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MUSCULOSKELETAL/RHEUM > PATHOPHYS > Flashcards

PATHOPHYS Flashcards

1
Q

what is the most sensitive test for ACL injury?

A

Lachman’s test

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2
Q

what percent of ACL injuries feel pop?

A

70%

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3
Q

The classic bone bruise on the tibial plateau of an MRI is found in what kind of injury?

A

ACL

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4
Q

if you wait more than 8 hours to evaluate a knee dislocation what could happen?

A

amputation (lack of vascularization from popliteal artery)

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5
Q

how could you test to see if someone had torn their achilles tendon?

A

squeeze the gastrocnemius and if normal you should see plantarflexion, if abnormal then you it shouldn’t move

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6
Q

what is the genetic defect in myotonic dystrophy?

A

autosomal dominant pattern

-increased CGT repeats of DNA on chromosome 19 which encodes a protein kinase

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7
Q

what is the metabolic problem in mcArdle’s disease

A

lack of muscle phosphorylase, so can’t break glycogen down to make ATP, lactate, & pyruvate

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8
Q

what is the main pathogenesis of Eaton-lambert syndrome?

A

abs that bind to the voltage gated Ca2+ channels and thus prevent release of ACh at the presynaptic neuromuscular synapse

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9
Q

what is the most common vasculitis in children?

A

HSP

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10
Q

what kind of vasculitis is present in HSP?

A

IgA immune complex small vessel vasculitis

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11
Q

which vasculitis is associated with asthma and eosinophilia?

A

churg-strauss syndrome

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12
Q

Name the 2 large vessel vasculitidies:

A

Temporal arteritis

Takayasu’s ateritis

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13
Q

Name the 3 medium vessel vasculitidies:

A

PAN
Buerger’s
Kawasaki’s disease

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14
Q

Name the small vessel vasculitidies:

A 
Wegener's
Churg Strauss
Microscopic Polyangiitis
HSP
Essential Cryoglobulinemia
Cutaneous Leukocytoclastic angiitis
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15
Q

Name the types of vasculitis that form granulomas:

A

temporal arteritis
Takyasu’s arteritis
Wegener’s
Churg Strauss

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16
Q

Name the types of vasculitis that have ANCAs:

A

Wegener’s–>C-ANCA
Churg Strauss–>P-ANCA
Microscopic Polyangiitis–>P-ANCA

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17
Q

How do you treat kawasaki’s disease?

A

aspirin & IVIG

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18
Q

what do you have to remember about the treatment of bacterial arthritis?

A

it is MEDICAL EMERGENCY

    1. aspirate fluid
      1. abx
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19
Q

what kind of arthritis is found in rheumatic fever?

A

migratory polyarthritis

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20
Q

what is the most common cause of viral arthritis in US?

A

ParvoB19

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21
Q

what is the antigen associated with RA?

A

HLADR4

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22
Q

which antigen do all the spondyloarthropathies have in common?

A

HLAB27

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23
Q

What is the best characterized cytokine involved in cartilage degradation?

A

IL-1

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24
Q

what is thought to be the 1st irreversible step in pathogenesis of OA?

A

degradation of collagen (signif. reduces mechanical properties of cartilage)

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25
Q

what is the most important MMP in OA?

A

MMP13, b/c it pref. degrades type II collagen

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26
Q

aggrecan is also degraded in OA mostly by what 2 enzymes?

A

MMP, ADAMTS-4

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27
Q

what is the most common form of arthritis?

A

OA

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28
Q

what are some of the etiologies of secondary OA?

A

trauma: fracture, surgery, charcot joint

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29
Q

what is the most common symptoms in OA?

A

pain

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30
Q

what are some non-pharm therapies that should be part of management plan for OA pt?

A

weight loss & exercise

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31
Q

Do hyaluronic acid derivatives work in OA?

A

nope

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32
Q

whats the plan of action when you diagnose a pt with infectious arthritis?

A

hospitalize the pt, Tap the knee, aspirate for gram stain and culture, blood culture, start IV abx

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33
Q

most cases of bacterial arthritis result from what kind of spread?

A

hematogenous seeding of the synovial membrane

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34
Q

why are the joints a common place for bacterial infection?

A

they have abundant vascular supply to synovium and lack a BM

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35
Q

what is the most common overall cause of septic arthritis?

A

Staph Aureus

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36
Q

What are some of the risk factors for developing septic arthritis?

A 
DM
prosthetic joint in knee or hip
recent joint surgery
skin infection
previous septic arthritis
recent intra-articular injection
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37
Q

what is the most common cause of bacterial arthritis in young sexually active women?

A

gonococcal infection

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38
Q

what are some of the risk factors for developing disseminated gonococcal infection?

A
  • recent menstruation
  • pregnancy or post-partum state
  • congenital or acquired complement def. (C5-C8)
  • SLE
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39
Q

what are the 2 presenting forms of GC arthritis?

A
  1. fever, chills, skin lesions, tenosynovitis, polyarthralgia, w/ GC being cultured from several sites
  2. arthritis MC in knee, wrist, or ankle & more than 1 joint can be infected simultaneously w/ GC freq. cultured from synovial fluid
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40
Q

what tests should be performed on all pts presenting w/ an inflamed joint?

A

arthrocentesis & synovial fluid analysis

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41
Q

describe the lab findings in a joint aspiration of bacterial arthritis?

A

protein conc. 1/3 of plasma

WBC>50,000 (w/ polys predom.)

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42
Q

a definite dx of bacterial arthritis can be made only by what?

A

visualizing bacteria on a gram stained smear or by culturing bacteria from SF

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43
Q

what gives better outcomes daily aspiration or surgical drainage?

A

daily aspiration

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44
Q

what is the antibiotic of choice for gonococcal arthritis?

A

ceftriaxone (about 1 wk course)

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45
Q

describe the type of arthritis in acute rheumatic fever?

A

migratory polyarthritis

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46
Q

what are the major manifestations of acute rheumatic fever?

A 
polyarthritis (J)
Carditis (O)
subq nodules (N)
erythema marginatum (E)
sydenham chorea (S)
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47
Q

what is the mainstay treatment of acute rheumatic fever?

A

antiinflamm. agents–>aspirin

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48
Q

Severe systemic symptoms of lyme disease should alert the clinician to consider what kind of coinfection with another tick-borne pathogen?

A

Babesia microti or anaplasma phagocytophilum (HGE)

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49
Q

how do you diagnose lyme disease?

A

ELISA followed by western blot for confirmation

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50
Q

how would you diagnose tuberculous arthritis?

A

synovial biopsy (with cultures)

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51
Q

how does musculoskeletal TB typically present?

A

Bone Pain, chronic localized infection, most commonly involving the spine, less often the hip or knee

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52
Q

which part of the spine is most commonly involved in HIV pts who have musculoskeletal TB?

A

lumbar spine

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53
Q

why are we seeing more fungal infections in our rheumatology pts?

A

they are taking DMARDs which are immunosuppressive

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54
Q

how would you diagnose a fungal infection of bones and joints?

A

histologic examination or culture of involved tissues

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55
Q

if you got a blastomycosis arthritis it most likely came by exposure to what?

A

soil, dust containing decomposed wood

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56
Q

what are some fungal infections that you might get after taking an anti-TNF agent?

A

coccidiomycosis, histoplasmosis, aspergillus, candida, pneumocystis

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57
Q

describe HIV-associated arthritis?

A

usually oligoarthritis predom. involving the lower extremities & tends to be self-limited

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58
Q

what is Diffuse infiltrative lymphocytosis syndrome?

A

characterized by salivary gland enlargement & peripheral CD8 lymphocytosis w/ sicca symptoms, massive parotid gland swelling, lymphocytic interstitial pneumonias (seen exclusively in HIV pts)

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59
Q

what is Immune reconstitution inflamm. syndrome (IRIS)?

A

paradoxical clinical deterioration that occurs in pts w/ HIV who receive HAART as a result of improvement in cellular immunity

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60
Q

ParvoB19 can be a cause of what in infants?

A

hydrops fetalis (b/c ParvoB19 replicates in erythroid precursors and may cause anemia)

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61
Q

what is the most useful test for ParvoB19 after the onset of joint symptoms?

A

anti-b19 IgM serology

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62
Q

Essential mixed cryoglobulinemia is a triad of what 3 things?

A

arthritis, palpable purpura, & cryoglobulinemia (associated w/ HCV infection in most cases)

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63
Q

which factor has the highest association with pseudogout?

A

old age like >70 y/o

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64
Q

if you diagnose CPPD in a pt younger than 55 y/o then what should you do next?

A

start ddx of primary metabolic or familial disorder

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65
Q

which joint is most commonly affected in pseudogout?

A

knee

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66
Q

what do CPP crystals look like under the microscope?

A

rhomboid, positively birefringent

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67
Q

what is a useful & sensitive alternative to diagnosing CPPD?

A

high resolution ultrasounds

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68
Q

how do you treat CPPD?

A

alleviate symptoms (NSAIDs) and prophylaxis of acute arthritic attacks (colchicine)

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69
Q

does septic arthritis present more often with monoarticular or polyarticular involvement?

A

monoarticular

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70
Q

underexcreters make up what % of primary hyperuricemia & gout pts?

A

90% , (the other 10% being the overproducers)

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71
Q

what is the genetic deficiency in Lesch-Nyhan syndrome?

A

HGPRT

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72
Q

what are some risk factors for nephrolithiasis?

A

high uric acid excretion, reduce urine volume, low pH of urine

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73
Q

which class of BP meds cause hyperuricemia?

A

thiazide diuretics

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74
Q

hyperuricemia is defined as a serum urate level greater than ____________

A

6.8 mg/dL

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75
Q

according to Dr. P. acute gout can be treated w/ 4 types of drugs?

A
  1. NSAIDs (prob. indomethacin)
  2. colchicine
  3. corticosteroids
  4. ACTH
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76
Q

before starting a specific urate-lowering agent the pt shoudl be treated w/ low-dose what what drugs?

A

low dose colchicine or NSAID

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77
Q

what is your uric acid target blood level?

A

less than 6 mg/dL

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78
Q

what kind of food and drink make gout worse?

A

alcohol (has lots of purines), seafood, red meat

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79
Q

___________ is associated w/ obesity, hypertriglyceridemia, glucose intolerance & metabolic syndrome, HTN, atherosclerosis, and hypothyroidism.

A

gout

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80
Q

tumor lysis syndrome could cause what renal complication?

A

urate nephropathy from acute hyperuricemia

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81
Q

alcohol use, lead intoxication, & cyclosporine treatment are all associated with ______________

A

hyperuricemia & gout

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82
Q

what would be the indication for using pegloticase?

A

used in a pt with refractory tophaceous gout

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83
Q

what’s more common anterior subluxation or posterior subluxation of the glenohumeral joint?

A

anterior subluxation

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84
Q

how much strength do you lose by rupturing the long head of the biceps tendon?

A

not much (the short head & brachioradialis have 85% of strength of elbow flexion)

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85
Q

what is a common chronic disorder often found with frozen shoulder?

A

diabetes

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86
Q

What is complex regional pain syndrome?

A

generally associated with minor trauma:
Phase 1: sympathetic overflow w/ diffuse swelling, pain, evidence of demineralization
Phase 2: atrophy & extremity may be cold and shiny
Phase 3: refers to prog. of trophic changes w/ irreversible flexion contractures, pale, cold painful extremity

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87
Q

what is de Quervain’s tenosynovitis?

A

inflammation of sheaths of thumb

presents as wrist pain, positive finklestein test on exam

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88
Q

what is meralgia peristhetica?

A

lateral femoral cutaneous nerve (L2-L3) entrapment causing diffuse lateral pain

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89
Q

what are the 2 most common sites of compression of lateral femoral cutaneous nerve?

A

inguinal ligament

psoas insertion

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90
Q

what is prepatellar bursitis?

A

housemaid’s knees

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91
Q

what is patellar tendonitis?

A

patellofemoral pain syndrome (from jumping a lot)

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92
Q

what radiographic finding do you commonly see in plantar fasciitis?

A

heel spurs

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93
Q

what is cavus feet?

A

having an unusually high arch

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94
Q

what is morton’s neuroma?

A

fibrotic lesion that can cause nerve entrapment in 3rd & 4th webspace

  • chronic irritation may be cause
  • aching or burning pain that radiates from webspace distally to affected toes
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95
Q

what kind of people might get morton’s neuroma?

A

women wearing high heels or tight-fitting shoes

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96
Q

what is hammertoe?

A

flexion of PIP joint and tip of toe points downward

most common in 2nd toe

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97
Q

what % of pts presenting w/ low back pain will be pain free in 8 wks?

98
Q

what is a major indication for back surgery?

A

serious neurologic deficit

99
Q

what are 3 mechanical causes of low back pain?

A

lumbar spondylosis
disk herniation
spinal stenosis

100
Q

how do you alleviate pain in spinal stenosis?

A

flexion of lumbar spine (gets worse with extension)

101
Q

what is hypertrophic osteoarthropathy?

A

excessive proliferation of skin & bone at distal parts of the extremities from excessive collagen deposition

  • clubbing
  • periostitis at ends of long bones
102
Q

hypertrophic osteoarthropathy is commonly associated with what 2 things?

A

chest malignancies

chronic lung infection

103
Q

what kind of transporters are involved in excretion of urate?

A

Organic anion transporters (OAT)

104
Q

___________activate the NLRP3 inflammasome

A

monosodium urate crystals

105
Q

in gout the inflammasome generates what cytokines?

A

IL-1beta, IL-18, IL-33

106
Q

what two factors lead to the fact that gout commonly flares at night in the big toe?

A

big toe is cold, hypoventilation–>acidosis, both lead to precipitation of urate crystals

107
Q

what are the 3 stages of gout?

A
  1. asymptomatic hyperuricemia
  2. acute gout
  3. chronic gouty arthritis
108
Q

what is a useful alternative diagnostic method used for gout?

A

ultrasound

109
Q

78% of these vasculitis pts have neuropathy like foot drop

110
Q

which organ does PAN characteristically spare?

111
Q

is PAN more common in men or women?

112
Q

HSP has immune complex of what kind of immunoglobulin?

113
Q

cryoglobulinemic vasculitis is most often associated with what long standing chronic infection?

A

hepatitis C

114
Q

what is the classic tetrad in HSP?

A

purpura
arthritis
abdominal pain
GN

115
Q

what are cryoglobulins?

A

contain immunoglobulins and complement proteins and basically aggregate when they get cold

116
Q

what are cryofibrinogens?

A

have fibrinogen, fibrin, fibronectin (undetectable in serum)

117
Q

what is type I Cryoglobulinemia?

A

monoclonal Ig that is most often due to Multiple myeloma or Waldenstrom’s macroglonulinemia

118
Q

what is type II cryoglobulinemia?

A

polyclonal IgG with monoclonal IgM against IgG

119
Q

what is type III cryoglobulinemia?

A

polyclonal IgG & IgM

120
Q

what is the most common manifestation of cryoglobulinemic vasculitis?

A

palpable purpura with ulcers

121
Q

is rheumatoid vasculitis a big deal?

A

yes-devastating complication of medium & small blood vessels and requires aggressive therapeutic interventions

122
Q

what is the most common presentation of rheumatoid vasculitis?

A

purpuric lesions w/ or w/o evidence of medium vessel vasculitis, & deep cutaneous ulcer over the malleoli are a hallmark of RV

123
Q

how do you diagnose microscopic polyangiitis?

124
Q

what is a potentially serious complication of giant cell arteritis that warrants ongoing monitoring?

A

thoracic aortic aneurysm

125
Q

Why is it important to begin steroids as soon as you diagnose giant cell arteritis?

A

the pt may go blind permanently (don’t wait for biopsy)

126
Q

what is the prognosis of temporal arteritis with treatment?

A

good with treatment

127
Q

which large vessel vasculitis is not associated with glomerulonephritis?

A

Takyasu’s arteritis

128
Q

what kind of pts get takyasu’s arteritis?

A

young asian women

129
Q

Kawasakis disease can cause necrotizing vasculitis in what arteries that are particularly dangeous?

130
Q

what is the treatment for kawasaki’s disease?

A

aspirin & IVIG

131
Q

what is primary angiitis of the central nervous system?

A

vasculitis confined only to brain, meninges, spinal cord

132
Q

which crazy complex multisystem disease causes oral and genital ulcers?

A

bechet’s disease (pts in 20’s & 30’s)

133
Q

Autosomal dominant familial CPPD has been linked in to mutations in what gene?

A

ANKH -encodes PPi transporter

134
Q

what is driving the cell responses to CPPD crystals?

A

NLRP3 (cryopyrin) inflammasome activation & caspase-1 activation & IL-1beta processing and secretion

135
Q

what is a helpful way of diagnosing CPPD?

A

Ultrasound

136
Q

ANKH is on which chromosome?

137
Q

how do you confirm the presence of CPPD crystals?

A

positive birefringence on light microscopy

138
Q

acute onset symmetric polyarthritis canbe caused by _______infection especially when accompanied by rash.

139
Q

hepatitis B virus infection presents as _______________________

A

an arthritis-urticaria syndrome

140
Q

what are some of the genes implicated in RA?

A

HLA-DR4 (MHC II)
PTPN22
peptidylarginine deiminases

141
Q

presence of what can be present for many years before the onset of clinical arthritis?

A

RF, anti-CCPs

142
Q

what are two major cytokines involved in the inflammation of RA?

143
Q

bone and cartilage destruction are primarily mediated by what two types of cells?

A

Osteoclasts, Fibroblast-like synoviocytes

144
Q

what is a major environmental risk factor for developing RA?

A

smoking (creates citrullinated peptides)

145
Q

autoantibodies in RA can recognize what two joint antigens?

A

type II collagen

glucose phosphate isomerase

146
Q

how can autoantibodies contribute to synovial inflammation?

A

can activate complement

147
Q

describe the inflammation of the synovium in RA?

A

intimal lining hyperplasia & sublining infiltration w/ CD4 Tcells, mphages, & Bcells

148
Q

what kind of T cells are sublining the synovium in RA?

A

CD4 memory T cells

149
Q

Are neutrophils found in the RA synovium?

A

no, but they are found in synovial effusions

150
Q

which type of cells are responsible for most of the IL-1 secretion?

151
Q

which 2 types of cells produce the chemokines that recruit inflammatory cells into the joint?

A

mphages, fibroblasts

152
Q

inducing apoptosis of inflammatory cells can have what effect in synovial inflammation?

A

suppress synovial inflamm & joint destruction

153
Q

what are the 3 angiogenic factors that can enhance BV prolif. in the synovium of RA?

A

IL-8
FGF
VEGF

154
Q

how long does morning stiffness last in RA?

A

at least 30 mins

155
Q

how long does morning stiffness last in OA?

156
Q

is joint involvement in RA symmetrical or asymmetrical?

A

symmetrical

157
Q

Cervical spine involvement in RA carries what risk?

A

risk of spinal cord compression ranging from sensory loss to catastrophic neurologic compromise & sudden death

158
Q

where do rheumatoid nodules usually show up?

A

extensor surfaces such as olecranon process & proximal ulna

159
Q

what are some of the exam findings in ankylosing spondylitis?

A
  1. sacroiliac tenderness
  2. limited ROM of spine in all directions
  3. Loss of lumbar lordosis, thoracic, & cervical kyphosis
  4. reduced chest wall expansion
  5. increased wall distance test
160
Q

what are the x-ray findings in ankylosing spondylitis?

A

squaring of the vertebral bodies

syndesmophyte formation

161
Q

what is important to remember about treating reactive arthritis?

A

FOLLOWUP, (2-3 months)
recurrence is common
20-50% of pts have chronic course

162
Q

what should be suspected in a pt with an asymmetric joint distribution pattern who may also have dactylitis, enthesitis, inflammatory-type back pain, & who is negative for RA?

A

psoriatic arthritis

163
Q

what are markers of poor outcome in psoriatic arthritis?

A

elevated ESR, polyarticular disease

164
Q

which disease has sausage fingers?

A

psoriatic arthritis

165
Q

which disease has the classic pencil in cup formation on radiography?

A

psoriatic arthritis

166
Q

you might find increased levels of IL-18 in the serum and synovial tissue of pts with what disease?

A

psoriatic arthritis

167
Q

what does IL-18 do?

A

stimulates angiogenesis (important in psoriatic arthritis)
upregulates chemokine expression on synovial fibroblasts
increases mononuclear cell recruitment

168
Q

this disease is characterized by chronic inflammation w/ variable degrees of collagen accumulation (fibrosis) in affected tissues & obliterative vasculopathy of peripheral and visceral vasculature

A

systemic sclerosis

169
Q

what is often the first sign of early limited sclerosis?

A

puffy fingers

170
Q

what is the antibody associated with diffuse scleroderma?

A

anti-scl70 (anti-DNA topoisomerase I)

171
Q

what is the antibody associated with limited scleroderma?

A

anti-centromere (remember in CREST syndrome)

172
Q

which is more common and also presents with severe symptoms: scleroderma pts w/ upper GI tract or lower GI tract involvement?

173
Q

scleroderma pts w/ dysfunction of lower GI tract are associated with what kind of prognosis?

A

poor prognosis

174
Q

what is the most common cause of death in scleroderma?

A

respiratory failure

175
Q

how do you treat scleroderma-related ILD?

A

immunosuppression

176
Q

what are risk factors for pulmonary artery hypertension in scleroderma?

A

late onset of scleroderma, limited scleroderma, numerous telangiectasias, anti-centromere abs

177
Q

how would you screen and monitor the status of interstitial lung disease in scleroderma pts?

A

pulmonary function tests

178
Q

what predicts the outcome of ILD in scleroderma pts?

A

degree of lung fibrosis on CT

179
Q

which scleroderma pts typically have the worse prognosis?

A

nonwhite & antitopoisomerase I abs (anti-scl70)

180
Q

what kind of of deficiencies have the highest correlation with the risk of developing lupus?

A

complement deficiencies

181
Q

mutations in ____________ point to impaired regulation of endogenous nucleic acids as an important pathogenic mechanism of lupus.

182
Q

what problems are caused by serositis in lupus?

A

pleura (pleuritic chest pain, pleural effusion)
Pericardium (chest pain, pericardial effusion)
Peritoneal cavity (abd pain, fluid accum.)

183
Q

what are some of the neuropsychiatric complications of lupus?

A

depression, psychosis

184
Q

what is libman sacks endocarditis?

A

In lupus: aseptic vegetations that deposit on both sides of cardiac valves, commonly mitral valve

185
Q

what are some of the obstetrical complications of lupus?

A

considered high risk for both maternal & fetal complications:
small for gestational age fetuses
recurrent fetal loss (antiphospholipid ab)
neonatal lupus

186
Q

how might you try to minimize the significant morbidity associated with lupus pts that get infections?

A

education
immunization
minimal GCs
prompt anti-microbial therapy

187
Q

Name the pathology:
this disease has fibrosis associated w/ sustained mesenchymal cell activation by growth factors, cytokines, chemokines, ROS, aberrant reactivation of developmental pathways

A

systemic scleroderma

188
Q

how do the early limited sclerosis pts present?

A

raynaud’s (1st symptom)
puffy fingers
limited skin thickening
anti-centromere antibody

189
Q

how do the early diffuse scleroderma pts present?

A 
lots of constitutional symptoms
Tendon friction rubs
Swollen, puffy HANDS
early diffuse skin
Anti-Scl70 & anti-RNA-polymerase III
190
Q

what pts typically get scleroderma?

A

young black women

191
Q

which disease has a watermelon stomach (gastric antral vascular ectasia-GAVE)?

A

Systemic sclerosis

192
Q

what is a life-threatening condition that occurs in 5-10% of systemic sclerosis pts?

A

scleroderma renal crisis

193
Q

what are some risk factors for developing scleroderma renal crisis?

A

early diffuse skin disease
use of GCs
presence of anti-RNA POL III

194
Q

what is the key to treating scleroderma renal crisis?

A

early use of ACE inhibitors

195
Q

what is the clinical presentation of scleroderma renal crisis?

A

aburupt onset of severe systemic HTN, visual alterations, & accelerated oliguric renal failure

196
Q

Myopathies are often accompanied by elevated levels of serum _________ and abnormal EMGs.

A

muscle enzymes

197
Q

what is Gottron’s sign and where is it found?

A

nodules associated w/ dermatomyositis (commonly seen around MCP, PIP, DIP)

198
Q

what kind of lymphocytes are involved in dermatomyositis?

A

CD4 T cells

199
Q

what kind of histologic findings are present in dermatomyositis?

A

perimysial inflammation (think of it as being closer to your skin)

200
Q

what disease has mechanics hands?

A

dermatomyositis-hyperkeratotic, crackling skin findings on tips of fingers

201
Q

what kind of lymphocytes are involved in polymyositis?

A

CD8 T cells

202
Q

what kind of histologic findings are present in polymyositis?

A

endomysial inflammation

203
Q

which antibody is associated with the inflammatory myopathies?

A

anti-Jo-1 (anti-histidyl-tRNA-synthetase)

204
Q

what is a heliotrope rash and what kinds of pts will have it?

A

rash around the orbits of the eye, found in dermatomyositis or polymyositis

205
Q

which inflammatory myopathy has an increased risk of occult malignancy?

A

dermatomyositis

206
Q

antiphospholipid abs are a family of autoantibodies directed against phospholipid binding plasma proteins, most commonly _____________

A

beta2-glycoprotein I

207
Q

when do pregnancy losses typically occur in antiphospholipid syndrome?

208
Q

____________ is the prototypical overlap disease w/ features of lupus, scleroderma, & inflammatory myositis.

A

mixed connective tissue diseases

209
Q

what is the most common presentation of MCTD?

A

Raynaud’s phenomenon

210
Q

MCTD is most commonly associated with which antibodies?

A

anti-U1-RNP

211
Q

what is the major cause of death in MCTD?

A

pulmonary hypertension

212
Q

Nearly all pts with a UCTD have ____________ in combo w/ an unexplained synovitis

A

raynaud’s phenomenon

213
Q

what is a useful way to evaluate the potential diagnosis of UCTD?

A

nail-fold capillary microscopy

214
Q

what kind of antibodies predict the differentiation of UCTD into MCTD?

A

anti-U1-RNP

215
Q

what kind of antibodies predict the differentiation of UCTD into SLE?

A

DNA antibodies

216
Q

What kind of antibodies predict the differentiation of UCTD into Systemic sclerosis?

A

nucleolar antibodies

217
Q

what kind of antibodies predict the differentiation of UCTD into a myositis overlap syndrome?

A

Synethetase & PM/Scl antibodies

218
Q

what are the main causes of morbidity & mortality in scleroderma overlaps?

A

pulmonary fibrosis

pulmonary hypertension

219
Q

how can you tell the difference between primary raynaud’s phenomenon and raynaud’s in the context of limited sclerosis?

A

primary raynaud’s will have normal caipillaries on nail-fold microscopy

220
Q

In myositis overlap, antibodies to U1-RNP, PM/Scl, or Ku are associated with _________________

A

corticosteroid responsiveness

221
Q

what finding is found in almost all pts with MCTD?

A

raynaud’s phenomenon

222
Q

what are the 3 phases of raynaud’s?

A

white–>blue–>red

223
Q

what are the clinical hallmarks of Sjogren’s syndrome? (3)

A

keratoconjunctivitis sicca
xerostomia
parotid gland swelling

224
Q

what is the characteristic histopathologic finding in sjogren’s syndrome?

A

chronic Lymphocyticl infiltration of the lacrimal & salivary glands

225
Q

how would you diagnose sjogren’s syndrome?

A

dry eyes, dry mouth, anti-SSA, anti-SSB, and by lip biopsy

226
Q

sjogren’s syndrome has a risk of what kind of malignancy?

A

44x greater risk of developing non-Hodgkin’s lymphoma

227
Q

which connective tissue disease has an increased association with dental caries?

A

sjogren’s syndrome

228
Q

what is spear tackler’s spine?

A

loss of cervical lordosis, cervical stenosis, arthritic changes

229
Q

what is stinger syndrome?

A

aka dead arm syndrome (happens in a pt walking off the field with a traction/tension injury)

  • stinging/burning electric shock sensation
  • arm numness or weakness
  • sensation of warmth
  • C5 most common
230
Q

what is the most common mechanism of C-spine fracture-dislocation?

A

axial load (C5-6 most common)

231
Q

if you have a pt who was a kid doing squats with heavy loads and crappy technique he might get what kind of injury?

A

stress fracture of pars

232
Q

most shoulder dislocations happen anterior or posterior?

A

90% are anterior dislocation

233
Q

what is a bankhart lesion?

A

tearing of the anterior inferior glenohumeral complex from the labrum

234
Q

what is a SLAP tear?

A

superior labral anterior posterior tear: lots of overhead athletes like baseball players

235
Q

What is OCD capitellum?

A 
osteochondritis dissicans (feels like someone threw a pebble into my elbow gears)
-happens in excessive axial loading like gymnasts, & weight lifters)
236
Q

how would you dislocate your elbow?

A

falling on an extended arm

237
Q

what is more serious a proximal or distal biceps tendon tear?

A

distal is way worse

238
Q

what are the signs & symptoms of an ulnar collateral ligament injury?

A

pain, tenderness inner side of elbow, especially when throwing (inability to throw at full speed, loss of control)

239
Q

if you have a scaphoid fracture where will you hurt?

A

pain and swelling at the anatomical snuffbox (difficult to heal because it has a poor blood supply)

240
Q

what are the most common sites for pelvic avulsion fractures?

A

ASIS, AIIS, Ischial Tuberosity

241
Q

what is the most common ligament involved in an ankle sprain?

A

lateral ligament

242
Q

how do you test for cervical radiculopathy?

A

spurling’s maneuver: apply axial load to head that’s extended and rotated toward painful shoulder–>this is going to hurt a lot

MUSCULOSKELETAL/RHEUM (8 decks)

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