Joint/muscle pathologies etc. Flashcards

1
Q

What collects in the joints in someone who has gout?

A

Monosodium urate crystals

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2
Q

Which is more common, the overproduction or uric acid or underexcretion?

A

Undersecretion of uric acid

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3
Q

Causes of undersecretion of uric acid

A

mostly idiopathic, but potentiated by renal failure

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4
Q

Causes of overproduction of uric acid

A

Lesch-Nyhan syndrome, PRPP excess, increased cell turnover

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5
Q

Findings under polarized light of joint fluid from someone with gout

A

Needle shaped crystals with - bifringence

-yellow under parallel light, blue under perpendicular light

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6
Q

Treatment of acute gout attack

A

NSAIDs, glucocorticoids, colchicine

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7
Q

Treatment of chronic gout attack

A

Xanthine oxidase inhibitors

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8
Q

What is calcium pyrophosphate deposition disease AKA

A

pseudogout

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9
Q

What deposits in the joints of someone with calcium pyrophosphate deposition disease?

A

calcium pyrophosphate

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10
Q

Most affected joint in calcium pyrophosphate deposition disease?

A

Knee

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11
Q

What will you see on xray of someone with calcium pyrophosphate deposition disease?

A

chondrocalcinosis

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12
Q

What do the crystals in calcium pyrophosphate deposition disease look like?

A

rhomboid and weakly + birefringent (blue when parallel to light)

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13
Q

acute treatment of calcium pyrophosphate deposition disease

A

NSAIDs, colchicine, glucocorticoids

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14
Q

Prophylaxis of calcium pyrophosphate deposition disease

A

colchicine

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15
Q

What is the presentation of systemic juvenile idiopathic arthritis?

A

Daily spikign fevers, salmon-pink macular rash, arthritis, leukocytosis, thrombocytosis, anemia,

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16
Q

Treatment of systemic juvenile idiopathic arthritis?

A

NSAIDs, steroids, methotrexate, TNF inhibitors

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17
Q

Sjogren syndrome pathophys

A

autoimmune disorder characterized by desctruction of exocrine glands by lymphocytes

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18
Q

Clinical findings in sjogrens syndrome

A

Inflammtory joint pain
Keratoconjunctivitis sicca (decreased tear production and corneal damage)
Xerostomia
Bilateral parotid enlargement

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19
Q

What will you find in the blood of someone with Sjogrens?

A

ANA antibodies, rheumatoid factor, and antiribonucleoprotein antibodies: SS-A, SS-B

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20
Q

In what condition other than Sjogrens may someone e have positive anti-SSA and anti-SSB antibodies?

A

SLE

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21
Q

Complications of sjogrens

A

dental caries

MALT (may present as parotid enlargement)

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22
Q

What confirms the diagnosis of sjogrens syndrome?

A

lymphocytic sialadenitis on labial salivary gland biopsy

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23
Q

What are the four types of seronegative spondyloarthritis?

A

Psoriatic arthritis
Ankylosing spondylitis
Inflammatory bowel disease
Reactive arthritis

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24
Q

What are seronegative spondyloarthritis’s?

A

arthritis without rheumatoid factor (no igG antibody)

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25
Q

what HLA type are seronegative spondyloarthritis’s associated with?

A

HLA-B27

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26
Q

What do the seronegative spondyloarthritis’s have in common as presentation ?

A

inflammatory back pain that improves with exercise, peripheral arthritis, enthesitis and dactylitis, uveitis

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27
Q

What may you see on XRAY of someone with psoriatic arthritis?

A

Pencil in cup deformity

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28
Q

What is the presentation of someone with ankylosing spondylitis?

A

Arthritis with symmetric involvement of spine and SI joints which leads to joint fusion
-also uveitis, aortic regurgitation and ankylosis

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29
Q

What may be seen on XRAY of someone with ankylosing spondylitis?

A

Bamboo spine

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30
Q

Complication of ankylosing spondylitis?

A

Restrictive lung disease

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31
Q

Explain the two different types of seronegative spondyloarthritis seen in IBD patients

A

Type I: <5 joints, large joints, worse w/ flares

Type II: >5 joints, small, independent

32
Q

What is the triad seen in reactive arthritis?

A

conjunctivitis, urethritis, arthritis

33
Q

What is SLE?

A

A relapsing and remitting autoimmune disease

34
Q

Pathophys of lupus?

A

organ damage primarily due to type III hypersensitivity (partially type II)
-associated with early complement protein deficiency leading to decreased clearance of immune complexes

35
Q

How does lupus classically present?

A

rash, joint pain, fever, in female of reproductive age (especially african-american or Hispanic women)

36
Q

What type of endocarditis is associated with SLE?

A

Libman-Sacks Endocarditis

37
Q

What is libman-sacks endocarditis?

A

nonbacterial thrombi on mitral or aoric valve that may be present on either side of the valve

38
Q

What is lupus nephritis?

A

glomerular deposition of DNA-anti-DNA immune complexes that leads to nephrotic or nephritic syndrome - most commonly diffuse proliferative

39
Q

What is an anti-SSA + pregnant women at risk of?

A

the newborn developing neonatal lupus

40
Q

Presentation of neonatal lupus?

A

congenital heart block, periorbital/diffuse rash, transaminitis, and cytopenias

41
Q

What is a sensitive antibody for lupus?

A

ANA

42
Q

What are some specific antibodies for lupus?

A

Sensitive - ANA

Specific - anti-dsDNA and anti-SM

43
Q

What is mixed connective tissue disease?

A

Disease with features of SLE, systemic sclerosis, and or polymyositis

44
Q

What antibody is associated with mixed connective tissue disease?

A

anti-U1 RNP antibodies

45
Q

How does antiphospholipid syndrome present?

A

venous/arterial thrombosis and reccurrent fetal loss

46
Q

What lab findings are present in antiphospholipid syndrome?

A

lupus anticoagulant, anticardiolipin, anti-B2 glycoprotein I antibodies

47
Q

Treatment of antiphospholipid syndrome ?

A

systemic anticoagulation

48
Q

antiphospholipid syndrome may occur secondarily to what?

A

SLE

49
Q

Presentation of polymyalgia rheumatica?

A

Bilateral pain and stiffness in proximal muscles with fever, malaise and weight loss. NO muscle weakness.

50
Q

What is polymyalgia rheumatica associated with?

A

giant cell arteritis

51
Q

Findings in polymyalgia rheumatica?

A

increased ESR, Increased CRP, normal CK

52
Q

Treatment for polymyalgia rheumatica?

A

corticosteroids (rapid response)

53
Q

Fibramyolgia presentation

A

Chronic widespread musculoskeletal pain associated wiht tender points, stiffness, paresthesias, poor sleep, cognitive disturance. More common in women 20-50 years old.

54
Q

Treatment of fibromyalgia

A

Regular exercise, antidepressants, neuropathic pain agents

55
Q

Antibodies found in polymyositis/dermatomyositis?

A

+ANA, anti-Jo-1, anti-SRP, anti-Mi-2

56
Q

polymyositis presentation

A

progressive symmetric proximal muscle weakness.

Usually involves shoulders.

57
Q

pathophys of polymyositis

A

Endomysial inflammation with CD8+ T cells.

58
Q

dermatomyositis presentation

A

Similar to polymyositis plus Gottron papules, photodistributed facial erythema, shawl and face rash., darkening and thickening of fingers tips.

59
Q

dermatomyositis pathophys

A

perimysial inflammation and atrophy with CD4+ cells

60
Q

pathophys of myasthenia gravis

A

autoantibodies to post-synaptic Ach receptors

61
Q

presentation of myasthenia gravis

A

Ptosis, diplopia, weakness (may lead to dyspnea if respiratory muscles involved, or dysphagia if bublar muscle involvement).
Worsen with muscle use.

62
Q

What is myasthenia gravis associated wtih?

A

thymoma, thymic hyperplasia

63
Q

Treatment of myasthenia gravis?

A

AchE inhibitors - pyridostigmine

64
Q

Tensilon test use

A

Determines whether a patient presenting with worsening symptoms of myasthenia gravis has an insufficient dose or is having a cholinergic crisis.

65
Q

Tensilon test findings

A
Administer edrophonium (a short acting AchE inhibitor).
If symptoms improve, patient needs higher dose. 
If symptoms gett worse, patient needs lower dose.
66
Q

Pathophys of lambert-eaton syndrome

A

autoantibodies to presynaptic Ca channels – decreased Ach release

67
Q

Presentation of lambert eaton syndrome

A

proximal muscle weakness, autonomic symptoms (dry mouth, impotence). Improves with muscle use.

68
Q

what is lambert-eastion syndrome associated with?

A

small cell lung cancer

69
Q

Treatment of Raynaud phenomonen ?

A

Ca channel blockers

70
Q

Scleroderma pathophys

A

Autoimmunity activates fibroblasts –> collagen deposition

71
Q

Diffuse scleroderma presentation

A

widespread skin involvment, rapid progression, early visceral involvment.

72
Q

Antibodies seen in diffuse scleroderma?

A

anti-scl-70

anti-RNA polymerase

73
Q

someone with anti-RNA polyermase is at increased risk for what?

A

renal crisis

74
Q

Limited scleroderma pathophys

A

skin involvement confined to fingers and face. Associated with CREST syndrome.

75
Q

What is CREST syndrome?

A

Calcinosis cutis, anti-centromere antibody, raynaud phenomenon, esophageal dysmotility, sclerodactyly, telangiectasia.

76
Q

Which antibody may be seen in limited scleroderma?

A

Anti-centromere antibody