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Clinical Medicine > MSK Quiz 2: Part 1 > Flashcards

MSK Quiz 2: Part 1 Flashcards

1
Q

How many joints are usually involved in crystal deposition disease?

A

1 joint

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2
Q

Crystals can be found in three locations:

A

synovium, cartilage, surrounding tissues

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3
Q

What crystals are responsible for gout?

A

monosodium urate crystals

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4
Q

What crystals are responsible for pseudogout?

A

calcium pryophosphate dehydrate crystals

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5
Q

What crystals are responsible for chondrocalcinosis?

A

calcium pyrophosphate dehydrate crystals

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6
Q

How do the crystals associated with gout form?

A

Urate saturation in the blood/body fluids forms monosodium urate crystals

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7
Q

What is the end-point for gout?

A

chronic, destructive and debilitating polyarthritis

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8
Q

Where are the most common areas for gout presentation?

A

1st metatarsophalangeal joint, ankle, midfoot, knee

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9
Q

What are the three overaching risk factors for hyperuricemia?

A

Syndromes, Medications, Diet

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10
Q

What syndromes put someone at risk for hyperuricemia?

A

hypertension, metabolic syndrome, and obesity

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11
Q

What medications put someone at risk for hyperuricemia?

A

thiazide diuretics and low dose ASA

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12
Q

What diets put someone at risk for hyperuricemia?

A

high purine diet, high-fructose corn syrup, excessive alcohol use

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13
Q

What are examples of purine rich foods?

A

organ meat, select seafoods

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14
Q

What are protective dietary foods for hyperuricemia?

A

vitamin C, coffee, cherries

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15
Q

What are the four phases of hyperuricemia?

A

1) asymptomatic hyperuricemia, 2) acute gouty flare 3) intercritical gout 4) chronic tophaceous gout

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16
Q

Asymptomatic hyperuricemia is defined as a serum urate concentration of?

A

> 7 mg/dL

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17
Q

There’s a clear correlation between the likelihood of developing gout and?

A

increased serum urate

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18
Q

Describe the etiology of gout

A

underexcretion (kidneys) and overproduction

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19
Q

Between underexcretion and overproduction what’s the most common etiology for gout?

A

underexcretion (90%)

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20
Q

Name the six causes of undersecretion in relation to gout:

A

reduced GFR/kidney disease, hypertension, obesity, systemic sclerosis, lead poisoning, drugs (diuretics, alcohol, ASA)

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21
Q

What are the seven causes of overproduction in relation to gout:

A

genetic disorders, obesity, psoriasis, nicotinic acid (B3), alcohol, red meat/organ meant/shellfish, high fructose corn syrup

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22
Q

What genetic disorder can lead to overproduction, causing gout?

A

hypoxanthine-guanine phosphoribosyltransferase deficiency

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23
Q

Who is more affected by gout, men or women?

A

Men (3-6x more likely)

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24
Q

Key age group for gout?

A

30-60

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25
Q

When are women more likely to experience gout?

A

after menopause

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26
Q

Describe the presentation of gout

A

sudden onset of pain, cardinal signs of inflammation, possible constitutional symptoms

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27
Q

Describe the inital gout attack?

A

monoarticular, lower extremity joints most common

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28
Q

Gout in the 1st metatarsophalangeal joint is called?

A

podagra

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29
Q

Advanced gout can lead to these four things?

A

subcutaenous tophus, urate kidney stones, joint damage, poly-articular attacks

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30
Q

DDx for gout?

A

cellulits, septic arthritis, trauma, sarcoidosis, pseudogout

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31
Q

DDx for advanced gout?

A

rheumatoid arthritis, reactive arthritis, CPPD arthropathy

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32
Q

What is the gold standard for diagnosing gout?

A

synovial fluid analysis

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33
Q

What will the synovial fluid analysis look like in gout?

A

needle-shaped crystals with strong negative birefringence

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34
Q

What tests would your order on someone with suspected gout?

A

synovial fluid analysis, serum urate level, urinary uric acid, CBC/ESR/CRP (r/o infection)

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35
Q

What imaging would your order for someone with suspected gout?

A

x-ray (r/o fracture), ultrasound (maybe)

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36
Q

Treatment for gout?

A

lifestyle modifications, RICE, NSAIDs or Colchicine or Corticosteroids, possibly opioids

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37
Q

What is the dosing for colchicine in acute gout?

A

1.2 po at first sign of flare, then 0.6 mg 1 hour later

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38
Q

What is the dosing for colchicine prophylaxis for gout?

A

0.6 mg po daily or q12 hours

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39
Q

What is the treatment for recurrent/advanced gout?

A

Xanthine oxidase inhibitor or probenecide or pegloticase

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40
Q

What does xanthine oxidase inhibitors do?

A

blocks uric acid production

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41
Q

Name two examples of xanthine oxidase inhibitors?

A

allopurinol and febuxostat

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42
Q

Describe dosing of allopurinol for gout?

A

100 mg po daily (increase weekly to 200-300 mg/day)

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43
Q

Describe dosing of febuxostat for gout?

A

40 mg po daily; can increase to 80 mg daily

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44
Q

Describe dosing for probenecide for gout?

A

250 mg po daily x 1 week; increase to 500 mg po bid

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45
Q

When do you consider discontinuing probenecid for gout?

A

If attacks do not occur for 4 months

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46
Q

How does probenecid work for gout?

A

lowers tissue stores by increasing renal excretion of uric acid

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47
Q

Do xanthine oxidase inhibitors work for overproducers or underexcretors?

A

Both

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48
Q

Does probenecid work for overproducers or underexretors?

A

Underexretors

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49
Q

Describe dosing for pegloticase?

A

8 mg IV q 2 weeks

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50
Q

How does pegloticase work?

A

converts uric acid to allantoin which is readily secreted by the kidneys

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51
Q

What’s the issue with pegloticase?

A

it’s expensive; blackbox warning for anaphylaxis

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52
Q

Name three examples of CPPD deposition disease?

A

pseudogout, chondrocalcinosis, pyrophosphate atrophy

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53
Q

What is chondrocalcinosis?

A

calcification of hyaline cartilage or fibrocartilage; extracellular pyrophosphate accumulation around chondrocytes

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54
Q

Is CPPD deposition disease more common in men or women?

A

women

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55
Q

What’s the cause of CPPD deposition disease?

A

Really it’s unknown, but maybe altered metabolism of pyrophosphate (PPI)…hereditary (familial), sporadic (idiopathic), metabolic

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56
Q

What are metabolic causes of CPPD deposition disease?

A

hemochromatosis, hyperparathyroidism, hypomagnesemia, hypophosphatasia

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57
Q

How many joints does pseudogout impact?

A

monoarticular

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58
Q

How does pseudogout differ from gout?

A

not as abrupt onset and tends to last longer; usually affects larger joints

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59
Q

What’s the most common location of pseudogout?

A

knee

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60
Q

What do you order to diagnose someone suspected of pseudogout deposition disease?

A

Xray, synovial fluid analysis

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61
Q

What will the synovial fluid look like in someone with pseduogout deposition disease?

A

squared off shape, positive birefringence

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62
Q

Treatment for pseudogout deposition disease

A

RICE, NSAIDs/corticosteroids/possibly colchicine

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63
Q

Symptoms of chondrocalcinosis?

A

asymptomatic; incidental finding on x-rays

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64
Q

Hydroxyapatite arthropathy is caused by?

A

a species of basic calcium phosphate

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65
Q

Hydroxyapatite arthropathy is identified by?

A

electron microscopy

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66
Q

What is hydroxyapatite arthropathy?

A

crystals in joints, tendons, ligaments and bursa

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67
Q

Demographic of those impacted by hydroxyapatite arthropathy?

A

younger

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68
Q

Causes of hydroxyapatite arthropathy

A

idiopathic, hereditary, metabolic (hypercalcemia)

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69
Q

What is a type of hydroxyapatite arthropathy that impacts the shoulder?

A

Calcific tendinitis

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70
Q

Calcific tendonitis impacts what muscle most often?

A

supraspinatus

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71
Q

What’s the cause of calcific tendinitis?

A

unknown

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72
Q

Presentation of calcific tendinitis?

A

sudden onset of pain without MOI, pain resolves, painful again during reabsorption phase

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73
Q

Treatment of calcific tendinitis?

A

conservative vs. surgical

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74
Q

What’s the condition where HA crystals destroy the RC and shoulder joint?

A

Milkwaukee Shoulder

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75
Q

Milwaukee SHoulder is most frequently seen in?

A

elderly females

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76
Q

Diffuse Idiopathic Skeletal Hyperostosis (DISH) is most commonly seen in?

A

elderly men

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77
Q

Symptoms of Diffuse Idiopathic Skeletal Hyperostosis (DISH)?

A

Largely asymptomatic, but large bridging causes more pain; dysphagia if in cervical spine

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78
Q

What is Diffuse Idiopathic Skeletal Hyperostosis?

A

the build up of calcium salts in the tendons and ligaments (calcification) and abnormal new bone growth (ossification) but the reason this happens is unknown

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79
Q

What is septic bursitis?

A

an infection of the bursa

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80
Q

Does septic bursitis impact superficial or deep more often?

A

superficial

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81
Q

Common sites of septic bursitis?

A

olecranon, prepatellar, infrapatellar, 1st MTP

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82
Q

Is septic bursitis more common in men or women?

A

men

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83
Q

What’s the cause of septic bursitis?

A

trauma to the skin (direct inoculation through the skin, rarely from cellulitis or hematogenous seeding)

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84
Q

Presentation of septic bursitis?

A

redness, warmth, swelling, usually no ROM restriction

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85
Q

How to diagnose septic bursitis?

A

x-ray (r/o other causes), aspiration

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86
Q

Aspiration of a septic bursa will likely show?

A

s. aureus

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87
Q

Three most common bugs in septic bursitis

A

s. aureus, beta hemolytic strep, aerobic gram negative bacilli

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88
Q

Chronic septic bursitis aspiration may show?

A

b. abortus, m. tuberculosis, fungus

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89
Q

DDx for septic bursitis?

A

gout, pseudogout, arthritis, trauma

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90
Q

Outpatient treatment for septic bursitis?

A

penicillin or 1st generation cephalosporin, if MRSA add tri/sulfa, if PCN allergy use clindamycin or linezolid

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91
Q

Inpatient treatment for septic bursitis?

A

IV nafcillin, oxacillin, or cefazolin; if MRSA, add vancomycin, daptomycin, or linezolid

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92
Q

What is septic arthritis?

A

infection of the joint, damages articular cartilage and bone

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93
Q

Septic arthritis is usually viral/bacterial/fungal?

A

most commonly bacterial; can be viral or fungal

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94
Q

Septic arthritis is usually caused by which organisms?

A

staphylococcus aureus or streptococci

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95
Q

Septic arthritis is usually caused by?

A

direct injury to the joint, hematogenous spread (indwelling catheters, IC, UTIs), contiguous osteomyelitis, rarely from arthrocentesis or arthroscopy

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96
Q

Septic arthritis risk factors

A

diabetes, alcoholism, cutaneous ulcers/skin infections, prosthetic joints, RA, OA, low economic status, immunosuppressive therapies, IV drug use

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97
Q

Where will an IV drug user typically present with septic arthritis?

A

SC or SI joint

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98
Q

If an IV drug user presents with an SC or SI septic arthritis what organism should be suspected?

A

pseudomonas aeroginosa

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99
Q

Presentation of septic arthritis?

A

very painful, red, hot, swollen joint; usually monoarticula, decreased ROM, possible fever

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100
Q

Which joint is most often affected by septic arthritis?

A

knee

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101
Q

What should you order for septic arthritis? (labs and imaging)

A

CBC with diff/ESR/CRP, synovial fluid analysis, plain films, blood cultures? cervical/urethral culture?

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102
Q

What will you see on plan films of septic arthritis?

A

usually normal, may see soft tissue swelling; radiolucent lines if prosthetic joint infection

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103
Q

What imaging can you order for chronic septic arthritis?

A

MRI (identify osteomyelitis), bone scan (evaluate for associated osteomyelitis)

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104
Q

Synovial fluid analysis of a septic arthritis will show?

A

WBCs >50,000, low glucose, high protein

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105
Q

Between ESR and CRP which is more specific and rises faster in relation to septic arthritis?

A

CRP

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106
Q

When would you order a cervical/urethra culture for septic arthritis?

A

if gonococcal

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107
Q

What would you order for chronic septic arthritis (labs)?

A

acid-fast, fungal, tick titers (Lyme disease)

108
Q

DDx for septic arthritis?

A

acute rheumatic fever, bursitis, crystal-induced arthritis, hemarthrosis, lyme disease, OA, RA

109
Q

Treatment of septic arthritis?

A

surgery, IV antibiotics based on culture and sensitivity for 4 weeks

110
Q

What is osteomyelitis?

A

infection of the bone

111
Q

Causes of osteomyelitis?

A

hematogenous spread, contiguous spread, inoculation at time of trauma or surgery

112
Q

Hematogenous spread of osteomyelitis is more common in males or females?

A

males

113
Q

Findings for osteomyelitis?

A

localized bone pain, possible sinus tract/swelling/abscess, possible constitutional symptoms

114
Q

DDx for osteomyelitis?

A

neuropathic arthropathy, malignancies, fractures

115
Q

Imaging for osteomyelitis?

A

Plain films (14% sensitivity, 76% specificity), MRI (will see bone marrow changes), CT scan (early cortical erosions), bone scan (high sensitivity, low specificity)

116
Q

Labs for osteomyelitis?

A

CBC with diff (leukocytosis), elevated Sed/CRP, biopsy/culture from affected area

117
Q

What’s the gold standard for testing osteomyelitis?

A

biopsy or culture from affected area

118
Q

Osteomyelitis treatment?

A

very difficult to eradicate, debridement and excision of infected bone (antibiotic spacer if in joint/infected prosthesis…can reconstruct bone later), IV antibiotics, antibiotic impregnated methylmethacrylate beads

119
Q

Low back pain is common in?

A

works 30-60 years old

120
Q

Low back pain symptoms usually resolve within?

A

30 days

121
Q

What is the spurling test?

A

narrows the neural foramen, will increase or reproduce radicular symptoms

122
Q

Straight-leg raise is used to test?

A

herniated disk; pain in lumbar spine when asymptomatic side is raised

123
Q

Seated Straight-leg raise is used to test?

A

Sciatic tension; if positive, patient should lead back when you raise the leg

124
Q

FABER (flexion-abduction-external rotation) test is used to test?

A

hip and SI joint pathology

125
Q

What are Waddell’s signs?

A

a group of physical signs that may indicate non-organic or psychological component to chronic low back pain

126
Q

What’s the difference between a strain and sprain in the neck?

A

used interchangeably because it’s difficult to determine muscle vs. ligament injury

127
Q

What causes a cervical strain?

A

injury (trauma, whiplash)

128
Q

What’s whiplash?

A

acceleration-deceleration with rapid flexion-extension

129
Q

Are adults or children impacted at higher rates for cervical strain?

A

adults

130
Q

Presentation of a cervical strain?

A

Pain (anywhere from base of skull to thoracic region/SCM/trapezius), headache, sleep disturbances, fatigue, difficulty concentrating, possible radicular symptoms; swelling, tenderness, limited ROM

131
Q

How to diagnose a cervical strain?

A

x-ray

132
Q

Treatment of cervical strain?

A

medications (NSAIDs, muscle relaxers, corticosteroids), possible soft cervical collar, massage, cervical traction, PT with modalities, self-limted

133
Q

Cervical strain resolves within?

A

4-6 weeks

134
Q

Whiplash associated cervical strain resolves within?

A

6-12 months

135
Q

What is cervical radiculopathy?

A

neurogenic pain in nerve roots; possibly with associated numbness, weakness, or loss of reflexes

136
Q

What are some causes of cervical radiculopathy?

A

disc herniation, degenerative changes

137
Q

Presentation of cervical radiculopathy?

A

neck and radicular pain with numbness and paresthesia, muscle spasms, muscle weakness, headaches, possible myelopathy signs, pain relief with hand over head (less compression of spinal nerve)

138
Q

What is cervical myelopathy?

A

neurologic deficit due to compression of the spinal cord

139
Q

Does cervical myelopathy happen gradually or suddenly?

A

gradual onset

140
Q

What are long-tract signs?

A

signs that indicate upper motor neuron lesion

141
Q

What are some long-tract signs?

A

palmar paresthesia, decreased finger dexterity, subtle gait differences, abnormal urinary function, pain is often absent, loss of vibration and position sense

142
Q

What’s the difference between cervical myelopathy and cervical radiculopathy?

A

Myelopathy is a loss of function in your upper and lower extremities because of compression of the spinal cord. Radiculopathy occurs when a nerve in your neck is compressed or irritated where it branches away from your spinal cord–can cause pain and muscle weakness.

143
Q

When is it normal to have a positive Babinski test?

A

In infants

144
Q

What is the positive babinski sign?

A

Positive sign is the toes fanning out

145
Q

Brudzinski-Kernig test is used for?

A

meningeal irritation

146
Q

Ankle clonus may show?

A

rhythmic dorsiflexion/plantar flexion they can’t control

147
Q

Cervical radiculopathy presentation?

A

TTP, decreased ROM, decreased lordosis, possible spurlings test positive, possible motor/sensory deficits

148
Q

Imaging for cervical radiculopathy?

A

x-rays, MRI, CT myelogram, EMG/NCS

149
Q

Treatment of cervical radiculopathy?

A

spontaneous resolution usually within 2-8 weeks, NSAIDs, cervical traction, avoid spinal manipulation

150
Q

Delayed treatment of cervical radiculopathy can lead to?

A

muscle paralysis, weakness, chronic pain syndromes, may progress to myelopathy with spinal cord involvement

151
Q

Cervical spondylosis is a general term that encompasses?

A

degenerative disc disease (herniation), bone spurs, changes in ligamentum flavum, neural foramen narrowing/stenosis

152
Q

What is the most frequent cause of spinal cord dysfunction >55 y/o?

A

cervical spondylosis

153
Q

Presentation of cervical spondylosis?

A

limited mobility, chronic neck pain that’s worse with upright activity, paraspinous muscle spasm, headaches, radicular symptoms, interference with ADLs, myelopathy symptoms, tenderness, decreased ROM with pain, possible gait issues (myelopathy)

154
Q

What special tests should you perform for cervical spondylosis?

A

Spurling’s test, Babinksi Sign, Brudzinski-Kernig Test, Ankle Clonus

155
Q

Imaging for cervical spondylosis?

A

x-ray, MRI, CT myelogram

156
Q

Treatment for cervical spndylosis?

A

conservative vs. surgical (decompression and fusion)

157
Q

What’s the most frequent cause of lost work time and disability in adults <45 years old?

A

Lumbar sprain/strain

158
Q

Most lumbar strains/sprains resolve within?

A

30 days

159
Q

What causes lumbar sprains/strains?

A

lifting/straining, trauma

160
Q

What are contributing factors to lumbar sprains/strains?

A

poor fitness, poor body mechanics, job dissatisfaction, smoking, psychosocial issues

161
Q

Presentation of lumbar sprain/strain?

A

LBP, radicular pain to buttocks/posterior thigh, difficulty ambulating, difficulty sleeping/finding comfortable position, low back or SI joint tenderness, decreased ROM, motor and sensory exam (radiculopathy; L4-S1), special tests

162
Q

What must you ask (r/o) for lumbar sprain/strain?

A

bowel and bladder function, saddle anesthesia, weakness in the lower extremities

163
Q

“bowel and bladder function, saddle anesthesia, weakness in the lower extremities” are used to r/o?

A

cauda equina syndrome

164
Q

What is cauda equina syndrome?

A

compression of the nerve roots distal to the conus medullaris

165
Q

What spinal nerves control bladder and anal sphincter function?

A

S2-S4

166
Q

What can cause cauda equina syndrome?

A

central disk herniation, epidural abscess, epidural hematoma, vertebral burst fracture

167
Q

How do you treat cauda equina syndrome?

A

Surgical emergency–immediate decompression syndrome

168
Q

Symptoms of cauda equina syndrome?

A

radicular pain and numbness in both legs, perineal numbness in saddle distribution, lower extremity weakness/paralysis (symmetric), difficulty raising from a seated position, unable to heel and toe walk, anal sphincter tone

169
Q

Imaging for cauda equina syndrome?

A

MRI, CT myelogram

170
Q

Imaging for lumbar sprain/strain

A

Possibly plain films (always after trauma or with atypical symptoms)

171
Q

Where do the ribs attach to the spine?

A

T12

172
Q

Treatment of lumbar sprain?

A

pain control, PT, patient education (body mechanics, lifting techniques)

173
Q

Chronic low back pain begins after x days?

A

90 days

174
Q

Presentation of chronic low back pain?

A

LBP radiating to 1 or both buttocks (mechanical pain; worse with movement), stiffness, intermittent pain down back of leg, pain relief with lying down; recurrent and episodic; TTP lumbar and/or SI joint, side or forward list due to muscle spasm, normal motor and sensory exam, decreased ROM, positive SLR

175
Q

Imaging for chronic low back paiN?

A

Plan films (look for degenerative changes, loss of joint space), MRI (structural changes).

176
Q

Treatment of chronic low back pain?

A

patient education, comprehensive pain management program (psychological testing, injections, biofeedback, cognitive/behavior conditioning programs, spinal cord stimulation, psychotherapy, detoxification programs)

177
Q

Lumbar herniated disc is caused by?

A

nucleus pulposus extrusion

178
Q

Why does nucleus pulposus extrusion occur?

A

posterolateral portion weakens over time

179
Q

Most common lumbar herniated discs?

A

L4-5; L5-S1

180
Q

Presentation of lumbar herniated disc?

A

abrupt vs insidious, low back pain with unilateral radicular leg pain, exacerbated (sitting, walking, standing, coughing, sneezing), radiates from buttock down posterior leg to foot (remember lumbar strain doesn’t go past knee); TTP lumbar spine, decreased ROM, sciatic (pain down posterior leg), positive seated SLR and SLR (asymptomatic leg is raised, increases pain on symptomatic side), if upper nerve roots then reverse SLR

181
Q

What’s sciatica?

A

inflammation of the sciatic nerve

182
Q

L3-L4 lumbar herniated disc findings?

A

ankle dorsiflexion; sensory loss of medial malleolus

183
Q

L4-L5 lumbar herniated disc findings?

A

great toe dorsiflexion; sensory loss of dorsal third metatarsophalangeal joint

184
Q

L5-S1 lumbar herniated disc findings?

A

ankle plantar flexion; sensory loss of lateral heel

185
Q

Imaging for lumbar herniated disc?

A

plain films (degenerative changes), MRI (neurologic changes and intolerable pain)

186
Q

Treatment of lumbar herniated disc

A

conservative (NSAIDs, rest, PT, epidural steroid injections, manipulative therapy, traction, acupuncture) vs. surgical decompression (microdisectomy, laminectomy)

187
Q

Define claudication?

A

Claudication is pain and/or cramping in the lower leg due to inadequate blood flow to the muscles.

188
Q

What is spinal stenosis?

A

narrowing of lumbar spinal canal with compress on nerve roots

189
Q

Common sites for spinal stenosis?

A

L3-4, L4-5, L2-3

190
Q

Presentation of spinal stenosis?

A

can be sudden or insidious, neurogenic claudication (fatigue and weakness from proximal to distal; sitting or lying relieves the pain), pain relief with sitting forward/leaning, possible low back pain

191
Q

PE of spinal stenosis?

A

proprioception may be impaired–positive Romberg test (eyes closed, estimate 30 seconds, feet together), segmental sensory changes, possible abnormal reflexes, normal tibial pulses, possible urinary or bowel symptoms (anal sphincter tone rarely affected)

192
Q

Imaging for spinal stenosis?

A

Plain films (up to T10); MRI; EMG/NCS

193
Q

Spinal stenosis treatment

A

Conservative (pain control, PT, water therapy, body mechanics), surgery (quality of life, decompression vs. spinal fusion)

194
Q

When does the SI joint move?

A

raising from sitting position

195
Q

Causes of SI joint dysfunction (6)?

A

trauma, leg-length inequalities, tight myofascial structures (iliopsoas), scoliosis, hip OA, pregnancy

196
Q

SI Joint Dysfunction presentation:

A

Pain: stabbing, knife-like; buttocks and posterior legs; worse with prolonged sitting/twisting/rotating

197
Q

PE of SI Joint Dysfunction:

A

evaluate symmetry, hip rotation, limb lengths, scoliosis; TTP; special tests

198
Q

Special tests for SI Joint dysfunction

A

Compression test (lay supine, hands on ASIS, press down on pelvis), FABER test

199
Q

Imaging for SI Joint dysfunction?

A

plain films, CT scan

200
Q

Treatment of SI Joint dysfunction?

A

conservative

201
Q

What’s coccydynia?

A

tailbone pain

202
Q

Is coccydynia more common in men or women?

A

women

203
Q

Causes of coccydynia?

A

Trauma (fall, childbirth), prolonged sitting on hard surfaces, degenerative changes, metastatic CA

204
Q

Presentation of coccydynia?

A

pain with sitting, BM, sexual intercourse

205
Q

PE of coccydynia?

A

TTP (need to check rectally), evaluate other areas of the lumbar spine, GI/gynecologic exams

206
Q

Imaging for coccydynia

A

plain films, MRI (r/o other metastatic disease if suspect it)

207
Q

Treatment of coccydynia

A

conservative (PT, change activity, nerve block) vs. surgical (coccygectomy)

208
Q

What’s spondylolysis?

A

pars interarticularis defect

209
Q

What’s spondylolisthesis?

A

forward translation of one vertebra to another

210
Q

Spondylolisthesis Grade 1

A

1-25%

211
Q

Spondylolisthesis Grade 2

A

25-50%

212
Q

Spondylolisthesis Grade 3

A

51-75%

213
Q

Spondylolisthesis Grade 4

A

76-100%

214
Q

What causes spondylolysis/spondylolisthesis?

A

repetitive hyperextension (gymnasts, football linemen)

215
Q

Most common locations for isthmic spondylolisthesis (pars interarticularis stress fracture)

A

L5-S1, then L4-L5

216
Q

What percentage of spondylolysis are not associated with spondylolisthesis?

A

50%

217
Q

Where are most common locations for degenerative spondylolisthesis (facet arthropathy)?

A

L4-L5

218
Q

Presentation of spondylolysis/spondylolisthesis?

A

back pain with movement, radiculopathy (can mimic spinal stenosis)

219
Q

PE of spondylolysis/spondylolisthesis

A

look at curvature, loss of lordosis, spinous process step-off; possible decreased DTRs, motor exam is usually normal, decreased strength test after walking, positive SLR

220
Q

Treatment of spondylolysis/spondylolisthesis

A

conservative (including weight loss) vs. surgical (skeletally immature, stabilization of defect)

221
Q

Adverse outcomes of spondylolysis/spondylolisthesis

A

progressive slippage of vertebral body, chronic back pain, paralysis, cauda equina syndroma

222
Q

What’s scoliosis?

A

lateral curvature of the spine

223
Q

What are causes of childhood scoliosis?

A

idiopathic, neuromuscular, congenital

224
Q

What are causes of scoliosis after skeletal maturity?

A

degenerative spondylosis, degenerative spondylolisthesis, osteoporosis, degenerative disc disease (DDD)

225
Q

Presentation of scoliosis?

A

pain, possible radiculopathy (common if L4-L5, extensor hallicis longus weakness), deformity (shorter, hump), cardiopulmonary decompensation (not common, associated with severe thoracic curves)

226
Q

PE of scoliosis?

A

inspection for deformity, gait analysis, neuro exam

227
Q

Imaging for scoliosis

A

full-length PA and lateral plain films; EMG (radiculopathy vs neuropathy)

228
Q

Treatment of scoliosis?

A

skeletally immature (observation, bracing, spinal fusion); skeletally mature (conservative vs. surgical)

229
Q

When is bracing warranted for skeletally immature scoliosis?

A

curves 25-45 with underarm orthosis 18-23 hours/ day

230
Q

When is spinal fusion warranted for skeletally immature scoliosis?

A

Curves >45

231
Q

When is surgery warranted for the skeletally mature scoliosis?

A

> 50-60

232
Q

Are primary tumors of the spine common?

A

no

233
Q

Common sites metastases to spine originated?

A

breast, lung, prostate, colon, thyroid, kidney

234
Q

Presentation metastatic disease

A

incident finding, back pain (primary tumor), neurologic finding; pain with weight bearing activities (relieved by rest), pain at night, radiculopathy, progression varies, possible constitutional symptoms (weight loss, fatigue, decreased appetite, night sweats, fever/chills)

235
Q

PE for metastatic disease

A

inspect for deformity, TTP, neuro exam

236
Q

Imaging for metastatic disease

A

AP/lateral plain films, bone scan to identify mets

237
Q

Treatment of metastatic disease

A

dependent on tumor type; chemo, radiation, hormone therapy; decompression and stabilization with post-op radiation

238
Q

Causes of vertebral fractures

A

Major trauma, minor trauma (osteoporosis, tumors, infections, LT steroid use)

239
Q

When should you ALWAYS suspect a cervical spine fracture?

A

traumatic brain injury, unconscious or intoxicated persons

240
Q

Cervical spine injuries impact men or women more?

A

men

241
Q

Presentation of vertebral fractures?

A

MOI specific; severe neck or back pain; paraspinous muscle spasm, bone tenderness, possible neurologic defects

242
Q

PE vertebral fractures?

A

swelling, ecchymosis, TTP, gap/step-off between vertebra, motor and sensory function, perianal sensation, sphincter tone, bulbocavernosus reflex

243
Q

Imaging for cervical vertebral fractures

A

x-ray (AP, lateral, odontoid view)

244
Q

Burst of C1 AKA

A

Jefferson Fracture

245
Q

Bilateral fracture of C2 pedicles AKA

A

Hangman’s fracture

246
Q

Hangman’s fracture MOI

A

hyperextension

247
Q

Spinous process avulsion AKA

A

Clay-Shoveler’s

248
Q

Common sites for Clay-Shoveler’s?

A

C7>C6>T1

249
Q

Treatment for cervical vertebral fracture?

A

Immobilization, methylprednisolone 30 mg/kg bolus followed by drip 5.4 mg/kg/h x 23 hours; conservative vs. surgical

250
Q

What are the goals of treating vertebral fractures?

A

preventing neurologic injury, restoring stability, restoring normal function

251
Q

Kyphoplasty is for which vertebra?

A

thoracic

252
Q

Vertebroplasty is for which vertebra?

A

lumbar

253
Q

What is a soft cervical collar used for?

A

short term use for cervical sprains

254
Q

What degree is the neck at in a soft cervical collar?

A

10 degree flexion

255
Q

When is a philadelphia collar used?

A

immobilizes c-spine when suspect a fracture

256
Q

The philadelphia collar allows for?

A

rotational control

257
Q

What’s the benefit of a rigid cervical orthosis?

A

greater limitation of c-spine movement

258
Q

What’s a halo brace?

A

4 screws with bars connecting to a plastic vest on the chest; immobilization of C-spine

259
Q

What does a three-point spine orthosis limit?

A

flexion and extension

260
Q

When is a three-point spine orthosis used?

A

thoracic sprains or minimal compression fractures

261
Q

When is a total-contact thoracolumbosacral orthosis (TLSO; clamshell) used?

A

thoracolumbar fractures, postop-spinal fusion

262
Q

Elastic belts provide?

A

abdominal support

263
Q

Elastic belts are used for?

A

mild lumbar sprains

264
Q

What does lumbosacral corset provide?

A

a little ROM restirction

265
Q

When is a lumbosacral corset used?

A

lumbar sprain/acute disk herniation

Clinical Medicine (13 decks)

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