Radiology Flashcards

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
Q

Can we adjust a segment with DISH?

A

no..

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26
Q

osteitis condensans ilii

A

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

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27
Q

which OAs have erosions?

A

erosive OA
RA
Psoriatic

28
Q
who gets these inflammatory arthridities?
RA
AS
EA
PA
reactive
A
RA: middle aged women
AS: younger men
EA: younger women
PA: middle aged, no gender bias
reactive: younger men
29
Q

what are some complications of inflammatory arthridities?

A

pain, erosions, ankylosis

30
Q

describe RA

A

common, autoimmune, multisystem (joints, lungs, kidneys) disease, aggressive and progressive

31
Q

describe the joints of someone with RA

A

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
Q

s/s in the extremities of RA

A

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
Q

RA in hands, wrists, feet

A
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
Q

RA in the shoulders

A

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
Q

RA in hips and knees

A

uniform loss in all joint spaces, joint deformities, subchondral cysts, baker’s cysts

36
Q

RA in spine

A

50% of patients with RA will have cervical spine involvement, causing erosions within facet capsules around ligament and tendon attachments

37
Q

management for RA

A

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
Q

SLE demographics

A

30-50yo females

blacks slightly higher than whites

39
Q

clinical findings of SLE

A

malar rash
joint deformities
serious multisystem disease of kidneys, liver, lymphatics, joints

40
Q

scleroderma demographics

A

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
Q

scleroderma in hands

A

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
Q

scleroderma management

A

chest films
chest CT
upper GI contrast studies
refer to rheumatologist

43
Q

seronegative spondyloarthropathies

A

AS
enteropathic
psoriasis
reactive

44
Q

most seronegative spondyloarthropathies have what lab finding?

A

HLA-B27 (present in most to varying degrees)
ESR, CRP elevated
ANA -

45
Q

Marie-Strumpell demographics

A

AS
most common inflammtory spondyloarthropathy, onset around late 20s and early 30s
males more than females

46
Q

AS in the spine and pelvis

A

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
Q

AS management

A

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
Q

enteropathic arthritis

causes

A

chron’s disease, ulcerative colitis, whipple disease, GI infections, cirrhosis

49
Q

enteropathic arthritis

what spine looks like on xray

A
squaring of the vertebrae
syndesmophytes
romanus lesion
shiny lesion
shiny corner sign
dagger sign
railroad sign
trolley track sign
50
Q

managment for enteropathic arthritis

A

almost same as AS, but HLA B27 in 60-70%, ESR up, RA and ANA -
refer to gastroenterologist, internist, rheumatologist

51
Q

psoriatic arthritis description

A

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
Q

how is PA similar to AS and RA? different?

A

similar: erosions, symmetrical joint space narrowing, eventual ankylosis
different: asymmetrical distribution about body and digit, normal bone density, peri-ostitis, acro-osteolysis

53
Q

PA in extremities

A
sausage digit
ray pattern
mouse ears
pencil in cup
osteolysis
54
Q

PA in spine and pelvis

A

SI erosions and eventual ankylosis

spine findings are key in distinguishing features of PA vs other causes of sacroiliitis

55
Q

PA managment

A

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
Q

reactive arthritis

A
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
Q

reactive arthritis treatment

A

treat infection first, then spondyloarthropathy may resolve

58
Q

metabolic and crystal-induced arthropathies

A

gout
CPPD
ochronosis

59
Q

gout

A

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
Q

gout managment

A

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
Q

chondrocalcinosis

A

CPPD
middle-aged and older
equal among males and females
associated with hyperparathyroidism, diabetes, hemochromatosis, gout, neuropathic arthropathies (syphilis, diabetes)

62
Q

chondrocalcinosis management

A

gold standard is joint aspiration to look for crystals
chiro care: exercise, joint mobilization
allopath: NSAIDs

63
Q

calcific tendonitis

A

HADD
not a crystal induced arthropathy, but can get mixed up with CPPD
typically monoarticular and MC in shoulder as dense calcification

64
Q

calcific tendonitis management

A

HADD

degenerative, treated as OA; some modalities may lessen symptoms (laser, US)

65
Q

septic arthritis

A

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
Q

septic arthritis management

A

CT for cortical destruction, MRI for marrow destruction, refer to ortho for aspiration, antibiotics, curretage, management of risk factors (HIV, diabetes, UTI)