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Rheumatology 2 Flashcards

1
Q

Treatment of ILD associated with systemic sclerosis

A

Mycophenolate

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2
Q

Specific lab feature for diagnosis of TB in pleural effusion

A

HIGH adenosine deaminase

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3
Q

Most common pulmonary manifestation of RA

A

Rheumatoid pleuritis

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4
Q

Specific lab feature of adult still disease

A

Extremely high serum ferritin

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5
Q

SE’s of lyrica

A
  • weight gain, peripheral edema, lethargy, dizziness
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6
Q

HSP diagnosis

A

Skin biopsy with immunofluorescence

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7
Q

Treatment of relapsed GPA

A

Rituximab

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8
Q

management of refractory SLE

A

Belimumab

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9
Q

what is acute cutaneous lupus erythematosus?

A
  • derm presentation of SLE – classic malar (butterfly) rash
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10
Q

clinical description of malar rash

A

bright patches over both cheeks AND nasal bridge

*No nasolabial fold involvement

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11
Q

What is subacute cutaneous lupus erythematous in general?

A
  • different subtype of cutaneous lupus
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12
Q

Rosacea vs. SLE

A

rosacea = inflammatory papules, pustules, telangiectasisas

*nasolabial fold involvement

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13
Q

Treatment of primary angiitis of the CNS

A

Cyclophosphamide

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14
Q

When patients on chronic steroids need to be on bisphosphonates

A

*moderate or high 10 yr risk of major fracture + at least 2.5 mg of pred daily for 3 months

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15
Q

subacute cutaneous lupus erythematosus clinical features

A

young woman with lupus features + annular rash with central clearing or papulosquamous with patchy erythematous plaques and papules

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16
Q

Treatment options for chronic calcium pyrophosphate arthropathy

A
  • low-dose steroids
  • low dose colchicine
  • NSAIDS
  • you don’t use allopurinol because allopurinol is urate-lowering therapy, but calcium pyrophosphate deposition results from calcium pyrophosphate rather than uric acid deposition
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17
Q

medical term for pseudogout

A

acute calcium pyrophosphate crystal arthritis

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18
Q

good treatment option for OA with NSAID contraindications

A

Duloxetine

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19
Q

c-ANCA (GPA) antigen

A

proteinase 3 (PR3)

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20
Q

p-ANCA antigen

A

myeloperoxidase (MPO)

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21
Q

CREST syndrome is

A

Calcinosis
Raynaud’s
Esophageal dysmotility, Sclerodactyly
Telangiectasias.

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22
Q

anti synthetase syndrome clinical features

A
  • myositis + raynaud’s + mechanic’s hand + ILD

- 1/3 of patients with immune-mediated myopathy have constellation of findings termed “antisynthetase syndrome”

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23
Q

Mechanic’s hands + clinical association

A
  • thickened skin resembling skin of mechanic

- feature of patients with myositis

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24
Q

Polyarteritis nodosa clinical features

A

He is pissing blood + has a BP cough around his neck + right foot and left hand in bowling water + covered in darts + in a wheelchair/presentation is multi-systemic: renal: glomerulonephritis + hypertension, nervous: peripheral neuropathy + mononeuritis multiplex, GI: mesenteric ischemia/bowel infarction, bleeding, Musculoskeletal: myositis, arthritis.

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25
Q

Medical term for Churg-Strauss

A

Eosinophilic granulomatosis with polyangiitis

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26
Q

Eosinophilic granulomatosis with polyangiitis clinical features

A

Poly Nichols laying in bed. Andrew purpura to the right of the bed + has big headphones on + red eyes + + feet and hands in a bucket. Polly Nichols has nails driven into her sinuses and wrist/foot drop + she’s using a huge inhaler/presentation = asthma + sinusitis + skin nodules or purpura + peripheral neuropathy (eg wrist/foot drop) + uveitis + conductive/hearing loss + muscle/joint pain.

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27
Q

Complement levels in mixed cryoglobulinemia

A
  • C3 is unaffected
  • C4 is low
  • CH50 is low (CH50 is total hemolytic complement)
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28
Q

anti-centromere antibodies association

A

CREST syndrome

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29
Q

antibody associated with systemic sclerosis

A

anti-topoisomerase

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30
Q

Principles of RA care

A

1) Care by rheumatologist
2) DMARD ASAP
3) Tight control, treat to target strategy (adjusting therapy to treat a composite clinical outcome)

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31
Q

Management of RA patient resistant to initial DMARD therapy

A

Combination of DMARDS
- MTX + sulfasalazine and hydroxychloroquine
OR
- MTX + TNF inhibitor

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32
Q

Screening prior to starting DMARD

A
  • Hep B AND C

* latent TB

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33
Q

Hep B testing prior to starting DMARD

A

Hep B surface antigen and HBV core antibody

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34
Q

Screening prior to starting hydroxychloroquine

A
  • baseline optho exam
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35
Q

Management of active RA

A
  • anti-inflammatory therapy with NSAID or steroid (depending on degree of disease activity)
  • start DMARD therapy with MTX (may take weeks to months to achieve optimal effects)
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36
Q

contraindication to DMARD

A

active infection

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37
Q

RA during pregnancy

A

RA often improves or remits completely during pregnancy

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38
Q

HPV screening age interval

A

21 to 65

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39
Q

HPV testing for different age groups per USPSTF

A

21-29 = Pap test q 3 years
30 and over = Pap test q 3 years OR primary HPV testing alone (only certain tests are approved) q 5 years OR contesting (Pap and HPV testing) q 5 years
*can cotest once you’re 30

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40
Q

Behcet’s disease clinical features

A

recurrent and painful oral ulcers + genital ulcerations + ocular disease (uveitis) + skin lesions, gastrointestinal involvement, neurologic disease, vascular disease, or arthritis

41
Q

Countries where Behcet’s incidence is higher

A
  • Turkey (80 to 370 cases per 100,000) while the prevalence ranges from 13.5 to 35 per 100,000 in Japan, Korea, China, Iran, Iraq, and Saudi Arabia
42
Q

Treatment of Behcet’s syndrome

A

IF oral or genital ulcers –> topical steroids
For prevention of recurrent oral and genital ulcers –> colchicine
IF more severe disease –> systemic steroids

43
Q

Anti-GBM disease is

A

Goodpasture’s

44
Q

Anti-GBM disease clinical features

A

Lungs on + and attacking the basement membrane with a pickaxe + pissing blood all over the place + coughing up blood all over himself (NEPHRITIC)/patients are typically young men with onset of pulmonary symptoms like fatigue, dyspnea, and hemoptysis and renal symptoms – dysuria, hematuria, and renal failure.

45
Q

Anti-GBM disease treatment

A

Diego hooked up to plasmapheresis machine/treatment = emergent plasmapheresis.

46
Q

Treatment of MPGN

A

IF immune complex-mediated (hep C or b associated) – treat underlying disease

47
Q

Initial treatment of GPA

A

steroids = rituxan

48
Q

Serology in RA

A
  • Many patients have “seronegative” RA, typically early on in disease course (thus often have negative ANA, RF, and CCP
  • RA is A CLINICAL DIAGNOSIS
49
Q

RA presentation

A
  • morning stiffness improving with activity
  • small joint involvement (PIP, MCP, MTP) sparing DIP
  • joints are warm and tender to touch
  • rheumatoid nodules
  • symmetric, polyarticular joint pain
50
Q

Derm presentation of systemic sclerosis

A
  • skin thickening over hands and fingers + digital ulceration
51
Q

Presentation of ILD associated with systemic sclerosis

A
  • basilar crackles

- interstitial markings on CXR

52
Q

alopecia areata clinical features

A
  • commonly associated with other autoimmune disorders
  • chronic, recurring, often spontaneously recover but commonly relapse
  • smooth, circular patches of hair loss
  • exclamation point hairs seen at margins (larger on top than at their base) + extractable with minimal traction
53
Q

management of alopecia areata

A
  • intralesional steroid injections (or topical if refusing steroids)
  • sometimes no treatment
54
Q

Management of AIHA

A

First line = steroids

Second line = splenectomy

55
Q

MAHA on peripheral smear

A

red cell fragmentation (schistocytes)

56
Q

Peutz-Jeghers syndrome presentation

A
  • mucocutaneous pigmentation (multiple brown spots on lips and buccal mucosa)
  • multiple hamartomatous GI tract polyps and pigmented mucocutaneous papules
  • GI symptoms: rectal bleeding, obstruction, abdominal pain
  • young age
57
Q

Peutz-Jeghers syndrome is associated with increased risk for what?

A
  • malignancy (both GI and non-GI malignancy)
58
Q

Screening for Peutz-Jeghers

A
  • c-scope at age 18
  • EGD and small-bowel series starting at age 8
  • early mammograms
  • testicular exam starting at age 12
59
Q

ovarian cancer presentation

A
  • subtle (bloating, pelvic pressure)
60
Q

Other clinical + lab features of eosinophilic granulomatosis with polyangiitis

A 
CLINICAL:
- ***asthma
- chronic rhinosinusitis with nasal polyps
- necrotizing glomerulonephritis
- tender subcutaneous nodules 
- migratory polyarthritis
LAB:
- eosinophilia
- granulomatous
61
Q

Treatment of churg strauss

A
  • systemic steroids with or without cyclophosphamide
62
Q

Diagnosis of churg strauss

A
  • tissue biopsy (lung or kidney)
63
Q

GPA vs. churg-strauss

A

Churg-strauss = asthma + nasal polyps + eosinophilia

64
Q

Management of joint destruction in RA causing refractory pain, functional disability

A

refer to orthopedics (pain is typically from mechanical stress of joint deformities and or destruction)

65
Q

Reactive arthritis features

A
  • asymmetric oligoarthritis
  • enthesisitis
  • conjunctivitis
  • OR oral ulcers
66
Q

First line therapy for reactive arthritis

67
Q

Most common complications of tattoos

A

1) local staph infections

2) hypersensitivity reactions from metals in ink

68
Q

Variable correlated with poorer functional outcomes in RA

A
  • High titer CCP
  • higher number of involved joints
  • positive RF
  • higher inflammatory markers
69
Q

Presentation of septic olecranon bursitis

A
  • warmth, swelling, fever of elbow joint
  • synovial fluid count greater than 3K
  • gram stain may be negative
70
Q

Treatment of septic olecranon bursitis

A

drain fluid + systemic anti-staphylococcal abx

71
Q

Finding that commonly causes DXA result to be inaccurate

A

osteophytes + other abnormal calcifications (this is why treatment decisions should be based on lowest bone density measurement)

72
Q

Antihypertensives of choice for patients with gout

A

Losartan

CCBs

73
Q

Meds that can increase risk of gout flair

A
  • diuretics

* beta blockers

74
Q

Next step after suspected Raynaud’s

A

Nailfold capillary examination (differentiates between primary and secondary raynaud’s – normal nail fold capillaroscopy suggests primary reynaud’s, abnormal suggests secondary, so patient should be evaluated for an underlying disorder)

75
Q

HSP clinical features

A
  • renal dysfunction
  • palpable purpura
  • abdominal pain
  • arthritis
  • can be in adults too
76
Q

description of palpable purpura

A
  • multiple raised, erythematous, non blanching lesions on lower extremities
77
Q

PMR clinical features

A
  • elevated ESR
  • elderly patient
  • neck, shoulder, proximal thigh or hip involvement (may not have hip)
  • decreased ROM in shoulders, neck, and hips
  • constitutional symptoms
78
Q

Diabetic amyotrophy clinical features

A
  • acute asymmetrical pain followed by gradually worsening proximal lower extremity and back weakness
79
Q

atypical features of hyperthyroidism in elderly patients

A
  • dyspnea, apathy (rather than hyperactivity), paradoxical constipation
  • Afib
80
Q

Long term complication of Sjogren syndrome

81
Q

What is a pleomorphic adenoma?

A

Common benign salivary gland tumor

82
Q

Treatment of Lofgren syndrome

83
Q

Lofgren syndrome clinical features

A
  • erythema nodosum + bilateral ankle arthritis + hilar adenopathy
    (variant of sarcoidosis)
84
Q

Sjogren syndrome clinical features

A
  • chronic dry eyes + dry mouth
  • 25% have extra glandular manifestations: *RTA + DI, chronic interstitial nephritis, lung, nervous system, heart involvement, *Rayonouds
85
Q

clinical features of mixed cryoglobulinemia

A
  • palpable purpura, arthralgias, MPGN, neuropathy

- can see skin necrosis and gangrene in some patients

86
Q

mixed cryoglobulinemia lab features

A
  • positive ANA + RF

- low C3 + C4 (confirm)

87
Q

Other presentation of GPA

A
  • ocular involvement
88
Q

Drugs causing drug-induced SLE

A
  • hydralazine
  • procainamide
  • minocycline
  • anti-tumor necrosis factor agents
89
Q

drug-induced SLE clinical and lab features (distinct from SLE

A
  • normal complement

- less likely to cause CNS, heme, or renal abnormalities

90
Q

autoantibodies positive in drug-induced SLE

A

histone autoantibodies

91
Q

Sarcoidosis diagnosis

A
  • requires biopsy (demonstrating pathologic evidence of noncaseating granulomas)
  • biopsy most accessible site of disease involvement, which is typically endobronchial ultrasound with nodal aspiration for mediastinal lymph node sampling
92
Q

pseudogout caveat

A
  • crystal microscopy has low sensitivity (CPPD crystals are small and often scarce)
93
Q

Preferred antihypertensive for suspected aortic dissection

A

First line: Beta blockers (labetalol) (you also want to decrease LV contractility to reduce aortic wall shear stress)
Second line: nitroprusside

94
Q

Symptomatic PDA presentation

A
  • continuous murmur
  • wide pulse pressure
  • bounding pulses
  • best auscultated pulmonic position
95
Q

Sequela of unprepared PDA

A

Increased risk of infective endarteritis

96
Q

description of murmur from PDA

A
  • continuous murmur in the left infraclavicular region
97
Q

Allopurinol titration in gout

A
  • never adjust dose or discontinue until 3-4 weeks after the acute inflammation subsides
  • typically increased until serum uric acid is below 6
98
Q

Management of dermatitis associated with SLE

A

Mild – topical steroids
Moderate – plaquenil
Severe – immunosuppressive drugs

99
Q

Limited cutaneous systemic sclerosis features

A
  • puffy fingers distal to MCP joints

- sclerosis distal to elbows and knees, sparing trunk and proximal extremities

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