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Musculoskeletal and Connective Tissue > FA 2 > Flashcards

FA 2 Flashcards

1
Q

systemic scleroderma is divided into

A
  1. diffuse scleroderma (both skin and visceral organs)

2. limited scleroderma (only skin)

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2
Q

diffuse scleroderma is associated with

A

anti-Scl 70 antibody (anti-DNA topoisomerase I antibody)

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3
Q

Limited sclerodermia - clinical manifestation

A
  • limited skin involvement (fingers and face)

- CREST: Calcinosis, Raynaud phenomenon, Esophangeal dysmotility, Sclerodactily, Talangiectasia

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4
Q

Limited sclerodermia is associated with

A

anti-centromere antibodies

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5
Q

myasthenia gravis - sex

A

MC seen in women

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6
Q

Lambert-Eaton myasthenic syndrome - symptoms

A
  1. proximal muscle weakness
  2. autonomic symptoms (dry mouth, impotence)
    improves with muscle use
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7
Q

fibromyalgia - most commonly seenin

A

females 20-50

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8
Q

fibromyalgia - clinical manifestation

A

(1) chronic, widespread musculoskeletal pain associated with (2)stiffness, (3) paresthesias, (4) poor sleep, (5) fatigue , 6. cognitive disturbance (“fibro fog”)

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9
Q

fibromyalgia - treatment

A
  1. regular exercise
  2. antidepressants (TCAs, SNRIs)
  3. anticonvulsants
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10
Q

polymyalgia rhematica - treatment

A

rapid response to low dose corticosteroids

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11
Q

polymyalgia rhematica - labs

A
  1. increased ESR
  2. increased CRP
  3. normal CK
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12
Q

polymyalgia rhematica - sex and age / associated with?

A

older women

- temporal (giant cell) arteritis

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13
Q

polymyalgia rhematica clinical manifestation

A
  1. pain and stiffness in shoulders and hips
  2. fever
  3. malaise
  4. weight loss
    (NO MUSCULAR WEAKNESS)
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14
Q

polymyalgia rhematica - muscular weakness

A

NO MUSCULAR WEAKNESS

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15
Q

polymyositis - clinical presentation / MC area

A

progressive SYMMETRIC proximal weakness

- shoulders

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16
Q

polymyositis - treatment

A

steroid followed by long term immunosuppressant therapy (methotrexate)

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17
Q

dermatomyositis - clinical presentation

A
  1. progressive symmetric proximal weakness (like polyomyositis)
  2. malar rash (similar to SLE)
  3. heliotrope rash
  4. Gottron papules
  5. shawl (or V-) and face rash
  6. mechanics hands
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18
Q

mechanics hands

A

Cracking (and hyperkeratosis) of the finger pad skin, commonly involving the first, second, and third fingers

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19
Q

dermatomyositis - treatment

A

steroid followed by long term immunosuppressant therapy (methotrexate) (same as polymyositis)

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20
Q

dermatomyositis vs polymyositis - labs

A

SAME:

  1. increased CK
  2. ANA +
  3. anti-Jo-1 +
  4. anti-SRP +
  5. anti-Mi-2+
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21
Q

polymyositis vs dermatomyositis regarding to cells

A

polymyositis –> CD8

dermatomyositis –> CD4

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22
Q

sarcoidosis - CD4/CD8 ratio

A

elavated in BRONCHOALVEOLAR LAVAGE

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23
Q

localized scleroderma - labs

A

antibodies against to DNA topoisomerase II

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24
Q

Raynaud phenomenon - Reynuad disease vs syndrome

A

disease –> when 1ry (idiopathic), women under 30
syndrome –> 2ry to a disease process such as mixed connective tissue disease, SLE, CREST, male older 40 –> digital ulceration

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25
Q

Lupus nephritis - MC

A

nephritic - diffuse proliferative glomerulonephritis
nephrotic - membranous glomerulonephritis
MC and severe type is diffuse proliferative

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26
Q

Common causes of death in SLE

A
  1. cardiovascular disease
  2. Infection
  3. Renal disease
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27
Q

SLE symptoms/findings/treatment etc

A

mnemonic: RASH OR PAIN
Rash, Arthritis, Soft tissues/Serositis, Hematologic disorders, Oral and nasopharyngeal ulcers, Renal disease/Raynaud phenomenon, Photosensitivity, Antinuclear antibodies, Immunologic disorfer (anti-dsDNA, anti-SM, antiphospholipids), Neurologic

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28
Q

SLE - heart

A

it can affect any layer of the heart (endo,myi,pericarditis)

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29
Q

SLE - treatment

A
  1. NSAID 2. Steroids 3. immunosuppressants

4. hydroxychloroquine

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30
Q

SLE - lab findings

A
  1. antinuclear antibodies (ANA)
  2. anti-dsDNA antibodies
  3. anti-Smith antibodies
  4. decreased C3, C4, CH50
  5. Anti-histone antibodies
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31
Q

SLE- sensitive, not specific test
SLE - specific, poor prognosis test
SLE - specific, not prognostic test

A
  • ANA
  • anti-dsDNA (renal disease)
  • anti-Smith
32
Q

SLE - sensitive for drug induced lupus

A

antihistone antibodies

33
Q

clinical criteria of antiphospholipid syndrome

A
  1. history of thrombosis (arterial or venous)

2. recurrent spontaneous abortion

34
Q

antiphospholipid syndrome arterial or venous thrombosis includes

A
  1. DVT
  2. hepatic vein thrombosis
  3. placental thrombosis
35
Q

antiphospholipid syndrome - lab findings

A
  1. lupus anticoagulants
  2. anticardiolipin
  3. anti-β2 glycoprotein antibodies
36
Q

antiphospholipid syndrome - lupus anticoagulants and anticardiolipin antibodies can cause …. (lab)

A

false positive VDRL/RPR

falsely elevated PTT

37
Q

Mixed connective tissue disease - clinical presentation

A

Feature of SLE, systemic sclerosis, and/or polyomyositis

38
Q

Mixed connective tissue disease - Labs

A

anti-U1 RNP antibodies (speckled ANA)

39
Q

SLE - lab findings (and their characteristics)

A
  1. antinuclear antibodies (ANA) - sensitive, Not specific
  2. anti-dsDNA antibodies - Specific, poor prognosis (renal disease)
  3. anti-Smith antibodies - Specific, not prognostic (directed against snRNPs)
  4. decreased C3, C4, CH50 - due to immune complex formation
  5. Anti-histone antibodies - sensitive for drug-induced lupus)
40
Q

Acute gout drugs?

A
  1. NSAID
  2. Glucocorticoids (oral or intra-articular)
  3. Colchicine
41
Q

salicilates - gout

A

do not salicylates –> all but the highest doses depress uric acid clearance. Even high doses (5-6g/day) have only minor uricosuric activity

42
Q

chronic gout drugs?

A
  1. allopurinol
  2. febuxostat
  3. pegloticase
  4. probenecid
43
Q

Clinical use of aspirin (and doses)

A 
Low dose, under 300 (inhibits platelet aggregation)
Intermediate dose (300-2400mg/day) --> antypyretic and analgesic
High dose (2400-4000mg/day) --> anti-inflammatory
44
Q

Bisphosphonates - clinical use

A
  1. osteoporosis
  2. hypercalcemia
  3. Paget disease of bone
  4. metastatic bone disease
  5. osteogenesis imperfecta
45
Q

Teriparatide - clinical use (explain)

A

osteoporosis –> causes increased growth compared to antirepsorptive therapies (eg. biphosphanates)
(PTH ANALOGUE)

46
Q

TNF-a inhibitors - drugs and mechanism of action

A
  1. etanercept - fusion protein (receptor for TNF-A+IgG1 FC) produced by recombinant DNA
  2. infliximab - anti-TNF-a monoclonal antibody
  3. adalimumab - anti-TNF-a monoclonal antibody
  4. certolizumab - anti-TNF-a monoclonal antibody
47
Q

Sjogren syndrome - clinical findings

A
  1. inflammatory joint pain
  2. xerophthalmia and subsequent corneal damage –> Keratoconjunctivitis sicca
  3. Xerostomia
  4. Bilateral parotid enlargment
48
Q

Sjogren syndrome - labs

A
  1. antinuclear antibodies (anti-ribonucleoprotein antibodies) –> SS-A (anti-Ro), SS-B (anti-La)
  2. ANA
49
Q

joint findings of osteoarthritis

A
  1. subchondral cysts
  2. sclerosis
  3. osteophytes (bone spurs)
  4. eburnations of the subchondral bone
  5. synovitis
  6. Heberden nodes (DIP)
  7. Bouchard nodes (PIP)
  8. 1st carpometacarpal (CMC)
  9. joint space narrowing
  10. synovial fluid non inflammatory (less than 2000 WBC)
    NO MCP
50
Q

osteoarthritis of the hand - which joints

A
  • DIP (Heberden nodes)
  • PIP (Bouchard nodes)
  • 1st carpometacarpal (CMC)
    NO MCP
51
Q

joint findings of Rheumatoid arthritis

A
  1. pannus formation in joints (MCP, PIP) - NOT DIP or 1st CMC
  2. subcutaneous rheumatoid nodules (fibrinoid necrosis) - soft tissue swelling
  3. ulnar deviation of fingers
  4. sublaxation
  5. swan neck deformity (rare)
  6. boutonniere deformity (rare)
  7. rare DIP involvement
  8. erosions
  9. joint space narrowing
  10. juxtaarticular osteopenia
  11. Synovial fluid inflammatory (WBC more than 2000)
52
Q

predisposing factor of Rheumatoid arthritis

A
  1. female (80% vs males)
  2. +Rheumatoid factor
  3. Anti-cyclic citrullinated peptide antibody (more specific)
  4. HLA-DR4
  5. SILICA exposure
53
Q

Heberden vs Bouchard nodes - area

A

Heberden: DIP
Bouchard: PIP

54
Q

Rheumatoid arthritis vs osteoarthritis - according to joint involvement distribution

A

RA –> symmetrical

Osteoarthritis –> asymmetrical

55
Q

Rheumatoid arthritis - x-rays

A

joint-space narrowing loss of cartilage

osteopenia

56
Q

Rheumatoid arthritis vs osteoarthritis - increased synovial fluid / wbc?

A

RA –> increased fluid

WBC –> less than 2000 in osteoarthritis, more in RA

57
Q

causes of septic arthritis

A
  1. Neisseria gonorrhoea (MCC)
  2. S. aureus (2nd MCC)
  3. Streptococcus
58
Q

infectious arthritis - presentation (clinical and labs)

A
  1. warm,red, painful joint with limited range of motion
    fever
  2. increased WBC and elevated ESR
  3. Synovial fluid purulent (more than 50000 WBCs
59
Q

Gonococcal arthritis is an STD that presents as a

A

STI either purulent arthritis (eg. knee) or triad of polyarthralgias, tenosynovitis (hand) ,dermatitis (pustules)

60
Q

Serenegative spondyloarthropathies - types

A
  1. Psoriatic arthritis
  2. Ankylosing spondylitis
  3. Inflammatory bowel disease
  4. Reactive arthritis
61
Q

Serenegative spondyloarthropathies - characteristics

A
  1. rheumatoid factor (-)
  2. HLA-B27 strong association
  3. Subtypes share variable occurrence of inflammatory back pain (morning stiffness, improves with exercise), peripheral arthrites, enthesitis (inflamed insertion sites of tendons eg. Achilles), dactylitis (sausage fingers), uveitis
62
Q

Psoriatic arthritis - clinical presentation

A
  • joint pain and stiffness associated with skin psoriasis and nail lesions
  • Asymmetric and patchy involvement
  • Dactylitis (sausage fingers)
  • sacroliti + spondilitis
  • athriting mutilans (destructive and deforming)
63
Q

Psoriatic arthritis - joints

A

axial and peripheral (DIP of hands and feet are MC)

64
Q

Reactive arthritis (Reiter syndrome) - clinical presentation

A 
Classic triad
1. Conjunctivitis and anterior uveitis  
2. Urethritis 
3. Arthritis 
weeks after GI infection (Shigella, Salmonella, Yersinia, Campylobacter) or chlamydia infection
65
Q

Ankylosing spondilitis causes (clinically) (and involves …)

A
  1. Symmetric involvement of spine and sacroiliac joints –> ankylosis (jonint fusion) and bamboo spine (vertebral fusion)
  2. uveitis
  3. aortic regurgitation
  4. dactylitis
66
Q

Gout - crystals?

A

monosodium urate crystals

67
Q

monosodium urate crystals - characteristics

A
  1. needle shaped
  2. (-) birefringent under polarized light
  3. blue under perpendicular light
  4. yellow under paraller light
68
Q

pseudogout present with

A

pain and effusion with acute infalmmation (pseudogout) and/or chronic degeneration (pseudo-osteoarthritis)
classically affects the knee

69
Q

pseudogout is caused by

A

deposition of calcium pyrophosphate crystals within the joint space

70
Q

x ray of pseudogout

A

chondrocalcinosis –> cartilage calcification

71
Q

pseudogout - which joints

A

usually affects large joints (classically the knee)

72
Q

diseases associated with pseudogout

A

Usually idiopathic

  1. hemochromatosis
  2. hyperparathyroidsm
  3. Joint trauma
73
Q

pseudogout - crystal characteristics

A
  1. basophilic, rhomboid crystals
  2. weakly birefringent under polarized light
  3. blue under paraller light
74
Q

pseudogout vs gout according crystals shape

A

pseudogout –> rhomboid

gout –> needle shape

75
Q

seronegative spondyloarthropathies are more common in

76
Q

seronegative spondyloarthropathies - inflammatory bowel disease ?

A

Crohn disease and ulcerative colitis are often accompanied by spondyloarthritis

77
Q

Felty syndrome

A
  1. RA
  2. neutropenia
  3. splenomegaly

Musculoskeletal and Connective Tissue (19 decks)

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