Musculoskeletal disorders Pt. II Flashcards
1
Q
What kind of lesions are found with fibrodisplasia?
A
Benign lesion, failure of body differentiation.
2
Q
How does fibrodysplasia affect bone growth?
A
Arrested development of bone
3
Q
How does FD affect size and morphology of bone?
A
Well circumscribed,intramedullary, variable size. Possible osseuous deformation.
4
Q
What are the three categories of FD
A
- ) Monostotic: single bone involvement
- ) Polyostotic: mutliple bone involvement
- ) Polyostotic + cafe au lait spots & endocrinopathy
5
Q
What is type 3 FD AKA
A
McCune-Albrite syndrome.
6
Q
What age is Monostotic FD normally seen?
A
Between ages 10-30
7
Q
Where is Monostotic FD detected?
A
ribs, femur, tibia, jabones, calvaria, humerus. Minimal bony distortion/enlargement
8
Q
T/F
Monostotic FD is very symptomatic?
A
False, asymptomatic.
9
Q
What are some features of polyostotic FD
A
No endocrinopathy, late childhood/adolescence
10
Q
What morphological bone features are noticed with polyostotic FD?
A
Severe deformation, pathologic fx, is common.
11
Q
Where is Polyostotic FD seen?
A
Femur, calvaria, tibia, humerus, pelvis
12
Q
How often is craniofacial involvement?
A
50% of all cases.
13
Q
What radiographic features are indicative of Polyostotic FD?
A
Well defined margins “ground glass” apprearance. “Shepherd’s crook” disorder
14
Q
What is the treatment for Polyostotic FD?
A
Excision, orthotic hardware.
15
Q
McCune-Albright syndrome is how much of polyostotic FD cases?
A
3% of all cases of FD.
16
Q
What are some specific endocrine related issues with MC-albrite syndrome?
A
Precocious puberty prompts evalutation, MC females. Endocrine hperfunction: hyperthyroidism, pituitary adenoma, adrenal hyperplasia.
17
Q
What are the 3 major aspects of A&P are affected by MC-Albrite syndrome?
A
Skin, skeletal, endocrinopathy.
18
Q
T/F
MC-Albrite syndrome is generally severe
A
False,
variable severity
19
Q
What is the disperal of lesions like with MC-Albrite syndrome?
A
Skin and bony lesions are commonly unilateral (femur, tibia)
20
Q
T/F
Ewing sarcoma and Primitive Neuroectodermal Tumor are variant of the same malignant tumor
A
True
21
Q
What are some features of Ewing Ssarcoma and PNET?
A
“Small round cell tumors” of bone.
Hemorrhage and necrosis, medulla and cortex.
22
Q
T/F
Ewing Sarcoma is highly differentiated?
A
False, highly undifferentiated
23
Q
What percent of primary bone cancers are Ewing’s sarocoma?
A
10%
24
Q
How common is Ewings sarcoma in pediatric bone CA?
A
2nd MC
25
Neural differentiation and Homer-Wright rosettes are indicative of what?
PNET
26
What is the MC age for Ewing Sarcoma and PNET, who is at risk?
10-20 years MC. Caucasian males most at risk
27
What morphological features are found with Ewing Sarcoma and PNET
Fempainful enlarging mass, loong bone diaphysis. "onion-skinning" or "sunburst" appeerance on the periosteum.
28
What areas are most affected by Ewing Sarcoma and PNET?
Femur (MC) or pelvis
29
Ewing Sarcoma and PNET stimulate proinflammatory cytokines which mimics what?
Infection. Elevating pyrexia, leukocytosis, and ESR
30
Onion skinning appearance of periosteum is indicative of what condition?
Ewing Sarcoma
31
What is the survival of 70% of Ewing Sarcoma PNET patients?
5-year survival
32
What gives for a worse prognosis for Ewing sarcoma and PNET?
Invasion of surrounding tissues
33
What is the treatment for Ewing Sarcoma and PNET?
Excision, chemotherapy
34
Ginat cell tumor of bone inolves what kind of cells?
Multinucleated giant cells (osteoclast-like), neoplastic monocunlear cells.
35
What age group is most associated with giant-cell tumor of bone?
Age 20-40
36
What kind of lesions are associated with Giant-cell tumor of bone?
Large, lytic, solitary, eccentric (off center) lesions
37
What areas are the lesions found with giant-cell tumor of bone
Knee (MC): dist. femur/prox. tibia. Locally invasive, erode cortex
Epiphysis/metapysis
At the ends of bones basically
38
How can giant-cell tumor of bone be identified
Biopsy
39
Is giant-cell bone tumor of bone painful?
Yes, arthritic like pain.
40
What x-ray features of giant-cell bone tumor?
Osteolytic, eccentric, thin shell of reactive bone.
41
Is it certain whether giant cell bone tumors are malignant or not?
No.
42
How many cases of giant-cell bone tumors metastasize?
2% MC lungs
43
What is the treatment for giant-cell bone tumors?
excision, radiation.
44
What are some radiographic features of giant cell bone tumor?
Thin "shell" of cortex
| "Soap bubble" appearance
45
What is secondary mets to bone?
Any cancer that spreads to bone
46
T/F
Secondary metastasis is more common than primary bone cancers
True
47
What are the mechanisms for secondary mets?
1. ) Direct extension (physical contact)
2. ) Circulation: lymphatic or hematogenous (sarcomas: hematogenous, carcinomas: lymphatics)
3. ) Intraspinal seeding
48
What does secondary mets do to bone?
Lytic, blastic, or mixed (MC)
49
Where is secondary mets found MC?
Axial skeleton, prox. femur/humerus because of
| red marrow: stasis, nutrient rich (implantation & growth)
50
What are the MC forms of secondary mets?
Adults: prostate (blastic), breast (lytic), lung
Children: neuroblastoma, Wilms tumor, osteosarcoma, Ewing sarcoma, rhabdomyosarcoma (malignancy of skeletal myocytes).
51
What are the 5 types of arthridites?
1. ) Degenerative (OA, DJD)
2. ) Immune-mediated (RA, ankylosing spodylitis)
3. ) Metabolic (Gout, pseudogout "CPDD")
4. ) Infectious
5. ) Neoplastic
52
T/F
Osteoarthritis is the major source of morbidity in the elderly
True
53
What is the most common joint disorder?
Osteoarthritis
54
What is osteoarthritis often confused with?
Rheumatoid arthritis
55
What does OA involve?
Degeneration of articular cartilage (collagen). Decreased proteoglycans = matrix breakdown
56
T/F
OA is always inflammatory
False, not necessarily inflammatory. Patient symptomotology does not always include pain.
57
What are secondary changes with OA
Subchondral changes. Mechanical wear and tear (age). Genetic influence.
58
What is primary OA
Insidious, oligoarticular (involves just a few joints). No trauma, adults
59
What is secondary OA
Predisposing injury or deformity. Trauma (obesity), deformity, systemic disease
60
What percentage of cases of OA occur in children?
5%, usually secondary to another condition.
61
Where does OA occur in the spine and extremeties?
Cervical, lumbar, DIP joints, 1st MCP joints, 1st TMT joint.
62
Where do females and males most experience OA?
Females: Knees and hands
Males: Hips
63
How can OA degrade a disk?
Decreasing proteoglycans which cause dehydration of the disk.
64
What bony changes happen with OA
Matrix cracks, softening/degradation (condromalacia), exposure of subchondral bone, sclerosis of bone (eburnation), osteophytosis. Inflammation may develop secondary to degeneration.
65
In advanced cases (all subchondral bone of affected area is exposed) what is seen in the bone?
Sunchondral fx -> exposure to synovial fluid -> subchondral cysts.
Possible joint mice: joint locking & pain.
66
What does eburnation mean?
"Ivory-like".
67
What properties provide elasticity and tensile strength to joints?
Proteoglycans and type II collagen (healthy condrocytes)
68
What does OA do to chondrocytes?
Distrupts functions, which decreases the resiliency of cartilage. Causes degeneration in normal cartilage.
69
What are some risks for OA?
Mechanical stress (age 50-60), genetics, increase bone density, increase estrogen. NOT simply wear-and-tear.
70
What are some features of OA?
Insidious, deep/achy pain, crepitus, decrease ROM, worse in morning. Generally slowly progressive.
71
What are some nervous system issues implicated in OA?
Osteophytes may impinge nerve roots. Radiculopathy (pain, weak, numb) spasm, atrophy.
72
What is the tx for OA?
Palliative
Ice, heat, NSAIDs, adjust, joint replacement.
73
What are some radiographic signs of OA?
Loss of joint space (dehydration). No ankylosis.
74
What kind of condition is RA?
Systemic, chornic autoimmune disease?
75
What cells are implicated in the autoimmunity of RA?
CD4+ T cells, cytokines, macrophages.
76
What is destroyed in RA?
In joints: increase collagenase and osteoclast activity
77
What are the 2 things that RA patients are tested for?
Anti-CCP antibodies (70% of cases) inflamamtion: smoking or infection.
IgM autoantibodies: 80% Rheuamtoid factor (RF), IgG immune complex. MC
78
What are the general features of RA?
Weakness, malaise, low-grade fever, cachexia. Insidious, aching, joint stiffness, decrease ROM.
79
T/F
RA affects large joints that are affected symmetrically
False,
Symmetric, small joints. Hands, feet, ankles, wrists, elbows, kness (although rare, usually it will be OA with the knee).
80
What are some features of joint harm with RA?
MC, MCP & PIP (Bouchard's). "Fusiform swelling"
Spine: 30% have atlanto-axial instability
81
What are some features of joint destruction with RA?
Pannus (granulation tissue), articular destruction/disability. 10-15 years to develop usually. Ulnar deviation, swan-neck deformity. Eventual ankylosis.
82
What are some key differences of RA and OA?
RA: autoimmune, inflammatory, ankylosis
OA: degenerative, non inflammatory, NO ankylosis.
83
What is Jevenile rheumatoid arthritis?
Autoimmune. Group of multifactorial disorders, MC neg. for RF.
84
What are some diagnostic criteria for JRA?
Early onset of pain (<16 years old), lasting up to or longer than 6 weeks.
85
What joints are MC affected by JRA
Large joints: knees, hips.
86
T/F
Males are more likely to develop JRA?
False,
Girls 2-3x more likely to develop than males.
87
What is the acronym for seronegative spondyloarthropothy categories?
P.E.A.R
P: Psoriatic arthritis (psoriasis)
E: Enteropathic arthritis (inflammatory bowel disease)
A: Ankylosing spondylitis
R: Reactive arthritis
88
What are some characteristics of seronegative spondyloarthropathies?
Sacroiliitis, spinal ligaments (syndesmophytes)
89
Ankylosing spondylitis is AKA?
Marie Strumpell disease
90
What are some features of AS?
Sacroiliitis (inflammation), referred gluteal pain.
| Syndesmophytes: bamboo spine, decreased lordosis, decreased flexion
91
What are some notable symtoms related to AS?
Morning stiffness
Nocturnal LBP (unrelieved when lying down)
Decreased chest expansion: ankylosing of rib joints
Fusion
92
T/F
95% of AS cases are HLA-B27 positive
True
93
What causes gout?
The result of abnormal purine metabolism. Uric acid accumulation, monosodium urate crystals (tophi). Failed crystal phagocytosis
94
What is the presentation of gout like?
Acute inflammation, recurrent (destruction, fibrosis)
95
What is primary gout?
Hyperuricemia (↑ uric acid production)
•Idiopathic, 90% of cases
•Hypothesized enzyme defects
96
What is secondary gout?
Co-morbid disease or drug exposure
| •Renal disease, leukemia, multiple myeloma, diuretics
97
Who is at risk for getting gout?
Males >30
98
Where does gout MC manifest?
In hallux (MTP) = podagra
99
What are the 3 types of gout?
1. Asymptomatic hyperuricemia
2. Acute gouty arthritis: cycles, hours-to-weeks (erythema)
3. Repeated: “chronic tophaceous arthritis”
•Fails to resolve between cycles
•20% die of renal failure (gouty nephropathy)
100
Where are the possible tophi deposition locations with gouty arthritis?
* Toes
* Fingers
* Helix of the ear
* Prepatellar bursa
* Olecranon
101
What is a late stage problem with gout?
Irreversible joint deformity
102
What is Pseudogout AKA?
Chondrocalcinosis or CPDD
103
What is pesudogout (CPDD)
Altered pyrophosphate metabolism. Pyrophosphate crystal deposition into joints
•Knee, wrist, shoulder, hip, elbow, ankle
104
T/F
Pseudogout (CPDD) is MC inherited
False
MC sporadic
105
What is the age of onset for CPDD?
>50
106
What happens with inflammation lasting weeks in CPDD?
Destruction of joint 50% of the time.
107
What are the tx for CPDD?
NSAIDS, corticosteroids (palliative meds)
108
What is HADD?
Hydroxyapatite deposition disease AKA calcific tendonitis
Hydroxyapatite accumulate in tendons, produces "soft tissue opacities"
109
What causes HADD?
Idiopathic, possible dystrophic Calcification
110
What symptoms are noted with HADD?
Pain, swelling, reduced ROM
111
At what locations does HADD appear?
Rotator cuff muscles (MC), elbow, wrist, hip, ankle
112
What is DISH and what is it AKA?
Diffuse idiopathic skeletal hyperostosis
AKA Forestier disease
113
What areas does DISH affect?
* Tendinous & ligamentous insertions
* Anterior longitudinal ligament (ALL)
* Spine: cervical, thoracic spine (T7-11)
114
What are the two types of infectious arthritis?
1. Suppurative arthritis
| 2. Lyme arthritis
115
What is suppurative arthritis?
Suppurative: pus forming
| •Bacteremia → seeds to joints
116
What are the features of suppurative arthritis?
Acute inflammation, ↓ ROM, fever, ↑ ESR
117
Where does suppurative arthritis occur?
90% monoarticular
| •Knee (MC), hip, shoulder, elbow, wrist, S-C joint
