GI calcium abosorption
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108
Q

What does calcitonin stimulate?

A

Osteoblastic activity

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109
Q

In regards to the kidney, what does calcitonin inhibit?

A

Renal tubular cell reabsorption of calcium

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110
Q

What is used to treat pagets disease?

A

Calcitonin, inhibits clastic activity

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111
Q

Where is osteoporosis most prevelant?

A

AXIAL SKELETON:

  • Vertebral column
  • Pelvis
  • Ribs
  • Sternum
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112
Q

What is the major cause of osteoporosis?

A

AGE RELATED CONDITIONS: Senile and postmenopausal states (by far most common and most often seen in clinical practice)

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113
Q

Describe the role of medications in regards to Osteoporosis:

A

Steroids (many pts; chronic use end up w/bone density issues), heparin

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114
Q

What are some endocrine states that would affect osteoporosis?

A

HPT, hyperthyroidism, Cushing’s, acromegaly, pregnancy, diabetes mellitus, hypogonadism

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115
Q

What are some deficiency states that could affect osteoporosis?

A

SCURVY***, malnutrition, calcium deficiency

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116
Q

Major causes of generalized osteoporosis:

A
  • Age related
  • medications
  • endocrine states
  • deficiency states
  • alcoholism
  • chronic liver disease
  • anemic states
  • osteogenesis imperfecta
  • idiopathic condition
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117
Q

What would be the reason for localized osteoporosis?

A

Immobilization and disuse (fracture healing)

  • Some degree of bone atrophy occurs; sustained Hyperemia in bone (too much blood flow in bone marrow) overstimulates osteoclasts
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118
Q

What is a VERY important reason for localized osteoporosis?

A

_Complex regional pain syndrome ***_

Sympathetically mediated pain syndrome, RSDS

had FOOSH injury 3-4 months ago

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119
Q

What is a type of osteoporosis that would cause pain?

A

Transient regional (localized) osteoporosis

  • Transient (temporary) osteoporosis of the hip (TOH)
    • Commonly seen in men
    • Regional Migratory Osteoporosis
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120
Q

what is pictured?

A

Complex Regional Pain Syndrome (CRPS) /Sympathetic Mediated Pain Syndrome (SMPS)

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121
Q

Describe the key points of Complex Regional Pain Syndrome (CRPS) / Sympathetic Mediated Pain Syndrome (SMPS):

A
  • Typically follows trauma
  • VERY PAINFUL (suicidal type of pain)
  • Just around joints (r wrist; can also be rheumatoid, lupus, scleroderma, etc)

*** Common in WRIST

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122
Q

Transient Osteoporosis of the hip usually involves?

A

Healthy middle aged men, rarely women, but almost exclusively during the 3rd trimester of pregnancy or the immediate postpartum period

  • Usually SINGLE HIP
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123
Q

Transient Osteoporosis of the hip is characterized by what?

A

Acute disabling pain in the hip and functional disability without a history of previous trauma

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124
Q

Histological exam of transient osteoporosis of the hip reveals what?

A

Focal areas of thin and disconnected bone trabeculae covered by osteoid and active osteoblasts, active osteocytes in the lacunae

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125
Q

what is this

A

TOH

Transient osteoporosis of the hip

  • should clear up on its own
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126
Q

What are the key features of regional migratory osteoporosis?

A

RMO was discovered by Duncan et al

  • Occurs in 5-41%
  • It may occur in different or same joint in an unpredictable time interval after the onset of the first symptoms
    • Can stay in left knee, jump to R knee, or diff joint
  • The joint nearest to the diseased one is the next to be involved
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127
Q

?

A

RMO of the ankle

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128
Q

What is general slowing down of osteoblastic activity?

A

Osteoporosis

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129
Q

What is the etiology of osteoporosis?

A

multifactorial

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130
Q

When does the gradual loss of bone occur with osteoporosis?

A

Beginning in the 5th or 6th decade in men and 4th decade in women

  • 40’s and 50’s in men
  • 30’s in women
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131
Q

> 50 y/o men lose bone at ______ ?

A

.4 % a year

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132
Q

> 35 y.o. women lose at _________ ?

A

.75-1% increasing to 2-3% post menopause

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133
Q

There is a significant loss of ____ bone in women who have osteoporosis?

A

Cortical

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134
Q

What disease may cause “fish vertebrae”?

A

Osteoporosis

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135
Q

Pic of osteoporosis byproducts

A
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136
Q

What type of bone is lost in osteoporosis?

A

Horizontal trabecular

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137
Q

When does the anterior wedge of osteoporosis normally occur?

A

Post Traumatic - Typically get with axial load trauma on normal bone. Edge anterior b/c vertebrae posterior is stronger

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138
Q

What is the worst sign when dealing with osteoporosis?

A

Losing posterior and ant. body height, commonly via Mets and Mult Myeloma

  • MOST COMMON PATHOLOGICAL COLLAPSE
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139
Q

What can cause fish vertebrae?

A

Biconcave (both endplate compression)

- Osteoporosis

- Mult Myeloma

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140
Q
A
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141
Q

where are common fracture sites of osteoporosis?

A
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142
Q

what could this be?

A

Osteoporosis, but could be multiple myeloma or Mets

  • Normally would have white cortex, grey medullary cavity, and very gray soft tissue
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143
Q
A
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144
Q

what is this?

A
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145
Q

Hemangioma is what?

A

Benign bone tumor

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146
Q

?

A
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147
Q

?

A
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148
Q

Percutaneous Verebroplasty fixes what? (pic)

A
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149
Q
A

Due to percutaneous vertebroplasty, ant. wedge fracture possibly

(liquid cement shows up extremely white on X ray)

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150
Q

When does an insufficiency fracture occur?

A

When the elastic strength of the bones is not sufficient to withstand normal physiologic stress (type of stress fracture)

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151
Q

Simplistic def. of insufficiency fracture?

A

normal stress on abnormal bone

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152
Q

What is a major cause of an insufficiency fx?

A

Osteoporosis

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153
Q

Characteristically, what does an insufficiency fracture involve?

A

Weight-bearing bones of the lower extremity, often bilateral

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154
Q

What are 2 main places of insuf. fx?

A

Sacrum and Pubic Rami

(MICRO fractures in trabeculae)

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155
Q
A

Insufficiency fracture

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156
Q

?

A

Honda sign!

Insufficiency fx. (associated with osteoporosis)

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157
Q

What are the osteoporosis risk factors?

A
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158
Q

Osteoporosis is not _____

A

a direct calcium deficiency, but an osteoblastic deficiency

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159
Q

Calcium deficiency =

A

Osteomalacia

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160
Q

What is the most sensitive meausure of bone mineral density?

A

DEXA/DXA Scan

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161
Q

DEXA/DXA Scan is dual ______

A

X-ray Absorptiometry (DEXA/DXA)

162
Q

What is the MAJOR feature of a DEXA/DXA scan?

A

Very sensitive scan to detect early bone (mineral) density loss (only thing we need to know about DEXA)

163
Q

What is an aka for Hypovitaminosis C?

A

Scurvy/Barlow’s Disease

164
Q

What is Hypovitaminosis C associated with?

A

Long term deficiency of Vit C, seen predominantly in infants

  • Children have specific and unique findings
  • 90-95% of osteoid is collagen
    • If it can’t produce, they slow down bone production
165
Q

What is Vit C essential for?

A

The formation of collagen, osteoid and endothelial linings - bleeding gums, muscles, soft tissues, cutaneous petechiae and hematuria

166
Q

What is the main “Hallmark” in regards to hypovitaminosis (Scurvy/Barlow’s disease)?

A

Spontaneous hemorrhage due to capillary fragility - bleeding in subperiosteum: Bone PAIN

167
Q

Osteopenia is defined as:

A

Decreased osteoblastic function

168
Q

T/F, you will have osteopenia with Hypovitaminosis C?

169
Q

An adult with Hypovitaminosis will present as similar to what disease?

A

Osteoporosis

170
Q

What is subject to bleeding in Hypovitaminosis C?

A

Capillary Fragility is why you are susceptible to bleeding

171
Q

Is Scurvy a mineralization disorder?

172
Q

What is the major sign in kids in regards to Scurvy

A

Trummerfield sign, band of radiolucency

173
Q

Major radiographic signs of Scurvy?

174
Q

What is a dense bright Zone of provisional mineralization (ZPM)?

A

White line of Frankel

175
Q

What is a dense cortical margin of epiphysis with radiolucent center?

A

Wimberger’s Ring

176
Q

What is an irregular metaphyseal margin?

A

Corner (angle sign)

177
Q

What is a Pelken’s sign?

A

Bony protuberances at margin of ZPM

178
Q

_What is Trummerfield/Scorbutic zone? ***_

A

Radiolucent metaphyseal band directly beneath ZPM, due to defective bone formation –> LEUKEMIA LINES

  • failure of normal bone formation
180
Q

3 big signs of Scurvy in CHILDREN?

A
  1. Frankel
  2. Trummerfield
  3. Subperiosteal Hemorrhage
181
Q

Define the name of Hypovitaminosis in adults and kids -

A

Kid = “Rickets”

Adult = “Osteomalacia”

182
Q

What is the major takeaway from Osteomalacia?

A

It is based on a QUALITY deficiency, and there is an abundance of unmineralized osteoid, thus causing BONE SOFTENING

183
Q

How does osteomalacia clinically present itself?

A

Muscle weakness and bone pain on palation

  • Deformities - Pelvis (sacrum could sink down into pelvis), femur (bows laterally), tibia, and spine (prone to compression fractures or scoliosis)
184
Q

What are the main bone softening disorders?

A

Osteomalacia, Paget’s, and Fibrous Dysplasia

185
Q

Describe the bone ratio in osteomalacia :

A

The ratio of mineral to osteoid is defective; not enough mineral to put on osteoid; Too much unmineralized osteoid; BONE SOFTENING = bowing deformities

186
Q

Osteomalacia can a lot of times occur due to:

A

Hypophasphotemia (renal disease), but can also be due to not enough Ca+

187
Q

What are the radiographic features of Osteomalacia?

A
  • Osteopenia
  • Coarsened Trabecular pattern
  • Pseudofractures
  • Loss of cortical definition
188
Q

Describe pseudofractures and their importance in bone softening disorders:

A

First described by Looser in 1930 and later by Milkman in 1934, they are defined as

  • Little band of unmineralized osteoid
189
Q

Pseudo fracures are only seen when?

A

BONE SOFTENING DISEASES

190
Q

What are deformities of Osteomalacia?

A

Weight bearing bones; triradiate pelvis, acetabular protrusion, femoral and tibial bowing, kyphoscoliosis and endplate concavity, bell-shaped thorax

191
Q

what are common locations for osteomalacia?

A

Femur, ribs, and pelvic rami

192
Q

?

195
Q

What is a seam of unmineralized osteoid?

A

Pseudofracture

196
Q

Where do pseudofractures occur?

A

Happens in ribs, boney pelvis, femur, but NOT SPINE

197
Q

Pseudofractures almost always ____ ?

A

Perpendicular to cortex

198
Q

Describe polyostotic Fibrous Dysplasia:

A

Not monostotic –> polyostotic = multiple bones

199
Q

What are the akas of Pseudofractures?

A

Looser’s lines, Milkman’s syndrome, increment fractures, osteoid seams, umbauzonen ***

200
Q

What is pediatric osteomalacia with same etiologies, may begin as early as 6-12 months?

201
Q

What is rickets defined as?

A

Renal tubular loss of phosphorus, not cured by administration of Vit D (resistant/refractory rickets) aka renal rickets (kidney losing phosphorus)

202
Q

Renal Rickets + Secondary HPT =

A

Renal Osteodystrophy

203
Q

What does Rickets clinically present with?

A

Muscle tetany, irritability, weakness, delayed bone development, small stature and bone deformities/bowing

  • Enlargement around growth plates (trumpeting) and rib ends (rachitic rosary)
204
Q

What is the most common cause of Rickets/Osteomalacia?****

A

KIDNEY DISEASE

205
Q

?

206
Q

Rickets presents with loss of _____ ?

A

Zone of Proliferative Mineralization

207
Q

Describe the mineral process of Rickets:

A

There is a mineral deficiency (calcium or phosphorus) - loss of ZPM & cant make bone after it

  • BONE SOFTENS
  • CANT MAKE NEW BONE IF YOU DONT HAVE A ZONE
208
Q

What is the “hallmark” finding of Rickets?

A

Loss of ZPM (easier to see in big bones)

209
Q

?

A

Trumpeting, associated with Rickets

210
Q

?

A

Richatic Rosary

211
Q

What is X linked Hypophosphatemia?

A

Genetically transmitted, X linked dominant trait

  • Renal tubular loss of phosphate, part of Fanconi Syndrome –> Resistant to Vit D administration (Not lack of Vit D intake)
212
Q

What develops from X-linked Hypophosphatemia?

A

Childhood rickets develops, and patients are short, bowlegged and stocky

213
Q

What happens in the adult skeleton from X-linked Hypophosphatemia?

A

Develops osteosclerosis and enthesopathic paravertebral ligament. Ossification may resemble AS or DISH

214
Q

What is a clinical finding of X-linked Hypophosphatemia?

A

Decreased pedicle length, lumbar spinal stenosis

215
Q

X-linked Hypophosphatemia is a type of ____

216
Q

X-linked Hypophosphatemia is a ______ of Osteomalacia?

A

Subtype (the phosphorus side of it)

217
Q

What is Hypophosphatasia?

A

Rare genetic disorder related to low serum alkaline phosphatase production by osteoblasts

  • This helps link collagen to osteoid (linkage disorder)
218
Q

What “resembles rickets”?

A

HypophosphaTASIA

219
Q

What are some clinical findings of Hypophosphatasia?

A

Peculiar radiolucent metaphyseal defects extending from the growth plate into the metaphysis

220
Q

What are some changes that occur due to Hyperparathyroidism HPT?

A

Histopathologic changes consist of osteoclastic and osteocytic bone resporption with fibrous tissue replacement (osteoitis fibrosa cystica, Recklinghausen’s disease of bone)

221
Q

What are some major bone changes that occur from Hyperparathyroidism?******

A

Osteopenia, accentuated trabecular pattern, loss of cortical definition, brown tumors and the radiographic/pathologic hallmark - subperiosteal bone resporption

  • Classic HPT finding = Pathognomonic
222
Q

What body part do we need to see if we suspect HPT?

223
Q

is HPT a bone softening disorder?

224
Q

What is actually occuring in HPT?

A

Clasts are working faster than blasts, the clasts take away both calcium and phosphorus (QUALITY prob.)

225
Q

HPT female/male:

A

3:1 female:male, and

typical patient is 30-50 y.o.

226
Q

Symptoms are usually related to ______ during HPT?

A

bone, renal, or GI

227
Q

Physical indicators of HPT?

A

Weakness (hypercalcemia), lethargy, polydipsia, polyuria, renal calculi, and bone tenderness

228
Q

Kidney loses calcium on a ______ in HPT?

A

Concentration basis

229
Q

Parathyroid Hormone general overview:

A
  • Osteoclastic and osteocytic stimulation –> Increase calcium from bone
  • Osteoblastic inhibition
  • Renal Conservation of calcium and inhibition of Phosphate resorption
  • Renal stimulation of 1-a-hydroxylase causing increase formation of 1,25 Vit D
  • Indirect effect on GI absorption of calcium
230
Q

Parathyroid hormone increases what?

A

Calcium and phosphorus out of the bone

231
Q

Describe Primary HPT:

A

Direct gland involvment: adenoma 90%, carcinoma, hyperplasia, or ectopic tumors (3o).

  • Renal function = Normal –> HYPERCALCEMIA and HYPOPHOSPHATEMIA
232
Q

Describe secondary HPT:

A

Sustained gland function from persistant hypocalcemia predominantly from RENAL DISEASE with loss of calcium and decrease Vit. D formation,

  • less likely GI malsorption –> low normal or HYPOCALCEMIA & HYPERPHOSPHATEMIA.
233
Q

In Secondary HPT, renal disease with hypocalcemia is associated with:

A

Soft tissue and vascular calcification and osteomalacia - Renal Osteodystrophy/uremic osteopathy (not rare)

234
Q

In secondary HPT, renal disease + Hypocalcemia =

A

Soft tissue & Vascular Calcification & Osteomalacia**

235
Q

Describe Tertiary HPT:

A

With chronic renal failure or malabsorption and long standing 2o who develop autonomous pathological function and HYPERCALCEMIA & HYPOPHOSPHATEMIA

  • “can be due to corrected secondary HPT”
236
Q

HPT bone changes:

A

Diffuse Osteopenia and Localized Bone Resorption

237
Q

In HPT, Subperiosteal Bone Resorption can be _____ ?

A

Seen in many locations but hand, middle phalanges radial aspect 2nd-4th digits pathognomonic ***** TEST

238
Q

What happens with cortical bone during HPT?

A

Intracortical bone resorption within Haversion Canals linear striations

239
Q

Describe Endosteal bone resorption within HPT?

A

Typically hands and other findings (know endosteal bone resorption happens with HPT)

240
Q

Describe Subchondral bone resorption when it comes to HPT:

A

Common, SI, SC, AC, SP (symphysis pubis), and DV junction, can mimic inflammatory joint disease. SI joint sacroiliitis

DRA (dialysis related arthropathy)

DRSA (dialysis related spondyloarthropathy)

* Typically related to secondary HPT

241
Q

Describe Trabecular bone resorption in HPT bone changes:

A

Diffuse in skeleton, very prominent in cranium, causes very granular appearance of diploic space “salt and pepper” or “pepper pot skull”

242
Q

Describe Subligamentous Bone resorption of HPT bone changes:

A

At entheses; trochanters, ischial and humeral tuberosities, elbow, calcaneus, inferior distal end of clavicle

243
Q

Describe brown tumor/osteoclastoma/Giant cell tumor in regards to HPT bone changes:

A

Localized cyst like bone resorption containing fibrous tissue, giant cells and hemorrhages, “brown” color Histopathologic

244
Q

Describe Acro-osteolysis in regards to HPT bone changes:

A

Distal tuft resorption, seen with many other conditions

245
Q

?

A

Subperiosteal bone resorption associated with HPT

  • Acro-osteolysis –> TUFTS (tuft resorption)
246
Q
A

Subperiosteal bone resorption

NOT pathognomonic in this location

250
Q

?

A

Salt and pepper skull

255
Q

What is common in Primary HPT?

A

Brown Tumor and Chondrocalcinosis

256
Q

What is rare in primary HPT?

A

Osteosclerosis and Periostitis

257
Q

What is common in Secondary HPT?

A

Osteosclerosis and Periostitis

258
Q

What is rare in Secondary HPT?

A

Brown tumor and Chondrocalcinosis

259
Q

Additional findings of renal osteodystrophy are observed _____ ?

A

In association with Secondary HPT, including rickets, osteomalacia, and soft tissue and vascular calcification

260
Q

What is renal osteodystrophy?

A

Renal disease leading to secondary HPT will push patient into rickets/osteomalacia if hypocalcemic

  • Renal Disease + Secondary HPT = RICKETS
261
Q

What is termed renal osteodystrophy/uremic osteopathy?

A

Comibnation of secondary HPT + osteomalacia + soft tissue and vascular calcification

262
Q

Osteosclerosis is more commonly seen in _____ ?

A

RO and predominates in the axial skeleton (rugger jersey spine)

264
Q

DRSA =

A

Dialysis Related Spondylo-Arthropathy

265
Q

Renal failure patients treated with hemodialysis will have _____

A

Resolution of RO bone changes

266
Q

Dialysis resolves what?

A

RO bone changes

267
Q

Normally after 3-5 years of dialysis, what happens?

A

Cervical spine involved is MC

268
Q

What occurs during DRSA?

A

Narrowing of disc height, subchondral cysts, endplate erosions, collapse, erosions of contiguous vertebral bodies, facet erosion, spondylolisthesis, peridiscal calcification****

  • Calcification in subcutaneous regions
269
Q

Hypoparathyroidism is acquired or genetic?

270
Q

Deficiency of Parathyroid hormone is most commonly from what?

A

Excision or trauma to the parathyroid gland during thyroidectomies

271
Q

What are the 2 main things that occur during Hypoparathyroidism?

A

HYPOCALCEMIA & HYPERPHOSPHATEMIA

272
Q

What are some underlying physical changes of Hypoparathyroidism?

A

Bone osteosclerosis (mc), thickening of cranial vault bones, calcification of basal ganglia, rarely choroid plexus and cerebellum***

test

273
Q

What is happneing within the spine during Hypoparathyroidism?

A

Rare spine changes of pain, stiffness with calcification of ALL and posterior spinal ligaments, resembling DISH

274
Q

Is hypoparathyroidism acquired? expand on it:

A

YES it is acquired

  • Has Ca and P levels like Secondary HPT
  • Osteosclerosis like Secondary HPT
275
Q

?

A

Hypoparathyroidism

276
Q

PHP stands for what?

A

Pseudohypoparathyroidism

277
Q

PHP is an ___

A

End - organ resistance to parathormone

278
Q

PHP main features:

A

X-linked dominant and more common in females

  • MAJOR DIFFERENCE:Genetic, unlike hypoparathyroidism (which is acquired)
    • End/Target-Organ restance to PTH
279
Q

In PHP, what conditions would you see?

A

Hypocalcemia, hyperphosphatemia and basal ganglia & soft tissue calcification

280
Q

What is another major difference between PHP and HPT (hypo)?

A

Characteristic somatotype:

Short stature, obesity, round face, and brachydactyly (short fingers and toes)

  • Tend to be mentally challenged

*** all above is PHP

281
Q

What does PPHP stand for?

A

Pseudopseudohypoparathyroidism

282
Q

Describe PPHP:

A

Normocalcemic form of PHP, same somatotype

  • Also GENETIC
  • Do not have a problem with PTH –> “false PHP”
283
Q

What is the major difference between PHP and PPHP?

A

PPHP is NORMOCALCEMIA & NORMOPHOSPHATEMIA

  • Also has Basal Ganglia & Soft tissue calcification
  • Both may occur in the same family –> STOP PROCREATING
284
Q

Neoplasm is described as what?

A

Widespread marrow infiltration with cancer cells (inhibits osteoblastic activity) and results in loss of bone density

285
Q

Neoplasm is often accompanied with what?

A

Other radiographic or clinical findings (punched out)

286
Q

Patients will be ____ in regards to a neoplasm?

287
Q

What is associated with Neoplasm?

A

Multiple Myeloma, leukemia in children, and lymphoma (non-Hodgkins) can cause diffuse osteopenia

288
Q

Osteoporosis review:

A

Reduced bone mass of normal quality; related to imbalance between osteoclastic and osteoblastic activity favoring osteoclastic resorption; serum calcium, phosphorus and alkaline phosphatase typically normal; generalized osteopenia with fractures frequent

289
Q

Osteomalacia/Rickets review:

A

Related to deficiency of calcium, Vit D or phosphorus with multitude of causes including dietary deficiency, malabsorption, liver disease and renal disease; abundance of unmineralized osteoid resulting in bone softening disease and osteopenia including pseudofractures; rickets in the child with radiographic findings including loss of zone of provisional calcification

290
Q

Hypophasphatemia Review:

A

Renal disease acquired or genetic resulting in Ph deficiency and leading to osteomalacia/rickets (Vit D resistant osteomalacia/rickets)

291
Q

Hyperparathyroidism Review:

A
  • Primary - Related to parathyroid tumor or hyperplasia
  • Secondary - Related to renal disease or GI malabsorption
  • Tertiary - Related to ectopic autonomous functioning tissue or chronic secondary HPT

Radiographic findings of HPT related to increased osteoclastic activity with localized resorption including subperiosteal at middle phalanges pathognomonic

292
Q

Hypoparathyroidism Review:

A

Acquired related to accidental removal/damge to parathyroid glands during thyroid surgery, radiation, infection, carcinoma; hypocalcemia and hyperphosphatemia; radiographic finding is osteosclerosis as well as calvarial thickening and hypoplastic dentition, may be associated with extensive calcification of spinal ligaments and basal ganglia calcification

293
Q

Pseudohypoparathyroidism PHP review:

A

PHP is a genetic disorder related to end organ resistance to parathyroid hromone with normal parathyroid hormone production; characteristic somatotype of short stature, obesity, round face, brachydactyly, abnormal dentition and mental retardation;

Radiographic findings: similar to hypoparathyroidism; hypocalcemia and hyperphosphatemia

294
Q

Pseudopseudohypoparathyroidism PPHP review:

A

Genetic disorder similar to PHP and frequently a sibling of; is the normal calcium and phosphorus version of PHP; produce and respond to parathyroid hormone; same somatotype and radiographic findings

295
Q

Hypophosphatemia Review:

A

Congenital abnormality related to decreased alkaline phosphatase production by osteoblasts resulting in findings similar to rickets; radiolucent metaphyseal defects

296
Q

Hypovitaminosis C Scurvy review:

A

Deficiency of Vit C resulting in decreased abilitiy to produce collagen with inadequate osteoid formation; is a form of osteoporosis; adult form identical to adult osteoporosis; childhood form changes at the bone and are characteristic with proper names

297
Q

Arthritic disorder affects 1 in ____

298
Q

What are the most prevelant types of arthritis:

A
  • DJD
  • RA
  • SLE = systemic lupus
  • PA = psoriatic arthritis
  • AS = Ankylosing spondylitis
  • Gout
  • JRA = Juvenile rheumatoid arthritis
  • PSS = Progressive Systemic Sclerosis (scleroderma)
299
Q

What remains the primary method of initial imaging in arthritic disorder?

A

The noncontrast radiograph

300
Q

What are synovial joints characterized by?

A

Joint capsule:

  • 2 layers: Outer fibrous & Inner Synovial
  • Articular/Hyaline cartilage, synovial membrane, synovial fluid, (anatomical) joint space (not radiographic space)
301
Q

Describe the synovial membrane:

A

Loose vascular connective tissue - secretes synovial fluid (blood plasma and mucoid substance) lubrication and nutrition; “bare area” –> major role in inflammatory

(no role in degnerative)

302
Q

Describe the articular cartilage:

A

Hyaline is most common intraarticular cartilage and consists of chondrocytes embedded in a matrix of collagen fibrils and ground substance (mucopolysaccharide chondroitin sulfate concentrated in water)

303
Q

Describe the subchondral bone plate:

A

Thin cortex and underlying cancellous trabeculae, abundant blood supply

304
Q

What is the bare area?

A

NO periosteum, no articular cartilage; btwn end of synovial membrane & articular cartilage

305
Q

What are the 2 branches of arthritis?

A

Mono and Poly arthritis

306
Q

What are the categories under monarthritis?

A
  • Traumatic
  • Infectious
  • Crystal induced (gout and psedo gout)
  • Rheumatoid
307
Q

What are the 4 categories under polyarthritis?

A
  1. Inflammatory Joint Disease
  2. Degenerative Joint Disease
  3. Metabolic Deposition Disease
  4. Hematological Disease
308
Q

What is under inflammatory Joint disease?

A

Painful Soft tissue swelling of joints

309
Q

What are the 2 subtypes of Inflammatory joint disease?

310
Q

What are under Rheumatoid types?

311
Q

What are under Rheumatoid Variants?

312
Q

What is under DJD?

313
Q

What goes under Metabolic Deposition disease?

314
Q

What goes under Hematological?

315
Q

Describe the Important Arthritis Chart as best you can:

316
Q

What are the only 2 types of arthritis in human beings?

A

Mechanical or Inflammatory

317
Q

Mechanical arthritis =

A

Osteophytes

318
Q

Inflammatory arthritis =

319
Q

All arthritis destroys what?

A

Articular Cartilage

320
Q

Gout starts where?

A

Single joint, nomally the big toe

321
Q

Metabolic Deposition Disease =

A

Accumulation of normal or abnormal metabolic biproducts in or around the joint

322
Q

Trauma: Bleed into joint —>

A

Inflammatory

323
Q

Describe the Rheumatoid factor in Polyarthritis:

A

IgM is reactive to IgG (serological blood test)

  • Rheumatoid types are autoimmune diseases, antigen-antibody reactions, IgM reacting to altered IgG
324
Q

What is the major key point of Rheumatoid?***

A

It is the ONLY one that is PRIMARY to the JOINT –> Main target is SYNOVIAL MEMBRANE —> Worst of the group

325
Q

HLA-B27 (+) / Rheumatoid (-) —>

A

Rheumatoid Variants (P.A.I.R)

326
Q

HLA-B27 (-) / Rheumatoid (+) –>

A

Rheumatoid Types (R.S.P.D.T/V.)

327
Q

In lupus, what is the “Secondary” target?

A

Synovial Membrane

328
Q

What is Reiter’s Syndrome aka?

A

Reactive Arthritis Syndrome

329
Q

Describe Psoriatic Arthritis:

A

Very Specific and common inflammatory, non-rheumatoid arthritis

330
Q

What can IBD patients develop?

A

Ankylosing Spondylitis that can act like rheumatoid arthritis

331
Q

What is “Primary” DJD?

A

(common joints; Spine) nothing else has happened to the joint

332
Q

What is the secondary DJD?

A

Joints involved where we don’t expect to see it, unpredictable joints (uncommon joints, any joint), and clinically we know something else has happened to that joint

333
Q

Bony enlargements come from _____ ?

A

Bony enlargements from DJD come from osteophytes

334
Q

Describe Metabolic Deposition Disease:

A

Accumulation of normal (uric acid –> Gout) or abnormal (amyloids –> amyloidosis)

Metabolic byproducts –> Creating “lumps and bumps” around a joint

335
Q

What is amyloid?

A

Abnormal Proteinacious material/metabolic byproduct

336
Q

In Metabolic Deposition Disease, describe uric acid:

A

Normal metabolic byproduct

MBB has amyloid and uric acid : gout

337
Q

All arthritis _______

A

Enlarges the joint

338
Q

THERE ARE ONLY 2 TYPES of ARTHRITIS IN HUMANS:

A

Joint Degenerates or Joint is INFLAMED

339
Q

What are the 4 things that inflame joints?

A
  1. Immune complexes
  2. Metabolic Byproducts
  3. Organisms
  4. Blood (Toxic/Inflammatory if outside of vascular system)
340
Q

All arthritis does one thing, what is it?

A

Desroys articular cartilage and narrows radiographic joint space

  • Radiographic joint space = bone-bone
341
Q

DJD is _______ whereas Inflammatory is _______?

A

DJD is mechanical stress across a joint (macro/microtrauma) and Inflammatory is chemical (typical lytic enzymes, collagenase –> Produced by synovial membrane due to being inflammed)

342
Q

Inflammation is to ______ what _______ are to Degeneration ? *****

A

EROSION, OSTEOPHYTES

343
Q

Relative frequency of arthritis, Weekly:

344
Q

Relative frequency of Arthritis, Monthly:

A

CPPD, RA, AS, PA, SCM (Joint mice)- Synovial Chondrometaplasia, DISH, OCI (OsteitisCondens)

345
Q

Relative Frequency of Arthritis, Yearly:

A

Gout, Infection RAS, Lupus, PSS (scleroderma)

346
Q

What are the ABCS of Anatomic - Radiographic Correlation?

A
  • A - Articular Alignment, adjacent bony relationships across the joint
  • B - Bone, for joint evaluation, focus on the subchondral bone
  • C - Cartilage, not visible but the space occupied is
    • All arthritic diseases destroy articular cartilage and narrow the radiographic joint space
  • S - Soft Tissues, periarticular soft tissues often enlarged by bone or soft tissue swelling
347
Q

Describe DJD:

A
  • Progressive, non-inflammatory joint disease characterized by degenerative pathologic changes to articular cartilage and its related components
    • Non-Uniform loss of joint space, Asymmetrical, Osteophytes, Mechanical Problem
348
Q

What are some findings of DJD?

A

Small joints of hands and feet as well as large weight bearing joint typically involved (spine also involved)

349
Q

Describe the etiology of DJD:

A

Exact etiology unkown, although pathologic sequence of change is well known

350
Q

What is the most common encountered Joint Disorder?

351
Q

Describe X ray findings and clinical findings:

A
  • Great disparity between radiographic findings and clinical presentation in any given patient
    • Just because X ray looks bad, it doesn’t mean the patient has symptoms
352
Q

Describe the symptoms of DJD:

A
  • Onset insidious with episodic moderate aching pain, stiffness and periarticular soft tissue swelling
    • Can be via inflammatory around joint, but NOT IN THE JOINT
353
Q

Stifness with prolonged inactivity, gradually decreasing with activity and returning with fatigue describes symptoms of ____

354
Q

Repetitive movements or recurrent chronic injury, first thoughts would be ____

355
Q

What lab values would DJD present with?

A

NORMAL LABS, no inflammatory or serological markers

356
Q

Periarticular swelling, soft tissue inflammatory episode (increase pain) -

357
Q

Once DJD is initiated it is :

A

IRREVERSIBLE (can be slowed down though)

358
Q

what is the actual process of DJD ?

A

“Trigger” is likely from abnormal mechanical forces across the joint that injure or kill chondrocytes with resulting loss of the surrounding matrix/chondroitin sulfate and destruction of collagen fibers

  • Macrotrauma
  • Rep. microtrauma
359
Q

Where does DJD begin?

A

At cartilage surface and extends toward subchondral bone - progressive asymmetrical joint space narrowing **

360
Q

Describe the subchondral findings of DJD:

A
  • Subchondral new bone due to cartilage loss (OSTEOPHYTES), subchondral synovial fluid intrusion - GEODES (subchondral cysts –> related to arthritic disease –> classic in DJD)
    • Subchondral Sclerosis (ONLY DJD, NOT in inflammatory)
361
Q

WHat is a hole in a rock?

362
Q

What are osteophytes?

A

The classic radiographic finding and lead to bony enlargement of the joint - visible in superficial joints

** CLASSIC finding in DJD

363
Q

How do osteophytes develop?

A

From the articular margin due to combination of cartilage metaplasia and increase capsular insertion stress

364
Q

Osteophytes are bony with ____ ,

A
  • Cortex, and unattached margin is capped with layer of cartilage
    • Osteophytes have cartilage caps
    • Doesn’t make a difference in extremities (hip, joint, knee, PIP, etc.)
    • Makes a big difference in spine
365
Q

Osteophytes only occur in _____

366
Q

?

367
Q

DJD is symmetrical or Asymmetric?

A

ASYMMETRIC

368
Q

Inflammatory is almost always _____ ?

A

Symmetrical

369
Q

4 main DJD radiographic findings: ****

A
  1. Non uniform loss of joint space - fundamental
  2. Osteophyte formation - Classic finding
  3. Subchondral sclerosis/eburnation - variable
  4. Subchondral cysts/geodes - variable

* Hips will have larger geodes than smaller joints

370
Q

Intra articular loose bodies are found in what disease? WHat are they?

A

Joint Mice, found in DJD, loose ossicles in the joint, SCM (synvoial chondrometaplasia) –> Cartilage pieces produced by synovial membrane)

371
Q

Geodes can weaken _____

A

Subchondral bone

372
Q

What is an articular deformity and what is it associated with?

A

Collapse of subchondral bone associated with DJD –> linked with Geodes

373
Q

?

374
Q

?

A

Heberdene’s Nodes (DIP)

Boucharde’s Nodes (PIP)

DJD

376
Q

DJD primary joints in hand:

A
  • DIP, PIP & 1st MCP occ. Scaphotrapezium
    • Not primary in MCP
    • Writst: Radioscaphoid = primary; Radiolunate = SECONDARY
377
Q

DJD Primary Joints, Shoulder:

378
Q

What are common PRIMARY areas of DJD?

A
  • HAND
  • SHOULDER
  • SPINE
  • KNEE
  • FOOT - DIP, PIP and 1st MTP
379
Q

What are secondary DJD?

A
  • HIP
  • ELBOW
  • ANKLE

** MOST COMMONLY SEEN IN POST MENOPAUSAL WOMEN

380
Q

?

382
Q

?

385
Q

What is CPPD?

A

Calcium Pyrophosphate Deposition DIsease

  • Common Metabolic Disease
  • Causes Pseudogout
386
Q

?

388
Q

?

389
Q

The bigger the joint,

A

The smaller the osteophytic bone

390
Q

If we see a geode, how do we differentiate this?

A
  • Is it next to a DJD (asymetrical joint space)
  • Is it up against the subchondral bone plate
392
Q

?

393
Q

What is the #1 cause of secondary DJD, and also common to cause primary?

A

Avascular Necrosis AVN

394
Q

?

A

Probably due to AVN in DJD

395
Q

?

A

Bilateral DJD

397
Q

?

A

Patella femoral DJD

5 SKEL RAD A (2 decks)

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