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MIDTERM Flashcards

1
Q

Bilateral symmetry is in what % of RA patients?

A

80%

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2
Q

What is juxta-articular osteopenia due to?

A

Hyperemia, disuse, and steroid therapy may lead to generalized form

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3
Q

Uniform loss of joint space is associated with what?

A

Collagenase/chemical destruction RA

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4
Q

Bare area bone destruction is what?

A

Marginal (rat bite) erosions

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5
Q

What is Pannus?

A

granulation tissue made up of new capillary growth and fibroblasts that grows into the joint

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6
Q

What can be infrequent, solid, or laminated in RA?

A

Juxta articular periostitis

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7
Q

What can deformity of RA be due to?

A

joint destruction, ligament laxity, and stenosing tenosynovitis

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8
Q

What is stenosing tenosynovitis?

A

Tendon sheaths scar, shrink, and pull

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9
Q

What are the areas of foot and hand affected by RA?

A

forefoot, MTP joints, PIP joints possible, dorsal dislocation on MTP, fibular dislocation on digits (Lanois deformity)

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10
Q

Primary DJD does not care about ____ but likes ______ ?

A

MCP, but does like DIP and PIP joints

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11
Q

RA likes ____ and does not involve ____ ?

A

Likes MCPs, and does not involve DIP joints (besides thumb) and entire wrist

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12
Q

What tendon does RA like?

A

the extensor carpi ulnaris tendon that runs right along side the ulnar styloid process, common for patients to complain of this before they get soft tissue swelling

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13
Q

Does RA create radial or ulnar deviation?

A

ulnar

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14
Q

Describe the Boutonniere hand deformity:

A

“BEFE”

boutonniere, extend DIP, flex PIP, extend MCP

Fingers are STUCK

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15
Q

Describe the “swan neck” hand deformity:

A

“FEF”

(Flex DIP, extend PIP, flex MCP)

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16
Q

Describe the Mallet finger RA:

A

DIP joint hyperflexion

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17
Q

What is the sign of RA that combines different hand deformities?

A

Arthritis Mutilans

  • boutonniere
  • swan neck
  • mallet finger
  • zig zag, ulnar deviation

(looks like your hand is in a blender)

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18
Q

What is the zig zag look associated with RA?

A

Radial carpal deviation with ulnar deviation

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19
Q

What are the exceptions of the hand deformities in RA?

A

Doesn’t like 2-5th DIP joints, but every other joint in upper extremity is fair game

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20
Q

What is rheumatoid’s primary focus?

A

Synovial Membrane

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21
Q

What is a deposition of immune complexes involving multiple systems?

A

Systemic Lupus Erythematous (SLE)

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22
Q

When does System Lupus Erythematous (SLE) occur?

A

Female childbearing years

48/100,000

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23
Q

What areas does SLE affect?

A

Skin and joints very common, kidney is severe

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24
Q

The butterfly rash is prevelant in how many percent of patients, and what disease is it involved with?

A

SLE and 40%

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25
Q

What are the symptoms of SLE?

A

90% joint symptoms, pain, swelling, and stiffness

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26
Q

How is the joint ivolvment in SLE?

A

Mile with little destruction, that’s why a lot of SLE deformities are reversible

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27
Q

What would you radiographically see on SLE?

A

Osteopenia, tuft resorption, and calcinosis

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28
Q

What are the corticosteroid changes that occur within SLE?

A

It is called, Corticosteroid Osteopothay, and one would see osteopenia, fractures, and AVN. Bone changes occur because of the steroid use

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29
Q

What are the early symptoms of SLE?

A

Chronic, episodic pain, stiffness, and soft tissue swelling

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30
Q

What is PSS?

A

Progressive _S_ystemic _S_clerosis

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31
Q

What is PSS main target?

A

(Scleroderma) Subcutaneous connective tissue

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32
Q

What is the main age group and gender of PSS?

A

Females 30-50 y.o.

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33
Q

What systems are affected by PSS?

A

systemic inflammatory then scarring disorder, skin, lungs, GI tract, heart, kidneys, MSK

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34
Q

90% of scleroderma patients have ______ ?

A

Raynaud’s

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35
Q

What does “CREST” stand for? What disease is it associated with?

A

Progressive Systemic Sclerosis

  • Calcinosis
  • Raynauds
  • Esophagus
  • Scleroderma
  • Teleangiectasia
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36
Q

Describe the Calcinosis portion of CREST in PSS:

A

Calcinosis Cutis, Circumscripta, and Universalis

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37
Q

Calcinosis Circumscripta pic:

A
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38
Q

Calcinosis Universalis pic

A
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39
Q

What are the components associated with the Esophagus in CREST (PSS)?

A

GERD is common, and there is difficulty swallowing

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40
Q

scleroderma x ray pic

A
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41
Q

Describe “Teleangiectasia” (CREST) associated with PSS:

A

Localized areas of redness

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42
Q

What’s the most common area of damage for PSS?

A

Hands, feet, and face

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43
Q

What happens to the skin during PSS?

A

It begins to tighten due to scarring

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44
Q

What type of arthritis is associated with PSS?

A

“Non-erosive arthritis”

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45
Q

Selective destruction of _____ is common in PSS?

A

1st MCC (base of thumb-trapezium) is distinctive

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46
Q

Tuft Resorption is associated with what?

A

(PSS) scleroderma is the default condition that causes this

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47
Q

What is the origin of Dermatomyositis/Polymyositis?

A

It is unknown

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48
Q

What is more common, Dermatomyositis or Polymyositis?

A

Dermatomyositis

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49
Q

What is dermatomyositis?

A

Dermatomyositis is an uncommon inflammatory disease marked by muscle weakness and a distinctive skin rash. Likely autoimmune

  • Muscle fascial inflammation
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50
Q

Dermatomyositis may occur _____ ?

A

secondary to neoplasm of lung, prostate, female pelvic organs, breast, and GI

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51
Q

What are the key features of Dermatomyositis?

A
  • Non - suppurative inflammation of skeletal muscle with
    • Weakness
    • Erythematous skin rash
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52
Q

What does the inflammation of Dermatomyositis lead to?

A

Eventual scarring of fascia and subsequent calcinosis universalis

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53
Q

Is there tuft resorption with Dermatomyositis?

A

YES, there is “non destructive small joint inflammation with tuft resorption”

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54
Q

The articular of Dermatomyositis resembles what?

A

PSS and SLE

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55
Q

What is Mixed Connective Tissue Disorder described as?

A

MCTD is characterized by overlapping clinical features of PSS, SLE, DM and possibly RA

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56
Q

What is common with Mixed Connective Tissue Disorder?

A

Arthropathy consisting of arthralgia and arthritis is common in the small joints of the hand, foot, and wrist

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57
Q

What is Jaccoud’s Arthropathy?

A

1867, Infrequent, deforming, non-erosive hand and foot arthropathy

  • Originally subsequent to rheumatic fever (from systemic strept)
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58
Q

What are the deformities of Jaccoud’s Arthropathy?

A
  • Ulnar deviation with flexion
  • Boutonniere and swan neck
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59
Q

KNOW THIS PIC :

A
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60
Q

What is the history of Sjogren’s Syndrome?

A

1930, A Swedish Opthalmomologist described a patient with low secretions from lacrimal and parotid glands

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61
Q

What is Sjogren’s syndrome due to?

A

Lymphocytic accumulation in and obstructing exocrine glands

  • Can be primary or secondary
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62
Q

Sjogren’s Syndrome is most common in _____

A

Females 40-50 year old

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63
Q

What does Sjogren’s Syndrome cause?

A
  • Keratoconjunctivitis sicca (dry eyes), xerostomia (dry mouth), as well as other areas of dryness (nose, skin, and vaginal)
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64
Q

What is the 3rd most common rheumatic autoimmune disorder next to RA and SLE?

A

Sjorgren’s syndrome

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65
Q

What is the clinical triad of Sjogren’s syndrome?

A
  1. Keratoconjunctivitis sicca
  2. Xerostomaia
  3. Autoimmune rheumatoid type disorder usually RA but can be SLE or PSS
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66
Q

Describe Juvenile chronic Arthritis:

A

Juvenile onset adult type RA (Rh factor +)

  • Rheumatoid in a child under the age 16
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67
Q

What are the radiologic signs in Juvenile Chronic Arthritis, (Juvenile onset adult type RA) Rh factor + ?

A
  • Bilateral symmetry
  • Starts in hands and moves toward axial skeleton
  • Longer term = Worse it gets
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68
Q

What are the 3 Juvenile chronic Arthritis subcategories?

A
  1. Juvenile Onset Adult type RA (Rh factor + )
  2. Still’s Disease (Rh factor - )
  3. Juvenile Onset Rheumatoid variant disease
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69
Q

What are the main characteristics of Still’s Disease?

A
  • Classic systemic form
  • Polyarticular form
  • Pauci - or monoarticular form - only have it in one joint or 2/3 but WON’T have a widespread form
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70
Q

Still’s disease is Rh +

t/f ?

A

FALSE (negatron)

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71
Q

Describe Juvenile onset Rheumatoid variant disease:

A

HLA-27 spondyloarthropathies, and Rheumatoid variants can Uncommonly happen in children

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72
Q

Juvenile onset adult type RA (Rh factor +), Still’s Disease (Rh factor - ), and Juvenile onset Rheumatoid variant disease are all _____ ?

A

Inflammatory arthritis

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73
Q

What is a bone infarct?

A

Ischemic death of the cellular elements of the bone and marrow

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74
Q

What does a bone infarct refer to?

A

Lesions occurring in the metaphysis and diaphysis of bone

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75
Q

Lesions in the epiphysis are called what?

A

Avascular Necrosis

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76
Q

What are the 3 classifications of Osteonecrosis?

A
  1. Bone ends children
  2. Bone ends adults
  3. Metaphysis and Diaphysis
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77
Q

In osteonecrosis, bone ends in children are called what?

A

Epiphyseal ischemic necrosis, femoral head is the most common location

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78
Q

What is adult osteonecrosis?

A

Chandler’s Disease

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79
Q

What is osteonecrosis in children?

A

Legg-Calves - Perthes disease, femoral head is the most common location

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80
Q

What is it called when osteonecrosis is found in the metaphysis and diaphysis?

A

Medullary infarction

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81
Q

What is the normal cause of osteonecrosis in the metaphysis and diaphysis?

A

It can be idiopathic or secondary to a number of conditions that reduce blood supply to the bone such as an intraluminal abnormality, extrinsic compression or combo of both

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82
Q

Osteonecrosis can be ____ or _____

A

Idiopathic or Secondary

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83
Q

Osteonecrosis can be idiopathic or secondary to a number of conditions that reduce blood supply to bone, what are they?

A
  • Intraluminal abnormality
  • An extrinsic compression
  • Combo of both
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84
Q

What does therapeutic radiation do in regards to Osteonecrosis?

A

Inflames the walls of arteries, narrows the lumen, and causes obstruction

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85
Q

Children usually develop ostenecrosis through ____

A

TRAUMA

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86
Q

What is the “gold standard” for detection of Osteonecrosis?

A

MRI

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87
Q

What plays a major role in diagnosing osteonecrosis at a young age?

A

CT scans, MRI, and bone scans, but if we see it on plain film, this means it is far along in its stages

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88
Q

AVN shows up how on a bone scan?

A

COLD AREA

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89
Q

What is the most common hematological condition of the skeleton?

A

AVN

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90
Q

What is AVN predisposed to?

A

Areas of tenuous blood supply with poor collateral circulation, that’s why the femoral head is the most common area - it gets most of its blood from one blood vessel (lateral peripheral artery)

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91
Q

Under the category of external vessel compression in osteonecrosis, what are the 3 subcategories?

A

infection, gaucher’s disease, hyperlipidemia

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92
Q

What is Gaucher’s disease?

A

Lipid storage disease, genetic disorder, accumulation of abnormal fatty material that accumulates in macrophages.

  • Cells accumulate in marrow – creates pressure — squishes vessels
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93
Q

What could cause external vessel compression?

A

Hyperlipidemia

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94
Q

Vessel wall disorders in the etiology of AVN is due to what?

A

Therapeutic levels of radiation used to treat cancers, it inflames blood vessels and narrows lumen

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95
Q

Under etiologies of AVN, Thrombo-embolic disorders are classified as:

A
  1. Alcoholism
  2. Sickle-cell
  3. Caisson’s disease
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96
Q

Why would alcoholism cause a thrombo-embolic disorder?

A

Causes pancreatitis, fatty embolism in the blood, and is one of the MORE COMMON causes of AVN

  • typically BILATERAL (long term alcoholics)
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97
Q

How would sickle cell cause a thrombo embolism?

A

Widespread AVN in femoral heads, humeral heads, etc. You can get an embolism in the kidneys or lungs

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98
Q

What is Caisson’s disease?

A
  • This could cause a nitrogen gas embolism
  • “Diver’s disease”
  • Rapid decompression in aircraft can cause it
  • Tends to involve in HUMERAL HEADS
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99
Q

Describe what corticosteroid use can do:

A

Prednisone for a period of time to treat rheumatoid type arthritis can cause AVN

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100
Q

_______ with prednisone leads to AVN?

A

LUPUS

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101
Q

What is the pneumonic for etiology list?

A

PLASTIC RAGS

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102
Q

Etiology of AVN - Pancreatitis:

A

Pregnancy, late stage pregnancy - particularly develop AVN in left hip

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103
Q

Patient with Cushing’s syndrome may develop AVN, t/f?

A

TRUE

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104
Q

What is the “I” in PLASTIC RAGS pneumonic?

A

_IDIOPATHIC****_

  • One of the more common ones, aka “SPONTANEOUS AVN”
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105
Q

What is the “C” in PLASTIC RAGS?

A

Caisson’s, rapid decompression, nitrogen embolism

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106
Q

What is the “A” in PLASTIC RAGS?

A

Amyloidosis:

  • Metabolic Arthritic disorders (lumpy bumpy)
  • Amyloid - abnormal protein material
  • Amyloid accumulating in bone marrow causes compression
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107
Q

What is the “G” in PLASTIC RAGS?

A

Gaucher’s

“Hematological disorder”

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108
Q

What would you see in the epiphyseal findings of osteonecrosis?

A
  • Deep dull joint pain, exacerbated by activity
  • Limp waddling gait
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109
Q

What would you notice with the medullary portion of bone in Osteonecrosis?

A

Medullary infarct typically asymptomatic

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110
Q

What is a _bolded**_ finding of ostenecrosis?

A

_Osteochondritis Dissecans**_ may cause joint locking

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111
Q

What are common locations of Osteochondritis Dissecans?

A

Knee and ankle

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112
Q

What are the main points of Osteochondritis Dissecans?

A
  • Specific, focal subchondral AVN
  • Does not involve entire epiphyseal area – right up at articular surface
  • Usually due to trauma
  • Late teens, early adults
  • Subchondral piece of cartilage that falls into joint (joint mouse)
  • Get secondary DJD from it
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113
Q

What are the 4 stages of Osteonecrosis?

A
  1. Avascular
  2. Revascularization
  3. Repair - Reossification
  4. Deformity - Healed
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114
Q

During the Avascular stage of AVN, what would you see?

A
  • Joint effusion – especially at the hip
    • Push the femur slightly lateral - increase medial joint space
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115
Q

How does the bone look during the Avascular stage of Osteonecrosis?

A

Normal, no radiographic changes

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116
Q

What can be a precursor to AVN?

A

TOH

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117
Q

What would describe, Avascular event has occured but has not started to heal yet?

A

Avascular stage of Osteonecrosis

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118
Q

What are the 3 stages to the principles of Infarction?

A

• Stage 1: cessation of intracellular metabolic activity at a

chemical level.

• Stage 2: alteration or interruption of intracellular enzyme

systems

• Stage 3: disruption or dissolution of intracellular nuclear

and cytoplasmic ultrastructure. Irreversible.

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119
Q

Adults rarely get beyond what stage of AVN?

A

Revascularization (2)

  • Deformity happens in this stage, once you deform the bone and the adult secondary DJD happens faster than they can get through being healed
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120
Q

What happens to the bone during the Revascularization stage of AVN

A

(2)

  • New osteoblasts/clasts
    • Clasts take away the dead bone
  • New vascular vessels/capillaries growing in the area - happens SLOWLY
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121
Q

What are the radiographic findings during Revascularization?

A
  • Look more radiolucent because clasts take away dead bone
  • Areas of increased bone density where blasts are building on dead trabeculae
  • Intermixed pattern of density in the femoral head
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122
Q

What are the signs you’d see during Revascularization stage of AVN?

A
  • Crescent sign - arc right under bone
  • Snow cap - osteosclerosis of femoral head
  • Fragmentation - well into second stage
    • can become extremely fragmented in CHILDREN
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123
Q

What is the overall quantity/quality of bone during Revascularization stage of AVN?

A

Net reduction in bone –> subchondral fracture

  • Femoral head collapses
  • FLATTEN FEMORAL HEAD - disrupt biomechanical integrity of articular cartilage –> DJD
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124
Q

What happens during the Repair - Reossification stage of AVN?

A
  • NEW BONE formation
  • More bone seen on the previous x-ray

** Fast is 2 years, and has been known to take 8 years **

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125
Q

Children need to be radiographed every _____ during Repair stage of AVN?

A

6 months

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126
Q

What is the last stage of AVN?

A

Deformity - Healed

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127
Q

What are the major findings in the last stage of AVN?

A
  • Normal bone density but shape change
  • Cox magna
  • Cox Plana
  • Reduced femoral neck angle
  • Large greater trochanter
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128
Q

What will happen to children during the Deformity stage of AVN?

A

They will heal but they may get secondary DJD years later

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129
Q

What will the signal look like taking an MRI for AVN?

A

Loss of signal in the marrow on a T1 weighted scan

  • T1 water is dark
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130
Q

Describe the epiphyseal on an MRI in AVN:

A

MRI are most sensitive, and it is often seen bilateral

  • May demonstrate joint effusion
  • GOLD STANDARD for early MRI imaging
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131
Q

What are the 4 main signs of AVN?

A
  1. SNOW CAP SIGN
  2. CRESCENT/RIM SIGN
  3. MUSHROOM Deformity
  4. HANGING ROPE SIGN
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132
Q

What can you also get from AVN (appears on X ray)?

A

Geodes - once you fracture articular surface, synovial fluid can leak down

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133
Q

Once the femoral head flattens in AVN it _____

A

PERMANENTLY Deformed

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134
Q

What would you think if you saw a bilateral case of AVN?

A

If it’s bilateral it’s probably not idiopathic - most likely alcohol or corticosteroids **

  • Sickle cell classically does it bilateral at multiple places
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135
Q

Adults typically don’t make it past what stage of AVN?

A

REVASCULARIZATION

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136
Q

Healed AVN has what signs?

A
  • Articular deformity
    • Early OA
  • Acetabular dysplasia, hanging rope
  • Trochanteric overgrowth
  • Mushroom cap deformity
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137
Q

Altered signal from fat and edema - ring of dark signal around the area of necrosis describes:

A

MRI findings of Osteonecrosis

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138
Q

What is a group of disorders that share certain features?

A

Osteochondroses

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139
Q

Osteochondroses has a predilection for what?

A

Immature skeleton

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140
Q

What does osteochondroses involve?

A

Involvement of the epiphysis, apophysis, oor epiphyseal equivalent

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141
Q

What are the radiographic pictures dominated by in Osteochondroses?

A
  • Fragmentation
  • Collapse
  • Sclerosis
  • Frequently, reossification with reconstruction of the osseous contour
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142
Q

Osteochondroses is more common in boys or girls?

A

BOYS

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143
Q

Legg Calves - Perthes discovered in 1910 affects patients from ______

A

4-8 years old, and is more common in boys (5:1)

  • Bilateral in 10-20%
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144
Q

What are the clinical signs of Legg-Calve Perthes Disease?

A
  • Limping
  • Pain
  • limiting movement (abduction and internal rotation) - or could be salter harris fracture

TRAUMA in 25% of cases

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145
Q

If parents smoke during pregnancy, it increase the risk of this disease in the child?

A

Legg Calve Perthe

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146
Q

What are the radiographic findings in Legg Calve Perthes disease?

A
  • Soft tissue swelling
  • Small epiphysis
  • Lateral displacement of ossification center
  • Flattening, fissuring, and fracture of the ossification center
  • Intraepiphyseal gas
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147
Q

What is Waldenstrong’s Radiographic Staging Initial stage?

A
  • Increased head-socket distance (medial joint space widens)
  • Subchondral plate thinning
  • Dense epiphysis
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148
Q

What are the 5 stages of Waldenstrom’s Radiographic Staging?

A
  1. Initial
  2. Fragmentation
  3. Reparative
  4. Growth
  5. Definitive
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149
Q

What happens during the Fragmentation stage of Waldenstrom’s?

A
  • Subchondral fracture
  • An inhomogenous dense epiphysis
  • Porous appearance with metaphyseal cysts
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150
Q

What happens during the Reparative Stage of Waldenstrom’s?

A
  • Normal bone in areas of resorption and removal of sclerotic bone
  • epiphysis has more homogenous appearance
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151
Q

What happens during the Growth stage of Waldenstrom’s?

A
  • Re-ossification
  • Normal femoral shape approached
  • Some degree of flattening does occur - earlier detection –> less deformity
    • Greater the deformity - higher chance of DJD
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152
Q

What happens during the Definitive stage during Waldenstrom’s?

A

Final shape is determined with joint congruency or incongruency

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153
Q

Waldenstrom’s Radiographic staging is under what category?

A

Legg-Calve Perthes Disease

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154
Q

What happens to the Metaphysis during Legg-Calves Perthes Disease?

A
  • Metaphyseal cysts - frayed looking areas
  • Widening and shortening of the femoral neck
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155
Q

Secondary OA is a problem in what?

A

Legg-Calve Perthe’s Disease

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156
Q

What is the basic problem of Legg-Calve Perthes

A

basic problem is osteonecrosis with
structural failure of bone, fragility of blood
supply

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157
Q

What is Legg Calve Perthe’s Disease different from?

A 
diff. from hypothyroidism and other
avascular necrosis (ie, sickle cell)
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158
Q

How long does healing for Legg Calve Perthe’s Disease last?

A

18 months

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159
Q

What are the main history components of Freidberg’s Infarction?

A
  • Affects children and adults
  • Usually unilateral
  • Woman 3 or 4:1
  • Ages 13-18
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160
Q

What are the clinical findings of Freiberg’s Infarction?

A
  • Local pain and swelling
  • Complain about MTP joint hurting
  • Increased density, flattened
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161
Q

What does Freiberg’s Infarction lead to?

A

DJD - Forefoot MTP joint most common place

  • DJD is secondary in Freiberg’s
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162
Q

What is the pathogenesis of Freiberg’s Infarction?

A

pathogenesis is AVN secondary to
single or repeated trauma

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163
Q

Healed osteonecrosis pic

A
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164
Q

What is AVN in the scaphoid?

A

Preiser’s Disease

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165
Q

What are the main points of Preiser’s Disease?

A
  • Scaphoid is most common carpal bone to fracture
  • Sclerosis analagous to snowcap appearance in femoral head
  • Eventually collapses like femoral head collapses
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166
Q

What usually happens secondary to fracture of scaphoid?

A

Preiser’s Disease

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167
Q

Radial carpal DJD – Secondary DJD describes what?

A

Preiser’s Disease

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168
Q

What suggests AVN of tarsal navicular navicular?

A

Kohler’s Disease

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169
Q

What are the main attributes of Kohler’s disease?

A
  • Boys 4 or 6:1
  • 3-6 years old
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170
Q

What are the radiographic findings of Kohler’s Disease?

A
  • Radiographs reveal patchy increased density and fragmentation
  • Local Pain, tenderness, and swelling
  • Look a little osteosclerotic, maybe radiolucent in areas, flattened
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171
Q

What is AVN of the lunate?

A

Kienbock’s Disease

172
Q

What happens during “Advanced Collapse” of Kienbock’s disease?

A
  • Very negative ulnar deviation
  • Very flattened lunate - almost looks like a crescent sign
173
Q

Describe the “ulnar variance” associated with Kienbock’s disease:

A
  • Patients that have negative ulnar variance have an increased risk of lunate AVN – causes excessive stress load on proximal carpal load
    • Patients should be followed
174
Q

What leads to DJD and decreased wrist function?

A

Kienbock’s Disease

175
Q

What are the main attributes of Vertebral body AVN?

A
  • May occur with corticosteroids, compression fracture, or osteoporosis
  • “Intravertebral Vacuum
176
Q

What are the radiograhic findings of Vertebral body AVN?

A
  • Radiolucency in vertebral body (almost looks like gas)
  • FLATTENING
177
Q

Aka for vertebral body AVN?

A

Kummel - Verneuli’s Disease

178
Q

What represents a focal subchondral infarction of sub-articular bone?

A

Osteochondritis Dissecans

179
Q

Describe what happens during Osteochondritis Dissecans:

A

The necrotic bone may become a free floating fragment separated from the parent bone

  • JOINT MOUSE: Damages hyaline cartilage and causes secondary DJD
180
Q

What case attributes are associated with Osteochondritis Dissecans?

A
  • Often associated with trauma
  • Seen in young individuals
  • Complain about joint pain
181
Q

What is the most common place for Osteochondritis Dissecans?

A

Knee is a common place, more common is lateral portion of medial femoral condyle

182
Q

Medullary Necrosis affects, ?

A

Large Tubular Bones

  • Tibia, Fibula, humerus, femur
183
Q

What are the main characteristics of Medullary Necrosis?

A
  • Medullary infarcts
    • Faint rim of calcification outlining area
  • Usually found by accident – traumatic determinism (x-ray after trauma and find this)
  • Can disappear overtime (go through all the stages to heal)
  • NO SYMPTOMS
184
Q

What classification is Medullary Necrosis in?

A

3rd in classification

  • Bone-ends children
  • Bone - ends adults
  • Everywhere else (diaphysis & metaphysis)
185
Q

What are the radiographic signs of medullary necrosis?

A
  • Snake like appearance in medullary cavity (twisted appearance)
  • One of the benign cartilage tumors (enchondroma) is in the differential with this – looks familiar
186
Q

What are the first few main points of Osteomyelitis?

A
  • Early diagnosis is intrinsic to appropriate therapy (antibiotics) being instituted
  • Often a high index of clinical suspicion is required rather than reliance on radiographic changes
  • Relatively short time frame for symptomatology
187
Q

most of the time, the infections of osteomyelitis are ______

188
Q

What is Cellulitis?

A

Infection of skin, subcutaneous fat, or connective tissue (tendons/ligaments/muscle)

189
Q

What is Osteomyelitis?

A

Infection of Bone (marrow spaces)

190
Q

What is Septic Arthritis?

A

Infection of joint (synovial tissue, articular surfaces)

191
Q

What is osteotitis?

A

Inflammatory condition usually confined to cortex

192
Q

What type of bacteria destroys joints very quickly?

A

Staph Aureus

193
Q

What are the “at risk groups” of osteomyelitis?

A
  • Immunosuppressed
  • Diabetics
  • Post surgical
  • Vascular insufficiency
  • Sickle Cell anemia
  • IV drug Users (pseudomonas aeruginosa)
194
Q

Explain Intravenous drug users in regards to Osteomyelitis:

A

“Mainliners Syndrome”

  • S JOINTS
    • ​spine - discovertebral
    • sacroiliacs
    • symphysis pubis
    • sternoclavicular
  • ALL ARE AXIAL JOINTS ****
195
Q

What are the categories under Osteonecrosis?

A
  • Osteochondroses
  • Legg-Calve Perthes Disease
  • Freiberg’s Infarction
  • Preiser’s Disease
  • Kohler’s Disease
  • Kienbock’s Disease
  • Vertebral Body AVN
  • Osteochondritis Dissecans
  • Medullary Necrosis
196
Q

What are the categories of Osteomyelitis?

A
  • Acute
  • Subacute
  • Chronic
197
Q

What are the clinical features of acute osteomyelitis?

A
  • Edema
  • Lymphadenopathy
  • Warm Skin
  • Cellulitis
  • Joint Pain
  • Happens within 2 weeks of disease onset
198
Q

Subacute Osteomyelitis develops _____

A

Within one to several months

199
Q

Chronic Osteomyelitis develops _____

A

After several months

200
Q

What are the classifications of Osteomyelitis?

A
  • Suppurative
  • Non-Suppurative
  • Syphilitic (lues) - Teponema Pallidum
201
Q

What are the aerobes associated with Osteomyelitis?

A
  • Myobacterium Tuberculosis****
  • Neisseria Gonorrhea
  • Pseudomonas
  • Fungus
202
Q

What are the anaerobic or faculative anaerobes associated with Osteomyelitis?

A

_****Staphylococcus Aureus**** (MOST COMMON)_

  • Streptococcus Pyogens
  • Treponema Palladium
203
Q

What is under the suppurative classification of Osteomyelitis?

A
  • Bone marrow infection by (pyogenic) non-tubercular organism (anything but TB)
  • Staylococcus aureus 90%
  • Haemophilus Influenza
  • Streptococcus Pneumonia
  • E. Coli
  • Pseudomonas
    • IV drug abuse
    • Mainliners Syndrome
    • Axial Joints
    • S joints
204
Q

What’s under the Non-suppurative category of Osteomyelitis?

A
  • Mycobacterium tuberculosis
  • Granulomatous
  • Fungal Infections
  • Blastomycosis - regional fungal infection
205
Q

What’s under the Syphilitic (lues) teponema pallidum?

A
  • Congenital
  • Acquired
206
Q

What is the Route of Contamination in Osteomyelitis?

A

Osseous and articular contamination by 4 principle mechanisms

207
Q

What are the 4 principle mechanisms of contamination in osteomyelitis?

A
  1. Hematogenous spread of infection - via bloodstream
  2. Spread from a contiguous source - cutaneous, sinus, and dental infections
  3. Direct Implantation - Penetrating injuries, particularly in the feet
  4. Postoperative Infection - contamination of surgical sites
208
Q

What are the clinical characteristics of Osteomyelitis?

A
  • Most often between 2-12
  • 3:1 male dominance
    • Boys have greater tendency to do things that make them vulnerable
  • Large tubular bones of extremities (metaphysis and richly vascularized)
    • Femur
    • Tibia
    • Humerus
    • Radius
209
Q

What are the Radiographic Findings associated with Osteomyelitis?

A
  1. Moth eaten ostelysis
  2. Periosteal reaction (involucrum - very substantial, mature, solid layer of bone around host bone)
  3. Cloaca
  4. Sequestra
  5. Marjolin’s Ulcer
210
Q

What is the “Cloaca” associated with the Radiographic finding of Osteomyelitis?

A
  • Hole through cortex and periosteal bone
  • Allows exudate out into the soft tissue
211
Q

What is “sequestra” associated with radiographic findings of Osteomyelitis?

A

Segments of necrotic bone separated from living bone by granulation tissue

212
Q

What is Marjolin’s Ulcer associated with Osteomyelitis radiographic findings?

A

Epidermoid carcinoma occuring at a sinus tract

  • Rare finding after 20-30 years with chronic disease
213
Q

How long does it take to see Radiographic evidence of Osteomyelitis?

A

10-14 days

214
Q

What is Brodie’s Abscess?

A

Low grade infection usually seen in children, may MIMIC osteoid osteoma

215
Q

What are the main points of Septic Arthritis?

A
  • May occur secondary to subarticular osteomyelitis or direct inoculation
  • Usually monoarticular
  • Spinal Involvement with TB frequently multi-disc level
  • Only 10% of skeletal infectious disease will be spinal
216
Q

What is Tom Smith Arthritis?

A
  • Spread of metaphyseal osteomyelitis to the adjacent joint when the metaphysis is intrascapular
  • Proximal and Distal femur and humerus as well as tibia
217
Q

What are the modes of infection occuring in Osteomyelitis?

A
  • Trauma/post - surgical
  • UTI - particularly bad for getting it into the spine
  • Pneumonia
  • Skin (open wound or cellulitis)
218
Q

What are the most common locations of Osteomyelitis?

A
  • Knee
  • Hip
  • Ankle
  • Shoulder
  • Spine
  • Venous Stasis and Gravity
219
Q

What are the 4 Radiographic Stages?

A
  1. Latent (Hidden) stage 1-10 days
    1. No radiographic findings
  2. Early Stage days 10-21 days
    1. Decreased bone density and soft tissue
    2. Periarticular Osteopenia - characteristic of RA
  3. Middle Stages - weeks
    1. ​Moth eaten destruction and periosteal reaction (solid)
    2. Lytic moth eaten destruction may cross anatomical barriers
  4. Late Stage - months
    1. ​Involucrum, sequestrum, cloaca
    2. Solid Periosteal Reaction - parallel to periosteal layer of bone
220
Q

What stage of osteomyelitis would you see moth eaten destruction and periosteal reaction?

A

Middle stage

221
Q

What is sequestrum?

A

Chalk, white area representing dead bone

222
Q

What is the vocabulary associated with Involucrum of Osteomyelitis?

A
  • Bony collar
  • Continuation of periosteal response
  • will eventually represent the new periosteum
  • Cloaca: Drainging sinus, more common with chronic disease
223
Q

What are the characteristics of arthritides?

A
  • Degenerative and Inflammatory
  • INFLAMMATORY:
    • Soft tissue swelling
    • osteoporosis
    • erosions
    • Septic arthritis
224
Q

What are common themese within Septic Arthritis?

A
  • Joint infection
  • MC in joints in which the capsules covers metaphysis
  • Joint capsule infected first
  • Completely eliminates both sides of the joint
225
Q

What are the radiographic features of Septic Arthritis?

A
  • Joint effusion
  • Juxtaarticular Osteoporosis
  • Erosions
  • Joint space loss
  • Lytic destruction that crosses the joint space

​

Tumors respect joints, INFECTIONS DONT!

226
Q

Describe Infectious Spondylodiscitis:

A

Infection that gets into the disc and starts at the end plates

  • Both suppurative and non-suppurative can do this
227
Q

Pediatric patient with disc space loss =

228
Q

What would give you the idea that you’re seeing infection vs. DJD?

A

Destruction on both sides of disc level with disc narrowing and prevertebral swelling - think infectious

229
Q

What “favors” TB?

A

Gibbus - hyperkyphosis with an angle

230
Q

DJD is the most common reason for having joint space narrowing but it does not _______

A

DESTROY end plates,

INFECTION DESTROYS END PLATES

231
Q

Metastasis can completely destroy the vertebral bodies, but _____

A

NOT touch the discs

232
Q

What does TB destroy?

A

More of the front of the vertebral body - segment begins to flex forward

233
Q

How much bone loss do you need for it to be detected on plain film?

234
Q

What imaging is more detailed, and more sensitive?

A

Computed Tomography

235
Q

Tuberculosis is simply ______

A

Non suppurative Osteomyelitis

236
Q

What is the most common cause of infection related death world wide?

A

Tuberculosis with 15 million people infected in the USA

237
Q

What are the clinical features of Tuberculosis?

A
  • Respiratory symptoms
    • _Pulmonary infection first (PRIMARY TB)**_
    • In an immunocompetent person, TB is asymptomatic 98% of the time
238
Q

What happens with the pulmonary infection in Tuberculosis?

A

Spreads through lymphatics and vascular system - _lymphohemotogenous dissemination - secondary TB***_

  • Can embed organisms in bone marrow and spine
239
Q

What is gohn’s tubercle?

A

Localized embedded areas of tubercular bascillus organisms that are walled off and contained

240
Q

What are the symptoms of Tuberculosis?

A
  • Respiratory symptoms
  • Weight loss
  • night sweats
  • vague joint/back pain
  • persistently elevated ESR
241
Q

What does TB really like?

A

The spine and joints - more so than suppurative

242
Q

What is spinal tuberculosis?

A

POTTS DISEASE

243
Q

What’s the most common place for TB?

244
Q

What are the radiographic features of TB?

A
  • similar to osteomyelitis in the spine, but:
    • Multiple levels
    • Paraspinal cold abscesses with Ca2+
    • Subligamentous spread to multiple vertebrla bodies
      • Spreads under ALL
245
Q

Explain the “Paraspinal cold abscesses with Ca2+” in the Radiographic features of TB:

A
  • New capillary growth with fibroblasts oozing from infectious site - granulation tissue can occur around the vertebra
  • Below diaphragm in lumbar area - granulation runs down psoas muscle - psoas abscesses
  • Calcifies because it scars
246
Q

What are the most common places for TB?

A

Spine, hips, and knees

247
Q

What is TB joint infection

A

Tuberculosis septic arthritis

248
Q

What will you see with Tuberculosis septic arthritis - TB joint infection?

A
  • PHEMISTER’S TRIAD
    • Juxtaarticular osteoporosis (osteopenia)
    • Marginal erosions
    • Slow joint space loss (uniform)
  • SCROFULA - associated with TB - cervical lymphadenitis
    • Cervical lymph nodes enlarged
249
Q

Osteitis Deformans =

A

Paget’s Disease

250
Q

What is Paget’s Disease?

A

Very common bone softening disease - many asymptomatic early in disease; progress with pain, bowing and enlargement with possible neurological complications (especially if it involves the spine)

251
Q

Where is Paget’s most common?

A

Great Britain and descendants

  • About 5% of the world (1 in 20)
  • Uncommon in Asia and Africa
  • In US slightly higher incidence the further north you go
252
Q

What is the etiology of Paget’s?

A

Undetermined, current thought is the latent Virus

253
Q

Describe the bone in Paget’s:

A

Bone is extrememly vascular - tremendously high increase in blood flow

  • This can overload the heart - high cardiac output –> lead to heart failure
254
Q

What does the lab report of Paget’s Disease look like?

A
  • Serum alkaline phosphatase - indication of liver activity and osteoblastic activity
  • Urinary and serum hydroxyproline - from collagen breakdown
255
Q

Describe the simple definition in early stage of Paget’s:

A

Bone/osteoclastic resorption - where you will find hydroxyproline

256
Q

Describe what simply happens in 2nd stage of Paget’s in regards to the lab findings:

A

Bone productive - high osteoblastic activity - significant elevation of alkaline phosphatase (20 x’s normal level)

257
Q

Patient with Paget’s disease frequently have ______

A

both stages going on at the same time - may see increase in both labs

258
Q

Where is Paget’s most common?

A

Big Tubular bones, pelvis, spine, and cranial vault

259
Q

What is a distinguishing characteristic of Paget’s?

A

Can jump over joints and involve the bones on the other side of the joint - typically subarticular (goes right up to the bone end)

  • Can also cause deformity of the subarticular bone - impact the integrity of the cartilage of the joint - secondary DJD
260
Q

Is there periosteal involvment in Paget’s?

261
Q

What is the age group of Paget’s ?

A

> 40 years old

262
Q

What are the stages of Paget’s?

A

4 stages

  1. Stage 1 - Osteoclastic Resorpiton
  2. Stage 2 - Bone Productive - mixed stage, biphastic stage
  3. Stage 3 - Osteosclerotic stage
  4. Stage 4 - Malignant Degeneration
263
Q

What happens during the 1st stage of Paget’s?

A
  • Seen with areas of radiolucency
  • Lytic Phase - radiographic findings depend on if it is a long bone or flat bone
264
Q

Describe the tubular component of Paget’s in regards to the 1st stage:

A

Tubular - progresses proximal to distal, or distal to proximal

  • Will have an area of radiolucency in a V shape (“blade of grass” or “candle flame”) or oblique line
265
Q

What happens to the skull in paget’s?

A

*1st stage***

  • Skull/flat bone - large well-defined geographic area of radiolucency “osteoporosis circumscripta”
    • IN SKULL ONLY
266
Q

What are some features of Stage 2 Paget’s?

A
  • Repair stage that comes behind
  • Osteoid is poor quality (lot of fibrous tissue)
  • Accentuate the bone cortex and thicken the trabeculae - increase bone density and increase size
267
Q

What stage do most patient’s stay in Paget’s?

268
Q

What will happen to the bone during Paget’s?

A
  • Sclerosis and lucency
  • Trabecular and cortical thickening
  • Bone enlargment - bone may lose vertical height (due to softening) but gain horizontal size
269
Q

What appearance will the Paget’s skull present with during stage 2?

A
  • Skull is cotton wool appearance - fluffy, non homogenous look
    • will cause enlargment of head
    • often spares facial bones
270
Q

What will the spine present with during Paget’s in the 2nd stage?

A

Vertebral body “picture frame” - name for cortical thickening - best illustrated in the lumbar layer

  • May see ivory vertebral body
  • Can extend posterior
271
Q

What is your differential diagnosis for ivory vertebra?

A

Pagets, blastic mets, lymphoma (Hodgkins)

272
Q

What is a “sign” in stage 2 of Paget’s?

A

“Brim/rim” sign - cortical thickening along the inside bony pelvic margin

* Bony enlargment in the spine can cause the neurological symptoms

273
Q

Describe Stage 3 of Paget’s:

A
  • Bone becomes homogenously osteosclerotic looking
  • Cannot distinguish trabeculae from cortex
274
Q

Describe stage 4 of Paget’s:

A

Most people do not get to this stage, and bone becomes very painful

275
Q

What can you use to diagnose Paget’s?

A
  • Radiographs
  • Bone scan can find areas of involvment
  • CT/MRI can asses for complications
276
Q

What are the complications of Paget’s?

A
  • Osseous Deformity
  • Fractures
  • Neurologic Symptoms
  • Arthropathy (secondary DJD)
  • Neoplasm (4th stage)***

KNOW THIS ****

277
Q

What are the “Osseous deformities associated with Paget’s?”

A
  • Due to bone softening
  • Bowing common
  • Acetabular protrusion with positive Kohler’s line
  • Basilar Invagination
  • Saber - shin deformity - bowing of tibia
278
Q

What type of fractures do you see in Paget’s?

A

Pseudofractures: Thin lines of radiolucency from unmineralized osteoid associated from softening

279
Q

Describe pseudofractures in Paget’s:

A
  • Can become true fractures
  • typical in femur, humerus, and pelvis
  • AKA: osteoid seam, Milkman’s syndrome, increment fracture, Looser’s lines, umbazone
280
Q

What is a Banan fracture in Paget’s?

A

Usually through a pseudofracture in big tubular bones, horizontal/transverse fracture

  • SPINE CAN HAVE COMPRESSION FRACTURES
281
Q

Describe Neoplasm symptoms in Paget’s:

A
  • Sacromatous transformation that are most often lytic (only about 1% of patients)
  • Occur in OLDER patients (55-80 y.o.)
  • May have soft tissue mass develop around it
282
Q

What are common sites of neoplasms?

A

FEMUR, pelvis, humerus

(UNCOMMON in spine)

283
Q

Osteosarcom neoplasm %

284
Q

Fibrosarcoma neoplasm %

285
Q

Chondrosarcoma neoplasm %

286
Q

What is a neoplasm?

A

Abnormal cellular growth that can be benign or malignant

  • Malignant: Ability to metastasize/spread
  • Benign: Does not metastasize, but this does not mean insignificant
287
Q

Any cell found in bone can produce ______

A

a tumor

* Subdivided by what type of cell it comes from

288
Q

If a tumor originates in bone it is called a _____

A

primary bone tumor

289
Q

What is a secondary bone tumor basic definition?

A

Starts somewhere else and metastasizes to bone

290
Q

What is a tumor like lesion?

A

Lesions that radiographically appear as tumors but are not histo-pathologically classified as a tumor - usually produce geographic radiolucency

291
Q

Primary bone tumors, benign category:

A
  1. Osteoma - MOST COMMON, intramembranous bone tumor, dont hurt
  2. Osteoid Osteoma - not as common, HURT
  3. Osteoblastoma - RARE, but half occur in spine
292
Q

Malignant bone tumr =

A

Osteosarcoma

293
Q

Describe conventional osteosarcomas:

A

Most of these are central sclerotic (about 75%) originate from inside the bone and loves the distal femoral metaphysis

  • 72% (over 2/3 of all osteosarcomas)
294
Q

What is multifocal Osteosarcomatosis?

A

Most often in children in first decade, nearly always fatal

295
Q

Osteosarcoma can be from post therapeutic radiation, t/f

296
Q

What type of malignant bone tumor is extremely vascular?

A

Telangiectatic

297
Q

What type of tumor can become an ostoesarcoma?

A

Dedifferentiated chondrosarcoma

298
Q

What osteosarcoma originates in the soft tissue attached to the bone?

A

Extraskeletal Osteosarcoma

299
Q

What are 2 of the most common benign bone tumors?

A

Chondroma and Solitary Osteochondroma - asymptomatic

300
Q

What is a tumor of the cortical bone?

A

Chondroma, and it is a common benign

301
Q

What is a benign bone tumor that is inside the bone?

A

Enchondroma

302
Q

Is osteochondroma benign or malignant?

303
Q

What is a fibromyxoid chondroma?

A

Tumor made of fibrous mucus cartilage

  • Dominant content is cartilage
  • Loves the TIBIA - rare to be anywhere else

BENIGN

304
Q

What is a chondroblastoma?

A

High concentration found in the epiphysis - where chondroblasts are located - may spread into rest of bone

BENIGN**

305
Q

What are the 3 Malignant cartilage Tumors?

A
  • Primary Chondrosarcoma
  • Secondary Chondrosarcoma
  • Clear cell chondrosarcoma
306
Q

What is primary chondrosarcoma?

A

Didn’t require anything else for it to be there, it originates by itself

307
Q

What is secondary chondrosarcoma?

A

From a preexisting benign tumor that malignantly degenerate - can be multiple

  • Central secondary chondrosarcoma - From ENCHONDROMA, central is inside the bone in medullary cavity or cortex
  • Peripheral - OSTEOCHONDROMA - located external to the bone, looks like a trunk/stalk of broccoli coming off
308
Q

Central secondary chondrosarcoma comes from _____

A

Enchondroma

309
Q

Peripheral secondary chondrosarcoma comes from _____ ?

A

Osteochondroma

310
Q

What is clear cell chondrosarcoma?

A

Usually near a joint, mistaken for chondroblastoma

311
Q

What is one of the more common bone tumors?

A

Giant cell tumor of bone/osteoclastoma

312
Q

What are the characteristics of Giant cell tumor?

A
  • Classically expansile soap bubble lesion
  • about 1 in 5 are malignant
  • “Quasi - malignant” can go either way - 80% malignant
313
Q

Where do giant cell tumors most likey occur?

A

At the knee (HURT)

314
Q

Marrow tumors, aka:

A

round cell tumors

315
Q

What is the common theme with marrow tumors (round cell tumors)?

A

_Occur in diaphysis and are all MALGINANT AND DESTRUCTIVE ******_

316
Q

Ewings Sarcoma is in what category?

A

Marrow tumor (round cell tumor)

  • Classically gives laminated periosteal reaction
  • moth eaten appearance
  • big tubular bone in young children
317
Q

What is the most common primary bone malignancy in first decade (peak in teenagers)?

A

EWINGS SARCOMA

  • dont confuse Leukemia, which is the most common malignancy in the first decade
318
Q

What category is Non-Hodgkin Lymphoma under? (NHL)

A

Marrow tumor (round cell tumor: malignant)

319
Q

What is the most common primary bone malignancy?

A

_Multiple Myeloma**** TEST_

320
Q

Where would you see true punched out lesions?

A

Multiple Myeloma

321
Q

Explain Myelomatosis:

A

Form of multiple myeloma:

  • Produces osteopenia, looks like osteoporosis - will also have weakness and fatigue due to anemia - radiographically will look the same
322
Q

What will plasmacytoma have?

A

Geographic soap bubble lesion

323
Q

What is “extra osseous” ?

A

Branch of multiple myeloma

  • Mass in nasal pharynx (difficulty breathing), very uncommon
324
Q

What is under the Benign Vascular and Connective Tissue tumor?

A

Hemangioma - produces localized coarsening of the trabecular pattern

325
Q

What is the “Malignant vascular tumor?’

A

Fibrosarcoma

326
Q

What is the notochord remnant tumor?

A

Chordoma - most often found in Clivus, C2, sacro-coccygeal, will cross the joint

327
Q

What are secondary tumors?

A

Metastatic tumors in bone

328
Q

Vast majority of secondary tumors are _____

A

Hematogenous

329
Q

Osteolytic mets is a _____

A

secondary tumor

330
Q

What has 75% occurence %, osteolytic mets or osteoblastic mets?

A

Osteolytic

331
Q

What are the key points of osteolytic mets?

A
  • Destroys by physical bulk and restricting osteoblasts
  • 80% of metastasis found in spine, ribs and pelvis with another 10% found in cranium
  • Rarely go beyond the elbow and knee
332
Q

What accelerates osteoblasts?

A

Osteoblastic mets

333
Q

Pic of mixed mets

334
Q

What is in the “Tumor Like” category?

A
  • Not exhaustive list
  • Fibrous dysplasia - as common as Paget’s
335
Q

How can tumors be classified?

A
  • They can be classified by location of where they originate - most often from the metaphysis
336
Q

If a tumor is most likely benign, what will it’s characteristics be?

A
  • Almost always originate before age of 30 (with exception of giant cell tumor 20-40 years old)

KNOW THIS***

337
Q

What are the top “Malignant Tumors” ?

A

MOCEF - top 5 primary malignant

  1. Multiple Myeloma: Over 40
  2. Osteosarcoma: under 30
  3. Chondrosarcoma: 40 - 60
  4. Ewing’s: Under 40
  5. Fibrosarcoma: 30 - 60
338
Q

Primary Bone Tumors:

A
  • Bone Forming Tumors
  • Cartilage Forming Tumors
  • Giant Cell Tumor of Bone/Osteoclastoma
  • Marrow Tumors (Round Cell Tumors)
  • Vascular and Connective Tissue Tumors
  • Notochord Remnant Tumor
339
Q

What are the Bone forming primary bone tumors?

A
  • Benign
    • Osteoma
    • Osteoid Osteoma
    • Osteoblastoma
  • Malignant - Osteosarcomas
    • Conventional Osteosarcoma
      • 72% central
      • 75% sclerotic
      • 25% lytic
    • Parosteal Os 4%
    • Periosteal Os 1%
    • Multifocal Os/osteosarcomatosis 1%
    • Osteosarcoma of Jaw - 6%
    • Post Radiation Os - 4%
    • Os in Paget’s disease - 3%
    • Os Degeneration from benign condition - 1%
    • Telangiectatic Os - 3%
    • Dedifferentiated Chondrosarcoma - 3%
    • Extraskeletal Os. < 1%
340
Q

What are the Benign Cartilage Forming Tumors?

A
  • Benign
    • Chodnroma/Enchondroma
    • Solitary Osteochondroma
    • Chondromyxoid Fibroma/Fibromyxoid Chondroma
    • Chondroblastoma
341
Q

What are the malignant Cartilage forming tumors?

A

Malignant

  • Primary Chondrosarcoma - arise de novo
  • Secondary Chondrosarcoma - from preexisting benign tumor
    • Central - From enchondroma
    • Peripheral - From Osteochondroma
  • Clear cell chondrosarcoma - mistaken form chondroblastoma, low grade
  • Extra Skeletal - Rare
342
Q

What are the marrow tumors (round cell tumors?)

A
  • Ewing’s Sarcoma
  • NHL (non hodgkin lymphoma) of bone/reticulum cell sarcoma
  • Multiple Myeloma
343
Q

What are the branches of multiple myeloma?

A
  • Classical MM
  • Myelomatosis
  • Plasmacytoma
  • Extra Osseous MM
344
Q

Vascular and Connective Tissue tumors are in what category, what are their subcategories?

A

It is in the category of “primary bone tumor”

  • Benign - Hemangioma
  • Malignant - Fibrosarcoma
345
Q

Metastatic Tumors in bone - most common skeletal malginancy

A
  • Osteolytic Mets
  • Osteoblastic Mets
  • Mixed Mets
346
Q

Tumor Like Conditions:

A

PRIMARY BONE TUMORS

  • Solitary bone cyst/Unicameral bone cyst
  • Aneurysmal bone cyst
  • Fibrous Cortical defect and nonossifying fibroma
  • Fibrous Dysplasia
  • Brown Tumor of hyperparathyroidism
  • Pseudotumors of Hemophilia
  • Large Arthritic Cysts/Geode
347
Q

If it’s a benign tumor they overwhelmingly originate when?

A

Before the Age of 30

348
Q

If a tumor is asymptomatic and benign, it may not show till ____

349
Q

When does Giant cell tumor usually occur?

A

20-40 this is an exception

350
Q

Metastisis happens how?

A

Through Vascular system

351
Q

Big 6 strongest potential to spread?

A
  1. Breast - females 70%
  2. Lung - 25%
  3. Prostate - Males 60%
  4. Kidney
  5. Ewing’s
  6. Neuroblastoma

*** Breast, lung, prostate, and kidney account for 80%

352
Q

Where does lytic Mets come from?

A

Physical bulk - pressure from the tumor taking up space which impedes the osteoblasts

  • More common (75% of metastasis destroys)
353
Q

Approximately 80% of all osseous metastases will be found _____

A

In the axial skeleton

  • 28% ribs
  • 39% vertebra
  • 13% bony pelvis

10 % of skeletal metastasis will be found in the cranium

10% extremities

354
Q

Is Enostosis primary or secondary bone tumor?

A

Primary

AKA BONE ISLAND

355
Q

What is enostosis classified as?

A

Tumorlike, usually an incidental finding, and is asymptomatic

356
Q

What are the characteristics of Enostosis?

A
  • Rare in children
  • Osteosclerotic bone lesion
  • Can be considered a hamartoma (benign tumor that is multicellular and has all the cells of the host tissue)
357
Q

Where is the location of Enostosis?

A

Intramedullary Location - usually up against inner surface of cortex

  • Composed of normal appearing compact lamellar bone with haversian canals
  • Blends with surround trabecular bone creating irregular margin
358
Q

What is the radiological appearance of Enostosis

A
  • Round to oval (.2 - 2 cm) osteoblastic area
  • Epiphyseal or metaphyseal
  • Bone scan NORMAL

95 % no need for further radiologic evaluation

359
Q

WHat is the differential diagnosis for Enostosis?

A

Osteoblastic Mets, osteoma, osteoid osteoma, low grade osteosarcoma

360
Q

Osteoblastic mets ____

361
Q

low grade osteosarcoma is ____

362
Q

When would you take a biopsy of Enostosis?

A

Increase in size of 25% in 6 months

363
Q

Bony pelivs is a common site to see ____

364
Q

Giant bone island is a _____

A

Enostosis that is > 2-3 cm in size

More likely to have increased activity on bone scan

365
Q

What are the possible diseases related to Enostosis?

A
  • Osteopoikilosis
  • Osteopathia Striata
  • Melorheostosis
366
Q

Osteopoikilosis =

A

Periarticular bone islands

367
Q

Osteopathia Striata =

A

Lesions are more elongated in periarticular pattern, Vooerheve disease, fan-like bands in flat bones

368
Q

What are the 3 common characteristics of Melorheostosis?

A
  • Osteosclerotic bone disorder
  • Often symptomatic (pain, decreased ROM, contractures, limb swelling, bowing)
  • Scleroderma - like skin lesions over osseous changes
369
Q

What is the radiology of Melorheostosis?

A

o Osseous excrescences often exuberant and lobulated along bone surface

o Single limb—more common lower extremity

o Also endosteal involvement may extend into marrow space

o Intense activity on bone scan

o Long drippy bone island

​

370
Q

Benign Bone forming:

A

OSTEOMA

OSTEOID OSTEOMA

OSTEOBLASTOMA

371
Q

Osteoma aka:

A

Ivory Exostosis

372
Q

What is a benign, slow growing hamartomatous lesion composed of well differentiated mature bone?

373
Q

What is the defect in Osteoma?

A

One resorption or formation during skeletal maturation

374
Q

What does osteoma arises beneath?

A

Endosteum from inner surface of cortex

375
Q

What causes surrounding reactive bone formation in Osteomas?

A

Elevation of periosteum from underlying bone

376
Q

Osteoma is a bone of _____

A

Intramembranous origin

377
Q

Extracranial Osteoms -

A

.03% of bone biopsied primary bone lesions

378
Q

Paranasal sinus osteomas -

A

.4%

Most have a osteosclerotic lesion in a frontal or ethmoid lesion

379
Q

What are the associated abnormailities with Osteoma?

A
  • Gardner’s Syndrome
  • Mutation of Adenmatous Polyposis Coli Gene (5q21)
  • Multiple osteomas, intestinal polypsos, soft tissue desmoid tumors
  • Bone lesions may precede intestinal polyposis
380
Q

Describe Gardner’s Syndrome in Osteoma:

A
  • Autosomal Dominant
    • Syndrome of hamartomatous tumors in different locations
    • One of the key findings - osteomas
    • Will develop color cancer (precursor to colon cancer)
381
Q

In osteoma, most just have ____

A

single solitary osteoma

382
Q

What are the clinical issues associated with Osteoma?

A
  • Small lesions usually asymptomatic
  • Project away from cortical surface
  • Palpable enlarging osseous mass
383
Q

What is the nasal issue with Osteoma?

A
  • Large oseomain paranasal sinus may obstruct nasal ducts
    • Can erode wall of cranial fossa and dura
    • Can cause mucocele, sinusitis, headache, pain
384
Q

What can osteoma tumors near orbit cause?

A

Cause exopthalmosis, double vision, vision loss

385
Q

What about the Hx of Osteoma:

A
  • Found before 30 but can be seen anytime
  • EQUAL GENDER
  • No malginant potential
386
Q

What looks identical to bone island but has different location?

387
Q

What does Osteoma look like radiographically?

(first 3)

A
  • Well defined round dense sclerotic lesion attach to underlying bone
  • Vast majority in frontal and ethmoid sinus
  • DENSE ivory like sclerotic mass
388
Q

What does Osteoma look like radiographically?

(last 3)

A
  • No satellite lesions
  • Low signal on MRI
  • Plain film is good to see them
389
Q

OSTEOID OSTEOMA: main characteristics

A
  • Painful!
  • Produce dense periosteal reaction
  • Can regress spontaneously - infarction
  • Local swelling and point tenderness
390
Q

What is Osteoid Osteoma characterized by?

A

Nidus less than 1 cm of osteoid/woven bone is vascular tissue surrounded by zone of reactive sclerosis

391
Q

What is elevated in Osteoid Osteoma?

A

Prostaglandin E2 elevated 100-1000 times within Nidus (pain and vasodilation)

392
Q

Describe the nidus in Osteoid osteoma:

A

Radiolucent and is the actual tumor

393
Q

Pain is worse at night with what tumor?

A

Osteoid Osteoma

394
Q

Whats the origin of Osteoid Osteoma?

A

Unknown, inflammatory, traumatic, vascular, viral

395
Q

What is a distinguishing characteristic of Osteoid Osteoma?

A

These can produce a painful scoliosis, and they happen in the spine (lean into a legion)

396
Q

Osteoid Osteoma is more common in ______

A

males 2-3:1

397
Q

What are the first 4 radiological features of Osteoid Osteoma?

A
  • Long bones are common
  • Metaphysis/Diaphysis
  • Phalanges of hands and feet
  • Spine (10%)
    • Posterior Elements 90% - posterior arch lamina
    • Vertebral body 10%
398
Q

What are the last 5-6 radiological features of osteoid osteoma?

A
  • Cortical: 70-80%
    • Radiolucent Nidus < 1.5 cm with surrounding dense sclerosis
    • Periosteal reaction may be present
  • Medullary: 25%
  • CT - well defined, round oval nidus surrounded by sclerosis
  • MRI - T1 WI nidus isointense to muscle
399
Q

What does osteoid osteoma look like on bone scan?

A

lights up

(will have a solid dense periosteal reaction)

400
Q

OSTEOBLASTOMA aka:

A

Giant osteoid osteoma, osteogenic fibroma

401
Q

What is Osteoblastoma characterized by?

A
  • Production of osteoid and woven bone
  • Lesion > 1.5 cm
  • Histology similar to osteoid osteoma
402
Q

What are the %’s associated with Osteoblastoma?

A

< 1% of primary bone tumors

3% benign bone tumor

403
Q

Describe Osteoblastoma:

A
  • Circumscribed mass, often surrounded by shell of cortical bone or periosteum
  • Sharp interphase between lesion and cancellous bone
404
Q

What does the nidus look like in Osteoblastoma?

A
  • 2-10 cm, friable, deep red (highly vascular)
  • Very vascular connective tissue stroma with interconnecting trabecular bone
405
Q

What are the symptoms of osteoblastoma?

A
  • Dull, localized pain of insidious onset
  • Pain rarely interferes with sleep
  • Localized swelling, tenderness, and decreased ROM
  • Doesnt respond well to aspirin
406
Q

Osteoblastoma originates ____

407
Q

Osteoblastoma gender pref.

A

2-3:1 in males

408
Q

WHat can Ostoeblastoma have?

A

Foci of aggressive stage 3 lesion (prone to aneurysmal bone cysts formation)

RECURRENCE AFTER resection = 10-25%

409
Q

In aggressive osteoblastoma, the recurrence is ____ %

410
Q

First 4 things of Osteoblastoma (radiology):

A
  • 30-50% SPINAL
    • Posterior elements –> 60% spinous, transverse process, pedicle
    • Posterior elements with extension into vertebral body 25%
    • Vertebral body 15%
  • Long bones, 30% originate in metaphysis
411
Q

What are the 5-8 radiographic features of Osteoblastoma?

A
  • Hands and feet 15%
  • Skull and Jaw 15%
  • Pelvis 5%
  • Expansile, lytic circumscribed lesion
  • Reactive sclerosis 60%
412
Q

Last radiologic features of Osteoblastoma:

A
  • CAN rapidly increase in size
  • Secondary aneurysmal bone cyst (ABC): 16% can look exactly the same
  • NECT: Expansile, lytic lesion with or without matrix mineralization
    • Can be purely radiolucent inside, speckled (inside matrix), or sclerotic looking

KEY IS EXPANSION

413
Q

MALIGNANT PRIMARY BONE TUMORS:

A

Osteosarcoma, aka Osteogenic Osteosarcoma

414
Q

What is the main definition of Osteosarcoma?

A

Malignant tumor with ability to produce osteoid directly from neoplastic cells

415
Q

Talk about the growth rate of Osteosarcoma:

A

Frequency of tumor occurence corresponds to greatest growth rate during adolescence

416
Q

What is chemically happening in osteosarcoma?

A

Overexpression of P-glycogen in OGS cells with propensity for metastasis and rx failure

alteration in Rb genes in OGS

417
Q

Think of osteosarcoma as ____

A

osteoblastic malignant tumor

418
Q

Periosteal reaction of osteosarcoma =

A

Spiculated

419
Q

2nd primary bone tumor is ____

A

Osteosarcoma (MOCEF)

420
Q

When does osteosarcoma peak?

421
Q

Where is the most common location for osteosarcoma?

A

Distal femoral metaphysis

422
Q

Osteosarcomatosis survival:

A

Change low

423
Q

Where will osteosarcoma metastasize to?

424
Q

Osteosarcoma has a majority of unknown origin, primary, but secondary to predisposing factors are:

A
  • Paget’s Disease (4th stage)
  • Bone infarction
  • Radiation
425
Q

What is the most common malignant primary bone tumor in young adults and children?

A

Osteosarcoma

6 SKEL B (5 decks)

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