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Shit you keep forgetting > Rheumatology, MSK, Skin > Flashcards

Rheumatology, MSK, Skin Flashcards

1
Q

What is the typical age presentation for ankylosing spondylitis?

A

20 - 40 years of age

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2
Q

What are the common clinical presentations of ankylosing spondylitis?

A

lower back pain, enthesitis, dactylitis, and extraarticular manifestations include restricitive lung disease and uveitis

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3
Q

What is the diagnosis for ankylosing Spondylitis?

A

MRI for acute presentation and X-ray for late presentation

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4
Q
A

Schober test less than 5cm is an indication of positive test for ankylosing spondylitis.

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5
Q

What is the treatment for ankylosing spondylitis?

A

NSAIDs for acute flares and if the treatment is refractory then we consider TNF inhibitors.

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6
Q

A patient with a history of psoriasis presents with joint pain serum studies are drawn what antigens do you expect to find in the blood?

A

Keep in mind that psoriatic arthritis is a seronegative arthropathy and thus even though HLA-B27 is associated with disease we typically don’t see it in the serum

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7
Q

What is the diagnosis of psoriatic arthritis?

A

Labs like the ESR and CRP will be elevated and RF and CCP are negative and a history of psoriasis or a family history

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8
Q

What are the joints most associated with psoriatic arthritis?

A

Knee, Ankle, and DIP

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9
Q

What is a definitive extraarticular manifestation of psoriatic arthritis?

A

Onycholysis (nail changes)

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10
Q
A

Is a manifestation of psoriatic arthritis. Called the pencil in cup deformity. Remember that the spondyloarthropathies are inflammatory disorders and therefore have the opportunity to destroy the joints.

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11
Q

What is the treatment for psoriatic arthritis?

A

First line is to start NSAIDs (diclofenac, ketorolac, aspirin, etc). Second line would be DMARD’s and we usually start with methotrexate or sulfasalazine. If those are not effective treatment then we move to TNF-a inhibitors.

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12
Q

What are the side affects of steroids?

A

bone fractures, psychosis, hypercalcemia

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13
Q

If you suspect that joint pain occurs do to an inflammatory bowel disorder what are the labs that you can draw?

A

Fecal Calprotectin and CRP

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14
Q

What is the most common bug to cause reactive arthritis?

A

Chlamydia, also consider gram negative organisms like salmonella, shigella, Yersinia, campylobacter and C. Diff

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15
Q

How does reactive arthritis usually present?

A

The patient typically presents with a viral infection 1-4 weeks before arthritic symptoms . Even though the infection is cleared. It’s because of the molecular mimicry that there is a residual reaction. I can’t, see I can’t pee I cant bend my knees.

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16
Q
A

Keratoderma blennorrhagica

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17
Q

What joints does pseudogout most commonly affect?

A

Larger joints like the knee

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18
Q

What is the finding on arthrocentesis of the joint in a patient with pseudogout ?

A

Calcium pyrophosphate crystals with rhomboid shape and positively birefringent

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19
Q

What is a common X-ray finding of pseudogout?

A

Chondrocalcinosis seen in cartilage and ligaments

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20
Q

What are the X-ray findings in gout?

A

Well-defined punched-out erosion with a thin rim of calcification.

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21
Q

What is the treatment for pseudogout?

A

NSAIDs, colchicine, and steroids if either is ineffective or contraindicated

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22
Q

What are the ways in which we end up with high levels of uric acid?

A

Either we produce to much or we don’t excrete it effectively (kidneys)

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23
Q

What is the presentation of gout/pseudogout?

A

Patients develop acute onset of joint pain that is severe.

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24
Q

What medications increase the risk of formation of uric acid stones?

A

Thiazides and loop diuretics, also aspirin

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25
Q
A

This is showing uric acid crystals

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26
Q

What is tophaceous gout?

A

This the chronic accumulation of urate crystals in the soft tissue

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27
Q

What is the contraindication to using Probenicid?

A

Patients with kidney disease

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28
Q

When should we start prophylactic gout attack medication?

A

2-4 weeks after an acute gout attack

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29
Q

What are the ways in which septic arthritis may be acquired?

A

Hematogenous, contiguous spread, and direct inoculation.

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30
Q

What is migratory arthritis?

A

There is inflammation of joints resolution and joint inflammation will start somewhere else.

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31
Q

What are common causes of migratory arthralgias?

A

SLE, rheumatic fever, lyme disease, DGI, Reactive arthritis

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32
Q

What are the most common risk factors for septic arthritis?

A

Rheumatoid arthritis and osteoarthritis

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33
Q

What criteria can we use to estimate the likely hood of septic arthritis?

A

Kocher test

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34
Q

In addition to antibiotic therapy what should be the next step in treatment for septic arthritis?

A

The patient should have joint drained

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35
Q

What is the classic triad for disseminated gonococcal infection?

A

Polyarthralgia, vesiculopustular rash, tenosynovitis

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36
Q

If you suspect a patient has DGI what test is necessary to confirm Nisseria gonorrhea (hint: the same test is used to diagnose chlamydia)

A

NAAT

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37
Q

When should we suspect a patient has tuberculosis arthritis?

A

If they are coming from an endemic area, infection with TB, immunocompromised, malnutrtion or alcholic

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38
Q

What are the diagnostic testing studies that would confirm a patient had TB arthritis?

A

Tuberculin skin test, IGRA and a synovial biopsy that shows granulomas.

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39
Q

This autoimmune arthritis typically upon waking in the morning takes only a few minutes to resolve?

A

Osteoarthritis

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40
Q

This autoimune disorder takes several minutes to hours to resolve upon waking in the morning.

A

Rheumatoid arthritis

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41
Q

_____ and _____ nodes are present in patients with osteoarthritis?

A

Herbden and Bouchard

42
Q

What are the X-ray and PE findings of osteoarthritis?

A

Xray shows joint space narrowing, osteophytes, subchondral calcinosis and even joint effusions. PE shows crepitus

43
Q

What is the treatment for osteoarthritis?

A

Acetaminophen is the first line treatment, NSAIDS are the second line, followed by steroids, consider joint replacement if no therapies are helpful.

44
Q

What are the antibodies for RA?

A

anti- CCP (citrulinated peptide), Anti- RF which is very non-specific

45
Q

What are the antibodies for systemic sclerosis that is diffuse

A

anti- scl-70

46
Q

What are the antibodies for mixed connective tissue disease

A

anti-URNP

47
Q

What are the antibodies for partial systemic sclerosis?

A

anti-centromere

48
Q

What are the antibodies for sjorens?

A

ant- Ro (SSA) and anti-La (SSB)

49
Q

What are the antibodies in dermatomyositis and polymyositis?

A

anti- Jo and anti- ANA

50
Q

What are the antibodies in SLE?

A

Anti- dsDNA, anti-smith, and ANA

51
Q

What are the joints affected in rheumatoid arthritis?

A

metatarsal, wrist, PIP,

52
Q

What is the treatment for RA?

A

Methotrexate is the first line, and sulfazalzine and methotrexate would be the second line, TNF inhibtors, surgery is an option for very severe presentations.

53
Q

What is the diagnostic work up for Sjorens?

A

Schrimer test and check serology for anti-Ro anti-La (SSA and SSB), and biopsy of the lip if necessary.

54
Q

What are the criteria that we use in order to diagnose SLE?

A
55
Q

What is the treatment for SLE?

A

hydoxychlorquine, steroids, immunosupressives

56
Q

What is the complication to the kidney of a patient with SLE?

A

Nephritic or nephrotic syndrome; this is the most common cause of morbidity and mortality in SLE and thus kidney function studies should always be checked.

57
Q

What are the antibodies that we can see in phospholipid syndrome?

A

anti b2, anti-cardiolipin, anti-phospholipid

58
Q

When should you start a work up for a patient that you may suspect to have anti-phospholipid syndrome?

A
  1. multiple incidences of vascular thrombosis, or at least 1 miscarriage after 10 weeks or
59
Q

What are complication that are we concerned about developing in SLE?

A

Libmann sac endocarditis, nephrotic syndrome of the kidneys, CNS seizure, psychosis, stroke, TIA, hyper coagulable state

60
Q

What is the criteria to diagnose SLE?

A

There must be at least 4 of the 11 of SOAP BRAIN MD

61
Q

What does SOAP BRAIN MD stand for?

A

Serositis, oral ulcers, Arthritis, Photosensitivity, Blood pathologies Renal anomalies, ANA (+), immunoglobulin (dsDNA and Smith) Malar, Discoid

62
Q

What is the immunoglobulin for drug induced lupus?

A

anti-histone

63
Q

What are the drugs that cause drug induced lupus?

A

HIPPE (hydralazine, isoniazid, phenytoin, procainamide, entancercept

64
Q

What are the concerning compliations of RA?

A

Cervical joint instability, and an increased risk for osteoporosis. Less important, but RA can also be associated with the development of a Baker’s cyst.

65
Q

What is Felty syndrome?

A

RA + neutropenia +splenomegaly

66
Q

What is the clinical presentation of systemic juvenile arthritis?

A

Still too FAST, usually presents in patients that are <35 yoA
Still = Still’s disease
Too = 2 weeks of fever spikes
F = Fever
A = arthritis
S = Skin rash (salmon-red/pink colored), Splenomegaly, Serositis
T = Tender lymphadenopathy

67
Q
A

Boutnierre is a manifestation of RA

68
Q

What are common side affects of methotrexate?

A

Bone marrow suppresion (leucvorin for saving), pulmonary fibrosis, and hepatoxcity.

69
Q

What are common complications of Sjorens?

A

Dental caries , dysphagia, and the formation of MALT lymphomas

70
Q

What are the treatments for Sjoren’s?

A

Artifical tears, saliva. Cholinergic agents like pilocarpine and cevlimine

71
Q

What is the workup for SLE?

A

If patient has any of the features of “SOAP BRAIN MD,” NSIDx is serum ANA (which is the screening test). If ANA is positive, NSIDx is anti-Smith and anti-dsDNA antibodies (these antibodies are specific to SLE, but not sensitive).

72
Q

____ drugs are absolutely contraindicated in patients that have active SLE?

A

OCP’s

73
Q

______ and _____ should be screening in pregnant patient because antibodies can cross the placenta and cause neo-natal lupus and congenital heart block.

A

SLE (ANA) and Anti-Ro

74
Q

Patients with a history of phospholipid syndrome should receive what medications surging pregnancy?

A

Heparin and low dose Aspirin

75
Q

What are complication of systemic sclerosis or scleroderma?

A

CREST: calcinosis, Raynaud/Renal, Esophageal dysmotility, scleordactly, and teleangectasia
Interstitial lung disease which leads to pulmonary HTN (cor pulmonale) this is the most common cause of death in this disease, restrictive cardiomyopathy, and hypertensive emergency

76
Q

What is the diagnostic work up for Dermatomyositis?

A

Creatnine kinase levels, then anti- Jo serology, electromyography, and then muscle biopsy

77
Q

Myasthenia gravis: ______

Dermatomyositis: _________

Lambert-Eaton:__________

A

MG: thymoma
Dermato/poly: Malignancy
LAMBE: small cell

78
Q
A

Charcot’s foot presents with reduced angle of the arch, osteopenia, osseous fragmentation, new bone formation, and subluxation or dislocation

79
Q

In Paget’s disease is the osteolytic or osteoblastic phase more predominate?

A

Osteoclastic

80
Q

What is pes ansurine bursitis?

A

This is inflammation of the bursa locate antero-medially on the tibial surface. Risks for inflammation are increased with overuse

81
Q

What are common causes of pseudogout?

A

hyperparathyroidism, hemochromatosis, hemosiderosis, hypothyroidism and wilsons disease

82
Q

What are common risk factors for osteoporosis?

A

age 65>, smoking, first degree relatives with fractures, RA, chronic steroid use, colle’s fracture, and vertebral compression fracture.

83
Q

What are the risk factors for avascular necrosis?

A

CHAOS; chronic steroid therapy, HIV, alcoholism, organ transplantation, sickle cell disease and SLE

84
Q

What is the pathophysiology of Paget’s disease?

A

Well-defined punched-out erosion with a thin rim of calcification

85
Q

What is the clinical presentation of Paget’s disease?

A

Symptomatic presentation is usually due to bony deformities causing nerve impingement (e.g., hearing loss, radiculopathic symptoms), morphological changes (increased hat size) or due to pathological fractures.

86
Q

What is a life threatening complication of Paget’s disease?

A

high output cardiac failure due to venous malformation and osteosarcoma

87
Q

E.G MODE is a pneumonic to help remember where cancers localize in the bone.

A

Epiphysis; Giant cell, Metaphysis osteosarcoma, and Diaphysis is Ewing

88
Q

Tenderness in the lateral elbow with Hx of repetitive wrist extension movements?

A

lateral epicondylitis

89
Q

Tenderness in medial elbow with history of frequent wrist extension

A

medial epicondyltits

90
Q

Duptyrens

A

Tight waxy skin in the palmar area with nodularities.
Extension of fingers is limited due to subcutaneous fibrosis and contracture of palmar fascia. Fourth and fifth fingers are most commonly involved. Risk factors include HIV,diabetes, and alcoholism

91
Q

Stenosing flexor tenosynovitis

A

Hand is routinely in a flexed position which results in difficulty extending.

92
Q

Tenderness in anatomic snuff box area. Passive flexion of thumb may exacerbate pain

A

Dequarvein tenosynovitis

93
Q

Superficial cystic nodules that can be tender. MC location is the extensor surface of wrist and hand joints.

A

Ganglion cyst

94
Q

Intermittent or persistent neuropathic pain, sweating, and redness of involved extremity. Livedo reticularis (vague purplish net-like rash) can be seen in affected extremities. In chronic cases, X-ray can reveal osteopenia of bones in the involved area.

A

Complex Regional Pain Syndrome (aka Reflex Sympathetic Dystrophy)

95
Q

What is the first step in work up for giant cell arteritis?

A

First obtain CRP and ESR levels.
ESR should be greater than 40

96
Q

What is the most common complication of Giant cell arteritis?

A

Aneurysm

97
Q

Asthma, Rhino-sinusitis, Eosinophilia is specific to what vasculidity?

A

Churgg strauss

97
Q

Percussion over the posterior tibial nerve elicits pain, parathesia, foot numbness.

A

Tarsal tunnel syndrome

98
Q

_____ vasculitis cause ANCA-positive necrotizing vasculitis, predominantly affecting vessels in lung (modular cavities), kidney, and ear-nose-throat.

A

Granulomatous with polyangitis

99
Q

Pain that is reproduced with medial-lateral squeezing of the calcaneus

A

Calcaneal stress fracture

100
Q

Swelling and tenderness on palpation of 2-6 cm proximal to tendon insertion.

A

Achilles tendinopathy

101
Q
A

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