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*Part IV Boards > Radiology > Flashcards

Radiology Flashcards

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1
Q

what do we do with new fractures?

A

refer to orthopedist

if in cervical spine, call 911

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2
Q

what makes a compression fracture new?

A

step defect
trabecular impaction
compare to old films

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3
Q

What will MRI show when looking at a new fracture? CT?

A

marrow edema

extent of body involvement and possible comminution

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4
Q

what do we do with degenerative arthritides?

A

we manage it
consider MRI for disc evaluation and CT/MRI for spinal canal stenosis
if it gets worse, consider orthopedic/neurological consult

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5
Q

what do we do with inflammatory/connective tissue arthridities?

A

co-manage with rheumatologist. lab studies support radiographic diagnoses.
erosions could lead to instabilities
perform cervical flexion, extension views, which may refer to orthopedist

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6
Q

what do we do with metabolic arthridities?

A

co-manage with rheumatologist

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7
Q

what do we do with benign tumors?

A

co manage
benign tumors are imaged with MRI to evaluate marrow characteristics and CT to evaluate cortical bone changes. some tumors simply need monitoring for future symptom development (osteochrondroma, hemangioma).
some benign tumors weaken bone and will need to be removed to avoid complications.
refer to orthopedist

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8
Q

what do we do with malignant tumors?

A

co-manage with oncologist
MRI will evaluate for bone destruction.
CT will define the extent of cortical destruction
radionuclide scintigrophy will reaveal multiple sites of involvement
chest films will evaluate metastatic spread to the lungs
lab studies may confirm bone destruction and most likely pathology
biopsy will reveal the particular pathology

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9
Q

what do we do with tumor like process?

A

co manage with oncologist and orthopedist, similar to malignant management. paget disease and fibrous dysplasia are benign, but have malignant potential

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10
Q

where does OA typically occur?

A

disc, posterior facets, extremities

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11
Q

associated conditions of OA

A

DISH, OPLL, OCI, risks for canal stenosis

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12
Q

who usually gets OA?

A

40 and older

may be seen in limited number of post-trauma, more likely in regions of anomalous joints (SCFE, DDH, healed AVN)

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13
Q

management for OA

A

chiro care unless with hypermobility

allopath: pain meds, surgical fusion, joint replacement

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14
Q

does OA cause erosions or lead to fusion?

A

NO

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15
Q

findings on xray with disc disease

A

decreased disc height, osteophytes, intercalary ossicles, vaccum phenomenon, posterior translation of vertebra, subchondral sclerosis (eburnation), uncinate hypertrophy (lushka joint hypertrophy)

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16
Q

findings on xray with posterior joint disease

A

posterior facet hypertrophy/arthrosis, anterior translation of vertebrae (spondylolisthesis), interspinous sclerosis (baastrup’s/kissing spinous process)

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17
Q

types of spondylolisthesis

A

I: dysplastic, congenital anomalies
II: isthmic, pars interarticularis defect
III: degenerative
IV: traumatic, fracture other than pars (Hangman’s fracture)
V: iatrogenic

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18
Q

bony causes of spinal canal stenosis

A

osteophytes, paget, hemangioma (when expansile), pedicle hypoplasia, congenital anomalies

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19
Q

soft tissue causes of spinal canal stenosis

A

disc herniations, OPLL, facet capsule ossification, ligamentum flavum thickening

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20
Q

C2-7 discs go with which nerve roots?

A 
C2 disc- C3 NR
C3 disc- C4 NR
C4 disc- C5 NR
C5 disc- C6 NR
C6 disc- C7 NR
C7 disc- C8 NR
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21
Q

if there was a PARACENTRAL disc herniation in the lumbars, which nerve roots would be affected?

A 
L1 disc- L2 NR
L2 disc- L3 NR
L3 disc- L4 NR
L4 disc- L5 NR
L5 disc- S1 NR
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22
Q

if there was a LATERAL disc herniation in the lumbars, which nerve roots would be affected?

A 
L1 disc- L1 NR
L2 disc- L2 NR
L3 disc- L3 NR
L4 disc- L4 NR
L5 disc- L5 NR
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23
Q

people who get DISH

A

people who get diabetes, middle age-older, overweight, metabolic syndrome, cardiovascular disease

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24
Q

what should you evaluate for for people with DISH? how?

A

diabetes

blood or urine analysis

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25
Can we adjust a segment with DISH?
no..
26
osteitis condensans ilii
most commonly seen in postpartum women, but could be seen in men iliac-based sclerosis, importantly WITHOUT EROSIONS if there is erosions, DDX of sacroiliitis
27
which OAs have erosions?
erosive OA RA Psoriatic
28
``` who gets these inflammatory arthridities? RA AS EA PA reactive ```
``` RA: middle aged women AS: younger men EA: younger women PA: middle aged, no gender bias reactive: younger men ```
29
what are some complications of inflammatory arthridities?
pain, erosions, ankylosis
30
describe RA
common, autoimmune, multisystem (joints, lungs, kidneys) disease, aggressive and progressive
31
describe the joints of someone with RA
hyperplastic synovitis (pannus) formation, causing symmetrical loss of joint space and erosions, usually polyarticular. bilateral and symmetrical prefers wrists, hands, shoulders, feet, knees, hips, cervical spine
32
s/s in the extremities of RA
soft tissue swelling hands achy in the morning hyperemia around joints leads to juxta-articular osteopenia bare area erosions region of RA will eventually becomes osteopenic joint deformities ankylosis
33
RA in hands, wrists, feet
``` usually first site of involvement bilateral and symmetrical within the body and within the involved joint MCP and PIP first swan neck deformity boutonniere deformity ulnar deviation of fingers at MCP fibular deviation of toes at MTP erosions around ulnar and radial styloid processes erosions within carpals ```
34
RA in the shoulders
erosions at AC joint, sometimes causing resorption of distal clavicle erosions around humeral head and acromion erosions around supraspinatus tendon leading to rotator cuff tear, which results in elevation of the humeral head and reduced acromiohumeral space
35
RA in hips and knees
uniform loss in all joint spaces, joint deformities, subchondral cysts, baker's cysts
36
RA in spine
50% of patients with RA will have cervical spine involvement, causing erosions within facet capsules around ligament and tendon attachments
37
management for RA
RA factor + (most of the time) anti-CCP antibodies present ESR and CRP elevated -ANA radiographic re-evaluation every 6-12 months until stable; MRI for panus and neuro effects don't adjust fused or hypermobile segments recommend adequate sleep, dietary changes, exercise refer to rheumatologist for pharmacology (NSAID, corticosteroids, anti-rheumatic drugs)
38
SLE demographics
30-50yo females | blacks slightly higher than whites
39
clinical findings of SLE
malar rash joint deformities serious multisystem disease of kidneys, liver, lymphatics, joints
40
scleroderma demographics
30-60 yo woman blacks more than whites serious multi-system disease of connective tissue may have CREST (calcinosis, raynaud's, esophageal lesions, sclerodactyly, telangiectasia
41
scleroderma in hands
ungual tuft resorption/acral osteolysis/distal tuft resorption soft tissue atrophy, soft tissue calcification, erosions in the DIPs, PIPs, and MCPs calcifications are distinctive (dense, globular, clumpy)
42
scleroderma management
chest films chest CT upper GI contrast studies refer to rheumatologist
43
seronegative spondyloarthropathies
AS enteropathic psoriasis reactive
44
most seronegative spondyloarthropathies have what lab finding?
HLA-B27 (present in most to varying degrees) ESR, CRP elevated ANA -
45
Marie-Strumpell demographics
AS most common inflammtory spondyloarthropathy, onset around late 20s and early 30s males more than females
46
AS in the spine and pelvis
SI is typically the first and most common site of involvement (50% will have full SI ankylosis) squaring of vertebrae, syndesmophytes (marginal, thin, gracile), romanus lesion, shiny corner sign, dagger sign, railroad sign, trolly track sign
47
AS management
plain films MRI and CT to further define osseous changes and characterize any neurological complications HLA-B27, ESR+, RA-, ANA- educate on safe activities joint mobilization, posture and thoracic expansion exercises allopaths (anti-inflammatories, rheumoatologist
48
enteropathic arthritis | causes
chron's disease, ulcerative colitis, whipple disease, GI infections, cirrhosis
49
enteropathic arthritis | what spine looks like on xray
``` squaring of the vertebrae syndesmophytes romanus lesion shiny lesion shiny corner sign dagger sign railroad sign trolley track sign ```
50
managment for enteropathic arthritis
almost same as AS, but HLA B27 in 60-70%, ESR up, RA and ANA - refer to gastroenterologist, internist, rheumatologist
51
psoriatic arthritis description
most people with dermatological psoriasis DON'T have inflammatory arthritis rarely would someone have arthritis and not skin lesions usually occurs around 30-50yo equal occurance in females and males
52
how is PA similar to AS and RA? different?
similar: erosions, symmetrical joint space narrowing, eventual ankylosis different: asymmetrical distribution about body and digit, normal bone density, peri-ostitis, acro-osteolysis
53
PA in extremities
``` sausage digit ray pattern mouse ears pencil in cup osteolysis ```
54
PA in spine and pelvis
SI erosions and eventual ankylosis | spine findings are key in distinguishing features of PA vs other causes of sacroiliitis
55
PA managment
evaluate skin and nails for lesions serological studies (HLA B27 up, RA and ANA - chiro care: be wary of hypermobility and ankylosis allopath: NSAIDs, anti-rheumatic drugs, refer to rheumatologist
56
reactive arthritis
``` non-marginal, thick, bulky, may be discontiguous not common males (adolescent-mid 30s usually follows gastrointestinal or genitourinary infection may also be linked to genetic factors iritis urethritis athritis ```
57
reactive arthritis treatment
treat infection first, then spondyloarthropathy may resolve
58
metabolic and crystal-induced arthropathies
gout CPPD ochronosis
59
gout
MC inflammatory arthritis in men older than 40 40-50 yo men too much uric acid in blood (produce too much or can't clear enough) most patients with gout don't develop tophacious gout crystals accumulate in and around joints, leading to erosions with "overhang", lump and bumpy digits
60
gout managment
plain films won't show tophi until years after the disease labs (hyperuricemia) lifestyle modifications- evaluation of triggers that lead to the attack allopath: anti-inflammatory medications, xanthene oxidase inhibitors
61
chondrocalcinosis
CPPD middle-aged and older equal among males and females associated with hyperparathyroidism, diabetes, hemochromatosis, gout, neuropathic arthropathies (syphilis, diabetes)
62
chondrocalcinosis management
gold standard is joint aspiration to look for crystals chiro care: exercise, joint mobilization allopath: NSAIDs
63
calcific tendonitis
HADD not a crystal induced arthropathy, but can get mixed up with CPPD typically monoarticular and MC in shoulder as dense calcification
64
calcific tendonitis management
HADD | degenerative, treated as OA; some modalities may lessen symptoms (laser, US)
65
septic arthritis
infections do not respect anatomical boundaries (they'll destroy all tissues) discs: rapid loss of disc height and development of endplate erosions joints: rapid loss of joint space and development of cortical erosions
66
septic arthritis management
CT for cortical destruction, MRI for marrow destruction, refer to ortho for aspiration, antibiotics, curretage, management of risk factors (HIV, diabetes, UTI)

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