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CMS150 > Joint Pain & Low Back Pain > Flashcards

Joint Pain & Low Back Pain Flashcards

1
Q

periarticular pain definition

A

pain from soft tissue surrounding the joint

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2
Q

referred pain definition

A

pain from proximal or distal structures to the joint or neurogenic

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3
Q

monoarticular vs oligoarticular vs polyarticular

A

monoarticular - involves a single joint
oligoarticular - involves 2-4 joints
poluarticular - involves 5 or more joints

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4
Q

inflammatory arthritis definition

A

a combination of redness, swelling, warmth, and/or tenderness

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5
Q

septic joint definition

A

generally refers to a bacterial infection of the joint

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6
Q

symmetrical arthritis vs asymmetrical arthritis

A

symmetrical - affecting both sides of the body
asymmetrical - spotty distribution of affected joints

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7
Q

migratory arthritis definition

A

development of new joint symptoms with improvement of previously affected joints

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8
Q

inflammatory vs non-inflammatory joint pain distinguishing features

A
  • both may or may not present with swelling and tenderness, but only inflammatory joint pain has warmth or redness present
  • inflammatory joint pain may worsen with inactivity and have joint stiffness or gelling in the morning vs non-inflammatory joint pain typically worsens with activity
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9
Q

what are some examples of inflammatory joint pain causes

A

infection
gout
calcium pyrophosphate deposition disease
RA, juvenile RA
SLE
polymyalgia rheumatica
sarcidosis
spondyloarthritides - reactive arthritis, psoriatic arthritis, anklyosing spondylitis, enteropathic arthritis

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10
Q

what are some examples of non-inflammatory joint pain causes

A

osteoarthritis
trauma

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11
Q

what conditions are commonly monoarticular or oligoarticular

A

septic arthritis
spondyloarthritides - reactive arthritis, psoriatic arthritis, ankylosing spondylitis, enteriopathic arthritis
gout
pseudogout - calcium pytophosphate deposition disease
osteoarthritis
trauma
hemochromatosis

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12
Q

what conditions are commonly polyarticular

A

rheumatoid arthritis
SLE
vasculides - polymyalgia rheumatica, polyarteritis nodosa
viral infections - ex. Parovirus B19
disseminated gonococcal infection
sjorgren syndrome
acute rheumatic fever
sarcoidosis

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13
Q

pls take this time to review the questions that should be asked as part of the history for a patient presenting with joint pain

A

yay, you did it! good job!

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14
Q

what is reactive arthritis
what question would we ask to screen for this?

A

comes on as an inflammatory response to antibodies that are created in response to a GI infection or STI and the antibodies attack the patient’s own cells, especially in the joints
comes on 2-6 weeks after the GI infection or STI
would ask if they have previously had any gastrointestinal or sexually transmitted disease

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15
Q

what are signs of a true intraarticular disorder?

A

effusion, redness, swelling
restricted AROM and PROM
maximum pain at end range
pain with motion in multiple directions

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16
Q

what is a sign of periarticular problem?

A

restriction of only AROM

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17
Q

what symptom is suggestive of tendonitis or bursitis?

A

pain on RROM

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18
Q

what should we assess when checking for extraarticular manifestations?

A

examine eyes, skin, oral cavity, lungs, heart

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19
Q

what tests should we consider if the workup of a case of joint pain? why?

A

synovial fluid analysis - differentiates between inflammatory vs non-inflammatory causes
blood tests: WBC elevated in infection
ESR and CRP - inflammatory markers
serum uric acid - elevated in gout
blood cultures and serology - important in cases of infection
rheumatoid factor - rheumatoid arthritis
anticitrullinated peptide antibodies - RA
ANA - lupus
ultrasound, x-ray, CT, MRI - show inflammation or trauma in intraarticular or periarticular areas

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20
Q

what happens in septic arthritis
what population is it most prevalent in
duration of condition

A

sudden onset
infection in a joint
commonly observed in children and persons >55 yo
increased risk with increasing age, immunosuppression, lower SES
duration: lasts until 6 weeks after effective antimicrobial treatment

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21
Q

what organisms are responsible for causing septic arthritis? which is most common?

A

caused by nongonococcal bacterial in more than 80% of cases
staphylococcus aureus is the most common causative pathogen, followed by staphylococcus species
can involve bacteria, viruses, fungi, mycobacterium
if gonococcal (20% of cases), most commonly caused by Niesseria gonorrheae

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22
Q

risk factors for septic arthritis

A

skin infection, cutaneous ulcers, osteomyelitis, septic bursitis, abscess
previous intraarticular injection, arthrocentesis, arthroscopy, prosthetic joint, recent joint surgery, trauma
diabetes mellitus, HIV infection, immunosuppressive mediations, IV drug abuse, other causes of sepsis, sexual activity (specifically for gonococcal arhtritis)

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23
Q

clinical presentation of septic arthritis

A

acute joint swelling, pain, erythema, warmth, joint immobility
usually monoarticular
knee most commonly affected, followed by hip, shoulder, ankle, elbow, wrist (ie larger joints more commonly affected)
constitutional symptoms such as fever, chills, rigors may be present

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24
Q

in septic arthritis, what joints are commonly affected in patients with history of IV drug abuse?

A

SC or SI joint infection more common in patients with history of IV drug abuse

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25
Q

should we rely on constitutional symptoms for diagnosis for septic arthritis? why or why not?

A

no, they aren’t as reliable. instead use a combination of other signs and symptoms

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26
Q

what provides the best evidence, if present, for septic arthritis?
what findings do not present good evidence for septic arthritis?

A

recent joint surgery
prosthetic implant and skin infection
arthrocentesis findings with increased WBCs showing better LR+
not as good: fever; serum lab values have limited usefulness

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27
Q

are elevated WBCs in a CBC enough evidence to rule in septic arthritis diagnosis?
if ESR and CRP are elevated, does this confirm that a patient has septic arthritis? what are these markers used for

A

no, they WBCs are not enough to rule in - need synovial fluid analysis with gram staining
ESR and CRP can be normal in septic arthritis - when elevated, these markers are used to monitor therapeutic response

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28
Q

what is the diagnostic criteria for ruling in septic arthritis?

A

WBCs >50,000 WBC/m^3
arthrocentesis for synovial fluid analysis showing >90% polymorphonuclear cells
gram stain of bacterial culture gives definitive diagnosis

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29
Q

if you are suspecting Lyme arthritis, what testing will not be helpful in ruling in?

A

synovial fluid analysis won’t be helpful because Borrelia burgdorferi cannot be cultured from synovial fluid
need to do PCR testing

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30
Q

how is septic arthritis managed? why?

A

this is a medical emergency and needs immediate diagnosis and urgent referral to treatment
failure to initiate appropriate antibiotic treatment within 24-48 hours of onset can lead to subchondral bone loss and permanent joint dysfunction

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31
Q

what happens in gout
most affected population
onset type?
duration of condition

A

middle aged men (increased prevalence with advancing age) and post-menopausal women
onset: sudden
duration: not constant; acute attacks last 3-14 days
morning pain or stiffness usually present but intermittent

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32
Q

in gout, is there a connection to hormones? what are the implications of this?

A

hormonal component to developing gout in women - later onset and comorbidities like chronic kidney disease and hypertension

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33
Q

demographic risk factors for developing gout

A

indigenous Taiwanese, Pacific Islander, New Zealand Maori
living in high-income countries like North America and Western Europe
male sex (2-6x higher incidence than females)

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34
Q

dietary risk factors for developing gout

A

high alcohol intake
diet rich in meat and seafood = high purine diet
high fructose consumption

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35
Q

what conditions can be comorbid with gout

A

hyperuricemia
metabolic syndrome
type 2 diabetes mellitus
cardiovascular disease
hypertension
hyperlipidemia
obesity
chronic kidney disease
diuretic use
obstructive sleep apnea
menopause
conditions with rapid cell turnover - psoriasis, hemolytic anemia, certain cancers
Lesch-Nyhan syndrome
Kelley-Seegmiller syndrome

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36
Q

what is metabolic syndrome?

A

combination of:
hypertension
high blood sugar
high cholesterol
central obesity
elevated waist circumference: >88cm for women, >102cm for men

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37
Q

why are conditions with rapid cell turnover often comorbid with gout

A

gout is an issue due to purine turnover which is due to increased protein breakdown
therefore, increased purines in the blood will contribute to elevated uric acid crystals in the bloodstream

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38
Q

what is Lesch-Nyhan syndrome?

A

a rare hereditary condition of purine metabolism
X-linked recessive pattern - only males affected
mutation of HPRT1 gene leading to deficiency or absence of HPRT enzyme causing elevated purine levels in these patients - they aren’t recycled
people have lower levels of dopamine and can see self injury behaviours like biting and head-banging specific to this syndrome

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39
Q

what is Kelley-Seegmiller syndrome?

A

a milder form of Lesch-Nyhan syndrome
a rare hereditary condition of purine metabolism
mutation of HPRT1 gene leading to DEFICIENCY of HPRT enzyme causing elevated purine levels in these patients - they aren’t recycled
patients have a higher risk of developing kidney stones and gout

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40
Q

clinical features of gout

A

acute, rapidly developing, self-limiting monoarthritis - commonly the first MTP joint or midfoot or knee
flares usually resolve within 14 days and are interspersed between asymptomatic and intercritical period
over time, flares become more frequent and severe and can be polyarticular, affecting upper limbs as well
presence of tophi -> tophaceous gout usually develops 10 years after initial gout flare

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41
Q

podagra definition

A

a gout flare at the first MTP joint (big toe)

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42
Q

what is an intercritical period (re: gout)

A

the time between flare ups where there is no joint pain

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43
Q

tophi definition

A

uric acid crystals that form lumps underneath the skin and can cause chronic pain and destroy the bones around the joint

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44
Q

where in the body are tophi most commonly found

A

first MTP joint
other joints and tendons of the foot and ankle (Achilles tendon)
prepatellar bursae
olecranon bursae
helix of ear

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45
Q

what is the gold standard for gout diagnosis

A

joint aspiration and microscopy analysis showing presence of monosodium urate crystals

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46
Q

what happens in pseudogout
what is the medical term for pseudogout
onset
duration of the condition
commonly affected population

A

calcium pyrophosphate dihydrate crystal deposition
common in ages >65yo
onset: sudden
duration: flares lasting days to weeks
usually with morning pain or stiffness

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47
Q

how is pseudogout diagnosed?

A

calcium pyrophosphate dihydrate crystals are polymorphic and weakly positive under birefringent microscopy
this is different from the MSU crystals that present with regular gout

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48
Q

what are the types of crystal-induced arthritis?

A

gout
pseudogout - calcium phyrophosphate dihydrate crystal deposition
calcium oxalate
hydroxyapatite

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49
Q

rheumatoid arthritis
overall description
implications
major risk factors

A

chronic relapsing descrtuctive synovitis - local inflammation, cartilage destruction, bone erosion
genetic disposition: HLA-DR1 and HLA-DR4
higher risk in women (2-3x higher than men)
cytokines drive chronic synovial inflammation

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50
Q

environmental risk factors for RA

A

smoking - dose response effect
airborne agents related to air pollution
overall microbiome
diet high in red meat, sugar, sodium
blue collar jobs
pesticide exposure
work stress
infectious exposure - parovirus 19, HCV, EBV

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51
Q

host-associated risk factors for RA

A

allergic and respiratory: rhinitis, atopic dermatitis, asthma, COPD
immune-mediated risk factors - autoimmune conditions (IBD, T1D, MS, autoimmune thyroid conditions)
sleep disorders
schizophrenia
neuroendocrine factors like decreased HPA axis function/relative adrenal insufficiency

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52
Q

clinical features of RA

A

symmetrical polyarticular pain and stiffness
morning stiffness >1hr
systemic symptoms: fatigue, weight loss, anemia
boggy swelling caused by synovitis and palpable synovial thickening

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53
Q

what joints are most commonly affected in RA

A

wrists
PIP joints
MCP joints
MTP joints

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54
Q

what is observed in advanced RA

A

ulnar deviation of MCP joints
MCP joint subluxation
swan neck deformity
Boutonniere deformity

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55
Q

what extra-articular manifestations can be observed in RA?

A

accelerated atherosclerosis
pericarditis
keratoconjunctivitis sicca
epicerlitis/scleritis
interstitial lung disease
pulmonary nodules
rheumatoid nodules
pleural effusion
vasculitis

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56
Q

what risk factors predispose someone to developing extra-articular manifestations of RA?

A

male sex
seropositivity for RA, anticitrullinated antibodies, antinuclear antibodies
smoking history - especially for nodules, vasculitis, and interstitial lung disease

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57
Q

anticitrullinated protein antibodies may be present for __ years before onset of ___ disease in RA

A

may be present for 10 years before onset of clinical disease in RA

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58
Q

serology markers you might test for in RA

A

rheumatoid factor
anticitrullinated protein antibodies

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59
Q

what does it mean to be seropositive for RA

A

if someone tests positive for rheumatoid factor and anticitrullinated protein antibodies

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60
Q

does a negative serum anticitrullinated protein antibody result rule out RA diagnosis?

A

no. but it is a little better than rheumatoid factor in predicting RA

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61
Q

what fraction of patients with RA are seronegative for rheumatoid factor?

A

1/3 - rheumatoid factor is not diagnostic of RA

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62
Q

how is RA managed? why?

A

there is a low threshold for referral to a rheumatologist
>12 week delay in treatment is associated with reduced chance of drug-free remission and increased risk for progressive joint damage

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63
Q

complications of RA

A

osteopenia and osteoporosis leading to fracture
lung manifestations - pleuritis, bronchiolitis, interstitial fibrosis
accelerated atherosclerosis
increased insulin resistance, diabetes mellitus
vasculitis, thromboembolic disease
anemia of chronic disease
depression due to low quality of life
felty syndrome

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64
Q

what implication does the complication of accelerated atherosclerosis have on disease outcomes in RA

A

increases risk for cardiac events
risk of mortality in RA is 3x that of the general population

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65
Q

what is felty syndrome?

A

combination of RA, splenomegaly and neutropenia (low WBC count)

66
Q

what happens in osteoarthritis
what populations are most affected
onset
duration of condition

A

degenerative disorder of articular cartilage associated with hypertrophic bone changes
usually no morning pain or stiffness
F>M
age 65+ >ages 45-64
onset: gradual
duration: lifelong with flares

67
Q

risk factors for OA

A

F>M
overweight and obese
previous joint injury
family history
frequent bending or squatting
repetitive impact

68
Q

clinical features of OA

A

asymmetric joint pain and stiffness, sometimes instability of joints
joint pain worse with movement, especially after a period of rest
joint swelling and tenderness WITHOUT significant inflammation (no erythema or warmth)
bony enlargement
pain on ROM and limited ROM
crepitus often in the knee
Bouchard nodes on PIPs
Heberden nodes on DIPs

69
Q

which joints are most commonly affected in OA

A

hands
knees
hips
feet spine

70
Q

what is the mnemonic for remembering bouchard nodes and heberden nodes

A

HD - Heberden nodes in DIPs
BP - Bouchard nodes in PIPs

71
Q

what sign is pathognomonic for OA?

A

Bouchard and Heberden nodes

72
Q

how is OA evalulated
is imaging required?
are lab testing required?

A

primarily clinical diagnosis based on history and physical exam
imaging not required in patients with risk factors and typical symptoms
lab testing not usually required because ESR and CRP are normal due to not being a lot of inflammation and unless we suspect gout or RA, we should not order RF, ACPA or serum uric acid levels because there is a risk of false positives

73
Q

radiculopathy definition

A

pinched nerve
injury or damage to nerve roots in the area they leave the spine that may result in pain, loss of sensation, and/or motor function depending on the severity of symptoms

74
Q

acute low back pain vs chronic low back pain

A

acute LBP - up to 12 weeks
chronic LBP - 3 months or more

75
Q

lumbago definition

A

often refers to acute back pain or a strain - related to soft tissues
typically either the quadratus lumborum or paraspinal muscles

76
Q

sciatica definition

A

often used to describe lumbosacral radiculopathy,
more specifically pain distributed along the sciatic nerve
not actually a diagnosis, but a description of the nerve pain someone is experiencing

77
Q

5 ways low back pain is classified in primary care

A
  1. a problem beyond the lumbar spine
  2. a serious disorder affecting the lumbar spine
  3. low back pain occurring with radicular pain
  4. neurogenic claudication
  5. nonspecific low back pain
78
Q

_____ (type of low back pain) accounts for 90% of low back pain in primary care

A

nonspecific low back pain

79
Q

specific low back pain definition
example?

A

where there is a clear relationship between anatomic abnormalities seen on imaging and symptoms
examples:
- lumbar radiculopathy due to herniated disc, osteophyte, facet hypertrophy
- spinal stenosis
- cauda equina syndrome

80
Q

how is low back pain due to systemic disease categorized?

A

serious and emergent vs serious but non emergent

81
Q

examples of serious and emergent diseases

A

neoplasm
infection

82
Q

examples of serious and nonemergent diseases

A

osteoporotic compression fracture
inflammatory arthritis

83
Q

differentiation between serious and emergent vs serious but nonemergent conditions

A

serious and emergent - requires specific and often rapid treatment
serious but nonemergent - requires specific treatment but not urgently

84
Q

what is low back pain due to visceral disease?

A

serious, requires specific and rapid diagnosis and treatment, could involve the pelvis, renal structures, GI structures

85
Q

what are considered red flag findings for low back pain? name them (7)

A

fecal incontinence or loss of bowel control
urinary retention or loss of bladder control
saddle anesthesia
unexplained fever
unexplained weight loss
focal neurological deficit, progressive or disabling symptoms
no improvement after 6 weeks of conservative management

86
Q

name 7 red flags regarding medical history concerning low back pain

A

immunosuppression or recent infection
chronic steroid use
osteoporosis
significant trauma at any age
mild trauma in ages 50+
history of cancer
IV drug use

87
Q

what red flag findings in low back pain have the best evidence for being good predictors of conditions

A

personal history of cancer as a predictor of malignancy
recent infection as a predictor of infection
for most conditions, combining the red flag findings improves the strength of diagnostic evidence

88
Q

what happens in cauda equina syndrome
mechanism?
classical symptoms?
how is it diagnosed?
management?

A

compression and disruption of function to cauda equina most commonly due to lumbar disc herniation
classical Sx: new urinary retention or overflow incontinence, fecal incontinence; saddle anesthesia; progresive motor and sensory loss
lower motor neuron weakness, significant deficits that encompass multiple nerve roots
diagnosis by MRI is gold standard
management: urgent ER referral - requires surgical decompression within 24-48 hours

89
Q

what nerve roots are affected in cauda equina syndrome

A

the cauda equina nerve roots: L3-L5

90
Q

saddle anesthesia definition

A

loss of sensation in the perineum and medial aspects of legs and thighs

91
Q

what types of cancers are most common to metastasize as spinal malignancy?

A

breast
lung
prostate
renal
GI
thyroid

92
Q

what happens in spinal malignancy

A

the most common tumours of the spine are metastases of other primary cancers

93
Q

presentation of spinal malignancy

A

personal history of cancer - current or distant past
back pain that is deep, aching
unexplained weight loss
possible sensory loss
weakness or radiculopathy

94
Q

how is spinal malignancy diagnosed?

A

imaging with x-ray or MRI
blood work and symptoms depend on type of primary cancers as there are different biomarkers for different types of cancers

95
Q

management of spinal malignancy

A

urgent referral back to oncologist or palliative care

96
Q

what happens in vertebral fracture
what do they result from (in most cases)

A

a break in one or more spinal vertebrae that can result from trauma and metastatic disease
in most cases, result from osteoporosis

97
Q

what level of the spine do vertebral fractures occur in the lower back?

A

T11-L2

98
Q

what is the second most cause of vertebral fracture?

A

trauma

99
Q

risk factors for vertebral fracture

A

low bone density: smoking, alcohol, anorexia, medications, vitamin D deficiency
female >50 yo
prolonged use of corticosteroids
trauma/fall
personal history of vertebral fracture

100
Q

patients with history of __ vertebral fractures have __x increased risk of having another compression fracture

A

with a history of 2 vertebral fractures have 12x increased risk of having another

101
Q

presentation of vertebral fracture

A

back pain that is acute or chronic, localized to the vertebral column
back pain aggravated with standing or walking
rarely has radiculopathy

102
Q

how is vertebral fracture diagnosed?

A

imaging by CT is diagnostic
tenderness over affected vertebra/vertebrae

103
Q

management of vertebral fracture

A

urgent referral for imaging, may require surgical intervention

104
Q

what is osteomyelitis

A

the most common vertebral infection often caused by hematogenous spread of Staphylococcus aureus

105
Q

how common is vertebral infection/osteomyelitis?

A

rare! and 3-5% are occurring after spinal surgery within 12 months, recent infection, wound in spinal region, history of IV drug use, immunosuppression

106
Q

presentation of vertebral infection (osteomyelitis)

A

back pain that begins as nonspecific/general LBP then as infection progresses the pain localizes
20% of patients don’t have spinal tenderness on physical exam
fever in 30-60% of cases
sensory loss
weakness or radiculopathy in 1/3 of cases

107
Q

how is vertebral infection diagnosed

A

imaging via MRI is preferred
CBC often normal, ESR & CRP elevated

108
Q

management of vertebral infection (osteomyleitis)

A

urgent ER referral and requires antibiotic therapy

109
Q

etiology of low back pain with radiculopathy

A

compression at the nerve roots in the lumbar spine
most commonly at the levels of L5 nerve root or S1 nerve root because it’s a particularly flexible part of the spine

110
Q

general & social risk factors for LBP with radiculopathy

A

M>F
increasing age - >40
certain jobs - repetitive lifting and twisting motions
chronic overloading of disc
smoking
overweight
sedentary - puts strain on lumbar spine

111
Q

medical history risk factors for LBP with radiculopathy

A

prior trauma
multiple pregnancies
history of back pain
chronic cough

112
Q

clinical presentation of LBP with radiculopathy

A

pain experience often described as tingling, electric, burning, sharp, little bugs crawling on skin
paresthesia
radiation of pain into lower limb
numbness/anesthesia
muscle weakness
absent ankle reflexes
absent knee reflexes (less common)

113
Q

what level of nerve root is most commonly affected in lumbar radiculopathy?

A

L5 radiculopathy

114
Q

what makes the pain better and worse with lumbar radiculopathy?

A

worse with: increased intradiscal pressure - weight bearing, sitting for prolonged periods; pressure increases (coughing, sneezing, bowel movements straining); forward flexion of lumbar spine
better with: extension of lumbar spine, recumbent position (knees flexed) alleviates tension on the nerve

115
Q

what are some associated signs and symptoms you should ask about in cases of lumbar radiculopathy

A

motor and sensory symptoms suggestive of nerve root or spinal cord compression
urinary retention or incontinence
hematuria
fever
malaise
weight loss
early morning stiffness
muscular spasms

116
Q

disc herniation pathology mechanism

A

displacement of intervertebral disc material (nucleous pulposus or annulus fibrosis) beyond the intervertebral disc splace

117
Q

who commonly presents with disc herniation

A

ages 30-40
M>F 2:1

118
Q

clinical presentation of disc herniation

A

acute-chronic pain
paresthesia
sensory change
loss of strength or reflexes - depends on affected nerve root

119
Q

what are the categories/progressions of disc hernation

A

bulging disc
herniation: protrusion/prolapse, extrusion, separation

120
Q

diagnosis of disc herniation

A

Straight leg raise + Hancock rule

121
Q

straight leg raise positive sign for disc herniation

A

ipsilateral leg pain at less than 45-60 degrees is positive sign for lumbar disc herniation

122
Q

Well leg raise/crossed SLR positive sign for disc herniation

A

reproduction of contralateral pain at less than 45 degrees is positive for lumbar disc herniation

123
Q

____ % of patients experience relief from lumbar disc herniation within _____ weeks without treatment

A

85-90% of patients experience relief within 6-12 weeks without treatment

124
Q

bulging disc definition

A

loss or damage of annular fibers allows the nucleus pulposus to shift without herniation
associated with trauma, repetitive stress, or aging

125
Q

herniated disc protrusion/prolapse definition

A

focal distention of the disc where annulus fibrosis remains intact

126
Q

herniated disc extrusion definition

A

nucleus pulposus breaks through the annulus fibrosis but remains within the intervertebral disc

127
Q

herniated disc separation definition

A

nucleus pulposus breaks through the annulus fibrosis and is displaced from the site of extrusion
considered a subtype of an extruded disc

128
Q

what type of disc herniation is considered a subtype of an extruded disc

A

separation

129
Q

what is the Hancock rule?
what is evaluated with it?

A

a clinical prediction rule for lumbar disc herniation
if 3 of 4 findings are present with a specific nerve root:
- dermatomal pain location
- sensory deficit
- reduced reflex
- motor weakness

130
Q

distribution of pain in L2, L3, L4 radiculopathies

A

radiating back pain to the anterior aspect of thigh which may progress into their knee, possibly to the medial aspect of the lower leg and into the foot

131
Q

physical exam findings for L2, L3, L4 radiculopathy
motor weakness?
paresthesia/sensory changes
absent reflexes
worse with what activities

A

motor weakness: knee extension, hip adduction, hip flexion
paresthesia/sensory change: anterior thigh along the area of pain
absent reflexes: patellar reflex
worse with: coughing, leg straightening, sneezing

132
Q

distribution of pain for L5 radiculopathy

A

acute back pain that radiates down into the lateral leg into the foot

133
Q

physical exam findings for L5 radiculopathy
motor weakness?
paresthesia/sensory changes
absent reflexes
atrophy of what if chronic

A

motor weakness: big toe extension, foot eversion and inversion, ankle dorsiflexion, hip abduction
paresthesia/sensory change: lateral thigh, lateral lower leg, dorsum of foot
absent reflexes: none
atrophy if chronic of extensor digitorum brevis and tibialis anterior

134
Q

distribution of pain in S1 radiculopathy

A

radiation of sacral or buttock pain into the posterior aspect of the patient leg, into the foot, or the perineum

135
Q

physical exam findings for S1 radiculopathy
motor weakness?
paresthesia/sensory changes
absent reflexes

A

motor weakness: plantar flexion
paresthesia/sensory changes: sole, lateral foot and ankle, fourth and fifth toes
absent reflexes: ankle reflex/Achilles reflex

136
Q

what are the serious disorders that can affect the lumbar spine

A

spondylosis
spinal stenosis
spondylolysis
spondylolisthesis

137
Q

spondylosis definition

A

an umbrella term for age-related degeneration of the spinal column
often involves degenerative disc disease and facet arthropathy

138
Q

spinal stenosis definition

A

narrowing of the spinal canal, neural foramen, and lateral recess which can lead to compression of the nerve roots and neurogenic claudication

139
Q

spondylolysis definition

A

weakness or stress fracture through the pars interarticularis

140
Q

spondylolisthesis definition

A

the slippage of one vertebral body with respect to the adjacent vertebral body

141
Q

spinal stenosis risk factors

A

age
most common ages 60-69

142
Q

presentation of spinal stenosis

A

LBP with bilateral lower extremity pain, numbness or loss of strength (depends on affected nerve root) aggravated by ambulation, standing and lumbar extension
neurogenic claudication

143
Q

neurogenic claudication definition

A

pain or discomfort with walking or prolonged standing that radiates into one or both extremities
relieved by rest/sitting, lumbar flexion

144
Q

diagnosis of spinal stenosis

A

imaging
pain elicited with passive and active lumbar extension
neurologic exam typically normal

145
Q

how common is it for patients with spinal stenosis to have repeat surgery?

A

20% of patient eventually repeat surgery

146
Q

what is spondylolysis

A

a unilateral or bilateral defect through the pars interarticularis

147
Q

what level does spondylolysis most often occur

A

L5

148
Q

what populations is spondylolysis most commonly observed in

A

ages 14+
up to 50% of young athletes
male > female 2:1

149
Q

risk factors for spondylolysis

A

excessive lumbar lordosis
family history

150
Q

clinical presentation of spondylolysis

A

asymptomatic in 90% of patients
insidious onset, can be progressive
recurrent axial LBP exacerbated with activity or lumbar hyperextension
may or may not have radiculopathy

151
Q

diagnosis of spondyloysis

A

imaging
increased lumbar lordosis, tight hamstrings, reduced lumbar ROM, tenderness overlying fracture site

152
Q

in what condition does pain not necessarily correlate with severity of condition?

A

spondylolysis

153
Q

at diagnosis, 50-75% of bilateral spondylolysis will have ____

A

spondylolisthesis

154
Q

what level does spondylolisthesis most commonly occur at?

A

anterior translation of L5 over S1
second most common is L4 over L5

155
Q

what population does spondylolisthesis most commonly present in

A

adults
M > F
obesity
family history of spondylolisthesis, scoliosis, spina bifida

156
Q

clinical presentation of spondylolisthesis

A

intermittent and localized LBP that radiates into buttock or posterior thigh
paresthesia, sensory change
loss of strength or reflexes
presents like a radiculopathy

157
Q

diagnosis of spondylolisthesis

A

imaging
pain elicited with lumbar flexion and extension
tenderness over affected vertebral segment

158
Q

co

A
159
Q

complications of lumbar radiculopathy

A

loss of function and decreased quality of life
emergent complications: cauda equina syndrome and severe lumbar radiculopathy
patients who d not improve within 6-12 weeks following pain onset can develop chronic pain
slowly progressive symptoms can lead to muscle atrophy
deconditioning if nerves aren’t interacting with muscles -> muscle atrophy

160
Q

what do we need to know about imaging and low back pain

A

imaging is not indicated in most patients with LBP due to a high prevalence of abnormal findings
usually LBP with radiculopathy is due to lumbar disc herniation and most of these (85-90%) resolve on their own in 6 weeks
conservative management for 6 weeks is recommended before imaging unless presenting with severe symptoms (disability) or red flag findings

CMS150 (6 decks)

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