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csv1 Flashcards

1
Q

1. In whom does RA most often present?

A

Women >50.

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2
Q
  1. Presentation of RA?
A

a. Joint pain and morning stiffness that is symmetrical and in multiple joints of the hands lasting for more than 1 hour in the morning with the symptomatic episode going on for at least 6 weeks. b. There is often a prodrome of malaise and weight loss, but this is not enough to make a clear diagnosis.

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3
Q
  1. Definition of RA?
A

Defined as having 4 or more of the following present for diagnosis: a. Morning stiffness lasting more than 1 hour b. Wrist and finger involvement (MCP, PIP) c. Swelling of at least 3 joints d. Symmetric involvement e. Rheumatoid nodules (not necessary to diagnose RA) f. X–ray abnormalities showing erosions (not necessary to diagnose RA) g. Positive rheumatoid factor or anti–CCP h. C–reactive protein (CRP) or ESR.

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4
Q
  1. Diagnostic testing for RA?
A

a. RA is diagnosed w/a constellation of physical findings, joint problems, and lab tests. b. There is no single diagnostic criteria to confirm the diagnosis. c. There is no single therapy to control and treat the disease.

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5
Q
  1. A 34 yo woman presents w/pains in both hands for the last few months and stiffness that improves as the day goes on. Multiple joints are swollen on exam. Xrays of the hands show some erosion. What is the single most accurate test? a. Rheumatoid factor b. Anti–cyclic citrullinated peptide (anti–ccp) c. Sed rate d. ANA e. Joint fluid aspiration
A
  1. Answer: B–Anti–CCP! 2. Rheumatoid factor (RF) is present in only 75–85% of pts w/RA. 3. It can also be present in a number of other diseases; hence the RF is rather nonspecific. 4. Anti–CCP is the single most accurate test for RA. It is >95% specific for RA, and it appears earlier in the course of the disease than RF. 5. There is nothing specific on joint aspiration to determine the diagnosis of RA.
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6
Q
  1. Other systems affected by RA?
A

a. Cardiac b. Lung c. Blood d. Nervous e. Skin

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7
Q
  1. Cardiac findings in RA?
A

a. Pericarditis b. Valvular disease

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8
Q
  1. Lung findings in RA?
A

Pleural effusion w/a very low glucose level, lung nodules.

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9
Q
  1. Blood findings in RA?
A

Anemia w/normal MCV

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10
Q
  1. Nerve findings in RA?
A

Mononeuritis multiplex.

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11
Q
  1. Skin findings in RA?
A

Nodules

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12
Q
  1. Joint findings in RA?
A

a. MCP swelling and pain b. Boutonniere deformity–Flexion of the PIP w/hyperextension of the DIP. c. Swan neck deformity–Extension of the PIP w/flexion of the DIP d. Baker’s cyst (outpocketing of synovium at the back of the knee) e. C1/C2 cervical spine subluxation f. Knee–Although the knee is commonly involved, multiple small joints are involved more commonly over time.

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13
Q
  1. Felty’s syndrome Triad?
A

a. RA b. Splenomegaly c. Neutropenia

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14
Q
  1. New alternate diagnostic criteria for RA?
A

a. Synovitis (a single joint is enough to diagnose RA) b. RF or anti–CCP c. ESR or CRP d. Prolonged duration (beyond 6 weeks)

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15
Q
  1. What type of anemia is very characteristic of RA?
A

Normocytic normochromic.

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16
Q
  1. CCS Tip: In addition to X–rays, RF, and CCP, what else should you order for RA?
A

a. CBC b. ESR c. CRP e. If the case describes a swollen joint w/an effusion, aspiration of the joint should also be done to establish the initial diagnosis.

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17
Q
  1. Which of the following will have the lowest glucose level on pleural effusion? a. CHF b. Pulmonary embolism c. Pneumonia d. Cancer e. RA f. Tuberculosis
A

Answer: E– RA has the lowest glucose levels of all the causes of pleural effusion described here.

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18
Q
  1. Which joint in spared in RA?!?
A

Sacroiliac. DIPs.

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19
Q
  1. Tx of RA?
A

a. NSAIDS combined w/a disease–modifying antirheumatic drug (DMAR) is the standard of care in patients w/RA. b. There is no therapeutic difference among NSAIDs, and you may use ibuprofen for any of the rheumatological diseases described. There is no point in waiting to use a DMARD in a patient w/severe RA or anyone w/joint erosions. c. NSAIDs will not delay the progression of disease.

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20
Q
  1. What is the best initial DMARD (and most widely used)?
A

Methotrexate. Add others if it is not effective.

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21
Q
  1. AE of Methotrexate?
A

Bone marrow suppression and pneumonitis.

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22
Q
  1. 3 DMARDs that are biological agents?
A

a. Infliximab b. Adalimumab c. Etanercept

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23
Q
  1. MOA of the Biological DMARDs (Infliximab, Adalimumab, and Etanercept)?
A

a. Block TNF (all of them do) b. Methotrexate and these agents can be used in combination. c. Anti–TNF agents are added if methotrexate fails.

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24
Q
  1. Role of Hydroxychloroquine in tx of RA?
A

Use with Mild disease!

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25
Q
  1. What will the patient on Hydroxychloroquine need (hint, to watch for an AE)?
A

a. Regular eye exams to check for retinopathy. b. Anti–TNF agents are added if methotrexate fails.

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26
Q
  1. AE of Sulfasalazine in RA?
A

a. Same drug that was used in the past for ulcerative colitis. b. It can suppress bone marrow.

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27
Q
  1. Other DMARDs for RA?
A

a. Rituximab b. Anakinra c. Toclizumab d. Leflunomide e. Abatacept f. Gold salts

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28
Q
  1. MOA of Rituximab?
A

Anti–CD–20 antibody.

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29
Q
  1. MOA of Anakinra?
A

IL–1 receptor antagonist

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30
Q
  1. MOA of Tocilizumab?
A

a. IL–6 receptor antagonist. b. Added to methotrexate, if it is ineffective.

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31
Q
  1. Leflunomide MOA?
A

Pyrimidine antagonist that is similar in effect to methotrexate, w/less toxicity.

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32
Q
  1. MOA of Abatacept?
A

Inhibits T–cell activation

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33
Q
  1. MOA of Gold Salts?
A

Rarely used because of toxicity, such as nephrotic syndrome.

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34
Q
  1. Why are DMARDs started early?
A

a. To prevent X–ray abnormalities. b. Eliminating an abnormal x–ray as a criterion for dx allows earlier tx w/DMARDs.

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35
Q
  1. Role of steroids for RA?
A

a. Glucocorticoids, such as prednisone, are not disease modifying. b. However, steroids do enable quick control of the disease and allow time for the other DMARDs to take effect. c. Steroids are a bridge to DMARD therapy!!! d. They are the answer for an acutely ill patient w/severe inflammation. e. Long–term glucocorticoid use should be avoided if at all possible.

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36
Q
  1. 4 diseases including under Seronegative Spondyloarthropathies?
A

a. Ankylosing Spondylitis b. Reactive arthritis (Reiter’s) c. Psoriatic arthritis d. Juvenile rheumatoid arthritis (adult–onset Still’s disease)

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37
Q
  1. What characteristics do all of the seronegative spondyloarthropathies have in common?
A

a. Negative test for rheumatoid factor!!! b. Predilection for Spine! c. Sacroiliac joint involvement d. Association w/HLA–B27.

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38
Q
  1. Presentation of Ankylosing Spondylitis (AS)?
A

a. AS presents in a young (<40) male patient w/spine or back stiffness. b. Peripheral joint involvement is less common. c. The pain is WORSE AT NIGHT and is relieved by leaning forward. d. This can lead to Kyphosis and diminished chest expansion.

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39
Q
  1. 3 Rare findings w/ankylosing spondylitis?
A

a. Uveitis (30%) b. Aortitis (3%) c. Restrictive lung disease (2–15%)

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40
Q
  1. A 27 year–old man presents w/months of back pain that is worse at night. He has diminished expansion of this chest on inhalation and flattening of the normal lumbar curvature. What is the most accurate tests? a. X–ray b. MRI c. HLA–B27 d. ESR e. Rheumatoid factor
A
  1. Answer: B–MRI of the SI joint is more sensitive that an x–ray, detecting edematous, inflammatory changes years before an x–ray in AS. 2. HLA–B27 can be present in 8% of the general population and is not necessary to confirm a diagnosis of AS. 3. In CCS case, all of these tests should be performed, w/the x–ray done first and then going on to the MRI if the x–ray is negative.
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41
Q
  1. What is the most common WRONG answer for AS?
A

a. Steroids! b. They do not work.

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42
Q
  1. Tx of AS?
A

a. NSAIDs b. Biological agents, such as infliximab or adalimumab c. Sulfasalazine d. DO NOT USE STEROIDS

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43
Q
  1. Presentation of Reactive Arthritis (formerly Reiter’s)?
A

a. Asymmetric arthritis w/a history of urethritis or gastrointestinal infection. b. There may be constitutional symptoms, such as fever, fatigue, or weight loss. c. Arthritis: May be monoarticular, oligoarticular, or more diffuse. d. Genital lesions: Circinate balanitis (around head of penis); urethritis or cervicitis in women. e. Conjunctivitis f. Keratoderma blennorrhagicum: A skin lesion characteristic of reactive arthritis.

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44
Q
  1. Diagnostic testing for reactive arthritis?
A

a. There is NO specific test. b. Look for the triad of: 1. Knee (joint) 2. Pee (urinary) 3. See (eye) Can’t see, pee, or clime a tree. c. Look for history of chlamydia, Shigella, salmonella, Yersinia, or campylobacter.

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45
Q
  1. Treatment of reactive arthritis?
A

NSAIDs

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46
Q
  1. Presentation of psoriatic arthritis?
A

a. Joint involvement w/a history of psoriasis. b. Rheumatoid factor is absent. c. The Sacroiliac spine is involved!, as it is in all seronegative spondyloarthropathies.

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47
Q
  1. Key features of psoriatic arthritis?
A

a. Nail pitting b. Distal interphalangeal (DIP) involvement (Remember RA involves the proximal joint) c. “Sausage–shaped” digits (dactylitis) d. Enthesitis: Inflammation of the tendinous insertion sites.

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48
Q
  1. What is the most common wrong answer for ankylosing spondylitis treatment?
A

Steroids. They do not work.

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49
Q
  1. Diagnostic testing for psoriatic arthritis?
A

No single test is specific for psoriatic arthritis.

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50
Q
  1. Treatment of psoriatic arthritis: best initial therapy?
A

NSAIDs

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51
Q
  1. Treatment of resistance psoriatic arthritis?
A

a. Methotrexate is used for resistant disease. b. Infliximab and other anti–TNF agents are effective.

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52
Q
  1. Note: No single test is specific for psoriatic arthritis.
A

Note: No single test is specific for psoriatic arthritis.

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53
Q

54.Presentation of Juvenile RA, or adult–onset Still’s disease?

A

a. Fever b. Salmon–coloured rash c. Polyarthritis d. Lymphadenopathy e. Myalgias. f. This can be a very difficult diagnosis to recognize.

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54
Q
  1. Additional minor criteria for JRA?
A

a. Hepatosplenomegaly b. Elevated transaminases.

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55
Q
  1. Diagnostic testing for Presentation of Juvenile RA, or adult–onset Still’s disease? 56.a.1.
A

a. Very high ferritin level b. Elevated WBC count c. Negative Rheumatoid factor and negative ANA are ESSENTIAL to establishing the diagnosis. There is no specific diagnostic test. JRA is characterized by the above.

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56
Q
  1. Treatment of JRA?
A

a. NSAIDs b. Unresponsive cases can be treated w/steroids. c. Those w/persistent symptoms need methotrexate or anti–TNF meds to get off steroids.

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57
Q
  1. Whipple disease presentation?
A

a. Diarrhea b. Fat malabsorption c. Weight loss

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58
Q
  1. what is the most common presentation of Whipple disease?
A

Joint pain.

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59
Q
  1. What is the most specific tests for Whipple disease?
A

Biopsy of the bowel showing PAS positive organisms.

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60
Q
  1. Treatment of Whipple disease?
A

TMP/SMX is curative

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61
Q
  1. What do you expect to see with biopsy of the bowel in Whipple disease?
A

PAS–positive organisms.

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62
Q
  1. With what two factors is osteoarthritis associated?
A

a. Aging b. increased use of the joint

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63
Q
  1. presentation of osteoarthritis?
A

a. Morning stiffness <30 Minutes in duratino. b. Crepitus on moving the joint

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64
Q
  1. which hand join is affected by osteoarthritis, as opposed to rheumatoid arthritis?
A

DIP joints (RA does not affect the DIP joints).

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65
Q
  1. Heberden’s node?
A

DIP osteophytes

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66
Q
  1. Bouchard’s nodes?
A

PIP osteophytes

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67
Q
  1. diagnostic testing for osteoarthritis: what is the best initial test?
A

X–ray of the joint

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68
Q
  1. for CCS, all of the following should be ordered for OA (there is no specific diagnostic test)?
A
  1. ANA 2. ESR 3. rheumatoid factor 4. anti–– CCP All other inflammatory markers will be normal. Joint fluid will have a low leukocyte count <2000 mm³.
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69
Q
  1. Treatment of osteoarthritis?
A

a. Acetaminophen b. weight loss and exercise help c. note: chondroitin sulfate is not clearly useful to slow joint deterioration

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70
Q
  1. note: glucosamine is a wrong answer. Glucosamine equals placebo.
A

note: glucosamine is a wrong answer. Glucosamine equals placebo.

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71
Q
  1. Morning stiffness and osteoarthritis vs. rheumatoid arthritis?
A

a. Osteoarthritis one hour

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72
Q
  1. DIP involvement in osteoarthritis vs. rheumatoid arthritis?
A

a. OA Yes b. RA NO

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73
Q
  1. PIP involvement in osteoarthritis vs. rheumatoid arthritis?
A

a. OA YES b. RA YES

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74
Q
  1. MCP involvement in osteoarthritis vs. rheumatoid arthritis?
A

a. OA No b. RA Yes

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75
Q
  1. RF, anti–CCP in osteoarthritis vs. rheumatoid arthritis?
A

a. OA No b. RA Yes

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76
Q
  1. joint fluid leukocyte count in osteoarthritis vs. rheumatoid arthritis?
A

a. OA <2,000 b. RA 5000 to 50,000

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77
Q
  1. how many criteria exist for lupus and how many are needed to confirm the diagnosis?
A

a. 11 criteria b. four are needed to confirm the diagnosis

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78
Q
  1. note: Rash + joint pain + fatigue= lupus.
A

note: Rash + joint pain + fatigue= lupus.

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79
Q
  1. Skin features of lupus?
A

a. Mallar rash b. photosensitivity rash c. oral ulcers rash d. discoid rash

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80
Q
  1. incidence of arthralgias in Lupus?
A

Present in 90% of patients

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81
Q
  1. blood findings with Lupus?
A

a. Leukopenia b. thrombocytopenia c. hemolysis Aany blood involvement counts as one criterion

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82
Q
  1. renal features of lupus?
A

Varies from benign proteinuria to end stage renal disease.

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83
Q
  1. Cerebral features of lupus (3)?
A

a. Behavioral change b. stroke c. seizure d. meningitis

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84
Q
  1. Serositis features of SLE?
A

a. Pericarditis b. pleuritic chest pain c. pulmonary hypertension d. pneumonia e. myocarditis

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85
Q
  1. in what percent of lupus patients is ANA positive?
A

95% sensitive

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86
Q
  1. in what percentage of lupus patients is double–stranded (DS–DNA) DNA positive?
A

60% sensitive

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87
Q
  1. note: each of the serologic abnormalities, counts as one criterion. Hence, if the person has joint pain, a rash, and both ANA and dsDNA, that patient would have four criteria.
A

Note: each of the serologic abnormalities, counts as one criterion. Hence, if the person has joint pain, a rash, and both ANA and dsDNA, that patient would have four criteria.

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88
Q
  1. Best initial diagnostic test for SLE?
A

ANA

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89
Q
  1. most specific test for SLE?
A

Anti–DS DNA or anti–SM (smith)

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90
Q
  1. for CCS, what test should be performed on all patients suspected of having lupus?
A

a. Complement levels b. anti–– SM c. anti–– DS DNA

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91
Q
  1. what is the best test for the severity of a lupus flare?
A

a. Complement levels (drop in a flare–up) b. and c. anti–DS DNA (Rise in a flare–up)

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92
Q
  1. as part of prenatal care, a woman with lupus is found to have a negative test for anti–cardiolipin antibodies, but she is positive for anti–Ro (SSA) antibody. What is the baby at risk for?
A

a. Heart block. b. The presence of anti–Ro or anti–SSA antibodies is a risk for the development of heart block.

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93
Q
  1. Other findings in lupus that are not part of specific diagnostic criteria?
A

a. Fatigue b. hair loss c. antiphospholipid syndrome d. elevated sedimentation rate

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94
Q
  1. Most common type of anemia with SLE?
A

Anemia of chronic disease (more common than hemolysis).

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95
Q
  1. Treatment of acute SLE flare–ups?
A

Prednisone and other glucocorticoids.

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96
Q
  1. For treatment of joint pain from SLE?
A

NSAIDS.

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97
Q
  1. Treatment of rash and joint pain, not responding to NSAIDs in SLE?
A

a. Hydroxychloroquine b. Antimalarials.

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98
Q
  1. Treatment of severe disease relapse upon cessation of steroids in SLE?
A
  1. Belimumab 2. Azathioprine 3. Cyclophosphamide
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99
Q
  1. Treatment of nephritis in SLE?
A
  1. Steroids 2. Mycophenolate mofetil (Mycophenolate is superior to cyclophosphamide).
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100
Q
  1. MOA of Belimumab?
A

It inhibits B cells as treatment of SLE.

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101
Q
  1. What are the three most common causes of drug–induced lupus?
A
  1. Hydralazine 2. Procainamide 3. Isoniazid
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102
Q
  1. What do you always see on labs with drug–induced lupus (very important)?
A

a. Anti–histone antibodies or b. positive ANA

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103
Q
  1. What is never seen with drug–induced lupus?
A

Renal or CNS involvement

104
Q
  1. Complement level and anti–DS DNA with drug–induced lupus?
A

Normal.

105
Q
  1. Presentation of Sjogren’s syndrome?
A

a. Look for: 1. Woman (9:1 female predominance) 2. dry eyes 3. dry mouth 4. sensation of sand under the eyelid b. There is often a loss of taste and smell from profound mouth dryness (You need saliva to wet food so you can taste it). c. Look for loss of teeth at an early age!!! because the saliva is critical to preventing dental cavities

106
Q
  1. most accurate test for Sjogren’s syndrome?
A

Lip biopsy

107
Q
  1. Schirmer test?
A

Decreased wetting of paper held to the eye shows decreased lack lacrimation.

108
Q
  1. Sensitivity and specificity of ANA with Sjogren’s syndrome?
A

ANA: 95%sensitive, but least specific.

109
Q
  1. Sensitivity of RF with Sjogren’s syndrome?
A

70% sensitive

110
Q
  1. Sensitivity and specificity of Anti–Ro/SSA with Sjogren’s syndrome?
A

50–65 percent sensitive but fairly specific

111
Q
  1. Sensitivity and specificity of Anti–La/SSB?
A

30–65% sensitive but fairly specific.

112
Q
  1. CCS tip: when you see anti–Ro (SSA) or anti–la (SSB), think?
A

Sjogren’s syndrome. They are present in a small number of people with lupus, and can help diagnose ANA negative lupus.

113
Q
  1. Treatment of Sjogren’s syndrome?
A

a. Keep the eyes and mouth moist b. Pilocarpine and Cevimeline.

114
Q
  1. MOA of Pilocarpine and Cevimeline?
A

Increase acetylcholine, which increases oral and ocular secretions.

115
Q
  1. Tight skin + heartburn + Raynaud’s= think?
A

Scleroderma.

116
Q
  1. Presentation of scleroderma (systemic sclerosis) [presents with three main symptoms]?
A
  1. Skin: look for a woman with tight, fibrous thickening of the skin that gives a tight face and tight, immobile fingers. 2. Raynaud’s phenomenon 3. Joint Pain.
117
Q
  1. What are tight, immobile fingers known as?
A

Sclerodactyly

118
Q
  1. Raynaud’s phenomenon?
A

a. This is a three–phase vascular hyperreactivity, with the skin of the fingers becoming white, then blue, then red. b. It can be quite painful c. Digital Ulceration may occur from infarction of the skin! d. There might also be abnormal giant capillaries in the nail folds!

119
Q
  1. Characteristics of joint pain with scleroderma (2)?
A

Mild and symmetrical.

120
Q
  1. 4 other organs affected by diffuse scleroderma?
A
  1. Lungs 2. G.I. 3. Heart 4. Renal
121
Q
  1. lung complications Of Diffuse Scleroderma?
A

Fibrosis and pulmonary hypertension (These are the leading cause of death)

122
Q
  1. G.I. Complications of diffuse scleroderma?
A
  1. Wide–mouthed clonic diverticula 2. Esophageal Dysmotility, this leads to reflux and Barrett’s esophagus 3. there is primary biliary or cirrhosis in 15% of patients!
123
Q
  1. Heart complications of scleroderma?
A

Restrictive cardiomyopathy

124
Q
  1. renal complications of scleroderma?
A

May lead to malignant hypertension

125
Q
  1. Diagnostic testing for scleroderma?
A

a. There is no single diagnostic test. b. ANA is present in 95% of cases, but is nonspecific. c. Anti–topoisomerase (anti–Scl 70) is only present in 30% of patients.

126
Q
  1. Treatment of systemic scleroderma?
A

a. No treatment has been proven effective in stopping scleroderma. b. Penicillamine is not effective in delaying progression of this disease. c. One can use the following therapies for treatment of each individual organ system

127
Q
  1. important: how is interstitial lung disease in scleroderma treated?
A

Cyclophosphamide.

128
Q
  1. treatment of renal involvement and hypertension in scleroderma?
A

Use ace inhibitors

129
Q
  1. Treatment of Pulmonary Hypertension in scleroderma (3 classes of agents)?
A
  1. Bosentan (endothelin antagonist) 2. Prostacyclin Analogs (epoprostenol, treprostinil, iloprost) 3. Sildenafil
130
Q
  1. treatment of Raynaud’s , with scleroderma?
A

Use calcium channel blockers.

131
Q
  1. Treatment of GERD in scleroderma?
A

Regular use of PPIs.

132
Q
  1. Treatment of lung fibrosis in scleroderma?
A

Cyclophosphamide.

133
Q
  1. What is crest syndrome composed of (limited scleroderma)?
A
  1. Calcinosis of the fingers 2. Raynaud’s 3. esophageal dysmotility 4. Sclerodactyly 5. Telangiectasia
134
Q
  1. What does CREST Syndrome NOT present with?
A
  1. Joint pain 2. heart involvement 3. lung involvement (except for pulmonary hypertension) 4. kidney involvement
135
Q
  1. Note: CREST DOES present with primary hypertension.
A

Note: CREST DOES present with primary hypertension.

136
Q
  1. Diagnostic testing for CREST Syndrome?
A

a. Anti–centromere antibodies!!! CREST is characterized by anticentromere antibodies. b. Crest syndrome does not involve anti–SCl70

137
Q
  1. presentation of eosinophilic fasciitis?
A

a. Thickened skin that looks like scleroderma. b. However, the following are not present: 1. hand involvement 2. Raynaud’s 3. heart, lung or kidney involvement c. there is marked eosinophilia, and the appearance of an “orange peel” (peau d’orange)

138
Q
  1. treatment of use and affiliate fasciitis?
A

Corticosteroids

139
Q
  1. what to look for with polymyositis and dermatomyositis?
A

a. In both conditions, the patient cannot get up from a seated position without using the arms. b. There can also be muscle pain and tenderness

140
Q
  1. what to look for with polymyositis?
A

a. Proximal muscle weakness b. signs of muscle inflammation on blood tests, electromyography, and biopsy

141
Q
  1. what to look for with dermatomyositis?
A

a. Polymyositis. Plus various rashes. b. Gottron’s papules: over metacarpophalangeal joint surfaces c. heliotrope rash: Periorbital and purplish lesion around the eyes d. shawl sign: shoulder and neck erythema

142
Q
  1. Diagnostic testing for Polymyositis and Dermatomyositis?
A

a. Elevated CPK b. Elevated Aldolase c. Abnormal EMG d. For CCS, order all the liver functino tests as well as ANA.

143
Q
  1. Weakness + Increased CPK + Increased aldolase + Biopsy =?
A

Polymyositis

144
Q
  1. Weakness + Increased CPK + Increased Aldolase + Biopsy + Skin Rash =?
A

Dermatomyositis

145
Q
  1. A 50–year–old patient presents with muscle weakness of the girdle with an increased CPK and aldolase. Her anti–Jo–1 antibody is positive. Which of the following is most likely to happen to her? a. Stroke. b. Myocardial infarction. c. Septic arthritis. d. DVT. e. Interstitial lung disease.
A

Answer: E–PM/DM presents with weakness and increase markers of muscle inflammation. The presence of anti–Jo–e indicates a markedly increased risk of interstitial lung disease.

146
Q
  1. What is the most common serious complication of PM/DM? a. Rhabdomyolysis. b. Hyperkalemia. c. Metabolic acidosis. d. Malignancy
A

Answer: D–. For unclear reasons, the most common serious threat to life from PM/DM is malignancy. DM has a greater risk than PM.

147
Q
  1. Fibromyalgia presentation?
A

a. Look for a woman (10x more common in females) with muscle aches and stiffness with trigger points on palpation and non–refreshing sleep. b. Depression and anxiety are common.

148
Q
  1. Diagnostic testing for Fibromyalgia?
A

a. All blood tests are normal. b. There is no objective evidence of disease. c. This is a pain syndrome w/tender trigger points.

149
Q
  1. What is the single most accurate test for PM/DM?
A

Biopsy!

150
Q
  1. Treatment of fibromyalgia (treat symptoms with the following)?
A

a. Exercise b. Milnacipran, duloxetine, or pregabalin (the best initial therapy) c. TCA, such as amitriptyline, are effective but have more adverse effects.

151
Q
  1. Are NSAIDs, the first–line treatment for fibromyalgia?
A

Nooo

152
Q
  1. How does polymyalgia rheumatica differ from polymyositis?
A

Pain is much more prominent than weakness in PMR (polymyalgia rheumatica)

153
Q
  1. presentation of polymyalgia rheumatica (PMR)?
A

a. Presents with a person >50 years old with profound pain and stiffness of the proximal muscles! (Such as shoulders and pelvic girdle) b. the stiffness is worse in the morning and is localized to the muscles rather than to the joints c. ESR is elevated d. there is an amazing response to steroids

154
Q
  1. Age >50 + proximal muscle pain + Increased ESR = PMR.
A

Age >50 + proximal muscle pain + Increased ESR = PMR.

155
Q
  1. Nonspecific features of polymyalgia rheumatica?
A

a. Fever, weight loss, and malaise b. Normocytic anemia him him c. NORMAL CPK, EMG, ALDOLASE, and Muscle Biopsy. d. No muscle atrophy.

156
Q
  1. Fatigue/Malaise with: a. Chronic Fatigue Syndrome b. Fibromyalgia c. Polymyalgia
A
  1. chronic fatigue syndrome: +++++ > 6 months 2. fibromyalgia: ++ 3. polymyalgia rheumatica ++
157
Q
  1. non–refreshing sleep with: a. Chronic Fatigue Syndrome b. Fibromyalgia c. Polymyalgia
A
  1. chronic fatigue syndrome: ++++++ 2. fibromyalgia:++ 3. polymyalgia rheumatica No
158
Q
  1. trigger points with: a. Chronic Fatigue Syndrome b. Fibromyalgia c. Polymyalgia
A
  1. chronic fatigue syndrome: No 2. fibromyalgia: yes 3. polymyalgia rheumatica: no
159
Q
  1. blood tests with: a. Chronic Fatigue Syndrome b. Fibromyalgia c. Polymyalgia
A
  1. chronic fatigue syndrome: all normal 2. fibromyalgia:all normal 3. polymyalgia rheumatica: increased ESR
160
Q
  1. Treatment of: a. Chronic Fatigue Syndrome b. Fibromyalgia c. Polymyalgia
A
  1. chronic fatigue syndrome: none 2. fibromyalgia: pain relief 3. polymyalgia rheumatica: prednisone
161
Q
  1. what features are common to all forms of vasculitis?
A

a. Fatigue, malaise, weight loss. b. Fever: may present as a fever of unknown origin (FUO). c. Skin lesions: palpable purpura, rash d. joint pain. e. Neuropathy: mononeuritis multiplex

162
Q
  1. common laboratory features of vasculitis?
A

a. Normocytic anemia b. Elevated ESR c. Thrombocytosis (Increased)

163
Q
  1. what is the most accurate test for vasculitis?
A

Biopsy

164
Q
  1. best initial therapy for vasculitis?
A

Prednisone and glucocorticoids

165
Q
  1. what should be used for vasculitis, if steroids are not effective? (4)
A
  1. Cyclophosphamide. 2. Azathioprine/6–mercaptopurine. 3. Methotrexate
166
Q
  1. presentation of polyarteritis nodosa (PAN)?
A

PAN has all of the features of vasculitis described above plus the following.

167
Q
  1. Features of Polyarteritis Nodosa, that allow you to establish the diagnosis as compared to other vasculitides?
A
  1. Abdominal pain (65%) 2. renal involvement (65%) 3. testicular involvement (35%) 4. pericarditis (35%) 5. hypertension (50%)
168
Q
  1. Which organ is not affected by polyarteritis nodosa?
A

Lungs!

169
Q
  1. Diagnostic testing for polyarteritis nodosa: best initial test?
A

Angiography of abdominal vessels

170
Q
  1. most accurate test for PAN?
A

Biopsy (of the skin, muscle, or sural nerve)

171
Q
  1. CCS Tip: there is no good blood test for pan.
A

CCS Tip: there is no good blood test for pan.

172
Q
  1. Treatment of PAN? (2 drugs)
A

Prednisone and cyclophosphamide

173
Q
  1. what surface antigen is found in 30% of patients with PAN?
A

Hepatitis B surface antigen

174
Q
  1. how can Wegener’s granulomatosis be distinguished?
A

a. This disorder,like PAN, can affect the majority the body. b. However, look for upper and lower respiratory findings!! and c. C–Anca!!!

175
Q
  1. Most accurate test for Wagner’s granulomatosis?
A

Biopsy.

176
Q
  1. What is the treatment of Wagner’s granulomatosis?
A

Steroids and cyclophosphamide

177
Q
  1. Upper + lower respiratory findings + c–ANCA =?
A

Wegener’s.

178
Q
  1. Presentation of Churg–Strauss? (3 features to look for)
A
  1. Vasculitis. 2. Eosinophilia. 3. Asthma b. Although Churg–Strausscan affect any organ in the body, the key is to recognize the above. c. Although the P–anca and anti–myeloperoxidase can be positive, too, these findings are not as uniquely suggestive of the presence of eosinophelia and asthma.
179
Q
  1. Most accurate diagnostic test for Churg–Strauss?
A

biopsy

180
Q
  1. Treatment of Churg–Strauss?
A

Excellent response to steroids

181
Q
  1. Temporal Arteritis?
A

a. A type of giant cell arteritis b. is related to polymyalgia rheumatica

182
Q
  1. presentation of temporal arteritis?
A

a. Fever b. weight loss c. malaise d. fatigue e. all of the above can be present,as they are in all forms of vasculitis

183
Q
  1. most accurate test for temporal arteritis?
A

Biopsy

184
Q
  1. The patient presents with headache, Jock claudication, and visual disturbance, and tenderness of the scalp. The ESR is elevated. What is the next best step in management?
A

Treatment with steroids is more important than getting a specific diagnostic test in temporal arteritis

185
Q
  1. young Asian female + diminished pulse = think?
A

Takayasu’s Arteritis

186
Q
  1. presentation of Takayasu’s Arteritis?
A

a. Young Asian female b. diminished pulses c. half of all patients with Takayasu’s Arteritis have the usual vasculitis findings present before the loss or decrease of pulse.! d. Fatigue, malaise, weight loss, arthralgia. e. Anemia, increased ESR

187
Q
  1. What are the special features of Takayasu’s Arteritis?
A

a. TIA and Stroke from vascular occlusion. b. Takayasu’s is also distinctive in that it is diagnosed with Aortic Arteriography or MRA.

188
Q
  1. Treatment of Takayasu’s Arteritis?
A

Steroids, like all vasculitis.

189
Q
  1. Diagnosis of Takayasu’s Arteritis?
A

a. Aortic Arteriography or MRA. b. The most accurate test for Takayasu’s is NOT a biopsy.

190
Q
  1. Two unique features of Cryoglobulinemia?
A

a. Association with: 1. Hepatitis C 2. Renal involvement. b. It also has the usual features of vasculitis, such as fatigue, malaise, skin lesions, and joint pain.

191
Q
  1. Treatment of Cryoglobulinemia?
A

Treat the hepatitis C with interferon and ribavirin. (Note: step three loves this question)

192
Q
  1. presentation of Behcet disease?
A

a. Present in patients of Middle Eastern or Asian ancestry. b. Look for: 1. oral and genital ulcers. 2. Ocular involvement (uveitis, optic neuritis): can lead to blindness! 3. Skin lesions: “Pathergy,” which is hyperreactivity to needle sticks, resulting in sterile skin abscesses

193
Q
  1. diagnosis of Behcet disease?
A

There is no specific test. Use the features described above.

194
Q
  1. Treatment of Behcet disease?
A

Prednisone and colchicine.

195
Q
  1. How do you diagnose inflamed joints?
A

a. You need to look at the fluid. b. Inflamed joints will generally have effusions. c. Joint aspiration is the most accurate test for gout, pseudogout, and septic arthritis

196
Q
  1. Note: the Gram stain lack sensitivity and, even in bacterial septic arthritis, won’t detect 50 to 60% of infections.
A

Note: the Gram stain lack sensitivity and, even in bacterial septic arthritis, won’t detect 50 to 60% of infections.

197
Q
  1. What is the best initial test for septic arthritis?
A

a. Cell count. b. There is still overlap

198
Q
  1. normal synovial fluid cell count?
A

< 2,000.

199
Q
  1. inflammatory synovial fluid cell count (gout/pseudogout)?
A

2,000 –50,000 WBCs.

200
Q
  1. Synovial fluid cell count with infectious arthritis?
A

>50,000.

201
Q
  1. Presentation of Gout?
A

a. Look for a man with a sudden onset of severe pain in the toe at night. b. The toe will be red, swollen and tender, and it can look very similar to a toe with infection.

202
Q
  1. What can precipitate acute gouty attacks?
A

a. Binge drinking of alcohol. b. Thiazides c. nicotinic acid

203
Q
  1. best initial diagnostic test for Gout?
A

Arthrocentesis ( aspiration of joint fluid)

204
Q
  1. Most accurate test for gout?
A

Polarized light examination of the fluid will show negatively birefringent needles!!!!

205
Q
  1. For CCS, what else should you do when working up Gout?
A

a. Joint fluid examination for cell count, culture, and protein levels. b. Serum uric acid level: however, do not rely on uric acid level to make an accurate diagnosis. c. X–ray of the toe d. extremity examination for tophi

206
Q
  1. what are you looking for with x–ray of the toe in gout?
A

May show “punched out” lesions.

207
Q
  1. Best initial therapy for an acute gouty attack?
A

NSAIDs

208
Q
  1. if there is insufficient response, or a contraindication to NSAIDs when treating gout, use?
A

Steroids to treat acute gouty attacks.

209
Q
  1. In what situations is colchicine useful for gout?
A

a. In the first 24 hours of an attack!!! b. When there is a contraindication to the use of NSAIDs, such as renal insufficiency. c. As part of preventive therapy to decrease the risk of a gouty attack!

210
Q
  1. AE of Colchicine?
A

a. Nausea and diarrhea b. bone marrow suppression.

211
Q
  1. Prevention of gout?
A
  1. Allopurinol 2. Probenecid 3. Silfinpuyrazone b. The above all lower the level of uric acid c. weight loss and avoiding alcohol! d. Febuxostat e. Uricase (rasburicase and pegloticase0
212
Q
  1. AE of Allopurinol? (3)
A
  1. Rash 2. allergic interstitial nephritis 3. hemolysis
213
Q
  1. MOA of Febuxostat?
A

A xanthine oxidase inhibitor that markedly lowers uric acid levels.

214
Q
  1. When is Febuxostat the answer?
A

When the patient is intolerant of allopurinol.

215
Q
  1. MOA of Rasburicase and Pegloticase (Uricase drugs)?
A

Benign drugs that break down uric acid.

216
Q
  1. when to use Rasburicase and Pegloticase (Uricase drugs)?
A

If allopurinol and Febuxostat are not enough.

217
Q
  1. What do Rasburicase and Pegloticase (Uricase drugs) break down uric acid to?
A

a. Allantoin. b. Use when allopurinol and Febuxostat are not enough.

218
Q
  1. Crystal type w/gout?
A

Negative birefringence

219
Q
  1. crystal type with pseudogout?
A

Positive birefringence (PP).

220
Q
  1. Note: of all gout patients. 30% can have at least one normal uric acid level, especially during the attack, because the uric acid is being deposited into the joints from the blood. An elevated uric acid level alone is not an indication for treatment in an asymptomatic patient. You must tap the joint!
A

Note: of all gout patients. 30% can have at least one normal uric acid level, especially during the attack, because the uric acid is being deposited into the joints from the blood. An elevated uric acid level alone is not an indication for treatment in an asymptomatic patient. You must tap the joint!

221
Q
  1. When to use colchicine for gout?
A

Only if NSAIDs and steroids cannot be used.

222
Q
  1. Should you start allopurinol during an acute attack of gout?
A

NO!

223
Q
  1. calcium pyrophosphate deposition disease ( pseudogout) presentation?
A

a. Knee and wrists are involve but NOT the toes. b. It has a much slower onset than gout, and the patient will NOT wake up with severe pain.

224
Q
  1. CCS TIP for psuedogout: in a case of pseudogout, expect hemochromatosis, hyperparathyroidism, acromegaly, or hypothyroidism in the history.
A

CCS TIP for psuedogout: in a case of pseudogout, expect hemochromatosis, hyperparathyroidism, acromegaly, or hypothyroidism in the history.

225
Q
  1. Diagnostic testing for pseudogout?
A

Tap the joint and look for positively birefringent rhomboid–shaped crystals.

226
Q
  1. Treatment of pseudogout?
A

a. NSAIDs are the best initial therapy. b. Colchicine is used, but is not effective. c. Acute management is the same as gout: NSAIDs or steroids.

227
Q
  1. Note: the more abnormal. The joint, the more likely a patient is to have septic arthritis: prosthetic joint > Rheumatoid arthritis > osteoarthritis > Normal joint.
A

Note: the more abnormal. The joint, the more likely a patient is to have septic arthritis: prosthetic joint > Rheumatoid arthritis > osteoarthritis > Normal joint.

228
Q
  1. Presentation of septic arthritis?
A

Swollen, red, immobile, tender joint!

229
Q
  1. Etiologies of septic arthritis?
A

a. Staphylococcus aureus (40%) b. Streptococcus (30%) c. gram–negative bacilli (20%).

230
Q
  1. CCS tip: : orthopedic surgery consult. We suspect a septic joint. The consultation will offer much on the CCS, but it needs to be done.
A

CCS tip: : orthopedic surgery consult. We suspect a septic joint. The consultation will offer much on the CCS, but it needs to be done.

231
Q
  1. Best initial diagnostic test for septic arthritis?
A

a. Arthrocentesis b. a finding of > 50,000 white cells is consistent with infection.

232
Q
  1. Sensitivity of Gram stain for septic arthritis?
A

50–60% sensitive.

233
Q
  1. Most accurate test for septic arthritis?
A

Culture. Culture is >90% sensitive, but is never available when you must make an acute treatment decision.

234
Q
  1. Treatment of septic arthritis?
A

a. Enteric therapy with ceftriaxone and vancomycin intravenously is effective. b. This is the choice for CCS when you have to write in one answer.

235
Q
  1. 3 Staph and strep drug options?
A
  1. Oxacillin 2. Nafcillin 3. Cefazolin
236
Q
  1. 3 Gram–negative bacilli drug options?
A
  1. Ceftriaxone. 2. Ceftazidime 3. Gentamicin
237
Q
  1. 4 staph and strep drug options for penicillin allergy?
A
  1. Vancomycin 2. Linezolid 3. Daptomycin 4. Clindamycin
238
Q
  1. 2 gram negative drug options for PCN allergy causing Anaphylaxis?
A

a. Aztreonam b. Fluoroquinolone.

239
Q
  1. Note: when treating septic arthritis. Use a combination of one drug for staff/strep and one for gram–negative bacilli.
A

Note: when treating septic arthritis. Use a combination of one drug for staff/strep and one for gram–negative bacilli.

240
Q
  1. Note: any arthritic joint or prosthetic showing is a risk factor for septic arthritis.
A

Note: any arthritic joint or prosthetic showing is a risk factor for septic arthritis.

241
Q
  1. Disseminated gonorrhea is diagnosed culture of?
A

a. Joint fluid 50% positive b. pharynx 10 – 20% positive c. rectum 10 – 20% positive d. urethra 10 – 20% positive e. cervix , 20 – 30% positive

242
Q
  1. Presentation of Paget’s Disease of Bone?
A

a. Often asymptomatic b. may lead to pain, stiffness, aching, and fractures c. soft bones lead to bowing of the tibias

243
Q
  1. Cancer Risk with Paget’s Disease of Bone?
A

Sarcoma arises in 1% of patients.

244
Q
  1. Diagnostic testing of Paget’s Disease of Bone: best initial test?
A

Alkaline phosphatase level; it will be elevated.

245
Q
  1. Most accurate test for Paget’s disease of bone?
A

X–ray

246
Q
  1. for CCS, also order the following for Paget’s disease of bone?
A

a. Urinary hydroxyproline b. serum calcium level– it will be normal c. serum phosphate level– it will be normal d. bone scan

247
Q
  1. treatment of Paget’s disease of bone? (2 drugs)
A
  1. Bisphosphonates 2. Calcitonin.
248
Q
  1. Note: in cases of Paget’s, ostiolytic lesions will be found initially. These may be replaced with osteoblastic lesions. So on Step 3, if osteolytic, then think Paget’s or osteoporosis; but if osteoblastic, think about metastatic prostate cancer in different diagnosis.
A

Note: in cases of Paget’s, ostiolytic lesions will be found initially. These may be replaced with osteoblastic lesions. So on Step 3, if osteolytic, then think Paget’s or osteoporosis; but if osteoblastic, think about metastatic prostate cancer in different diagnosis.

249
Q
  1. Baker’s cyst pathophys?
A

A Baker’s cyst is a posterior herniation of the synovium of the knee.

250
Q
  1. Presentation of Baker cyst?
A

a. Before a patient with osteoarthritis or rheumatoid arthritis with a swollen calf. b. A ruptured Baker’s cyst is a “pseudo–phlebitis”. c. Unruptured cysts can be palpated

251
Q
  1. diagnostic testing for Baker’s cyst?
A

Excluding DVT with ultrasound.

252
Q
  1. Treatment of Baker cyst?
A

NSAIDs and, occasionally, with steroid injection.

253
Q
  1. Where’s the pain with plantar fasciitis and tarsal tunnel syndrome?
A

Pain on bottom of foot.

254
Q
  1. Presentation of pain with plantar fasciitis VS. Tarsal tunnel syndrome?
A

a. Plantar fasciitis: very severe in the morning, better with walking a few steps. b. Tarsal tunnel syndrome: more painful with more use; like carpal tunnel of the foot; may have numbness of the soul, too.

255
Q
  1. Treatment of plantar fasciitis VS. Tarsal tunnel syndrome?
A

a. Plantar fasciitis: stretch the foot and calf b. tarsal tunnel syndrome:avoid boots and high heels; may need steroid injection.

256
Q
  1. Prognosis of plantar fasciitis VS. Tarsal tunnel syndrome?
A

a. Plantar fasciitis: results spontaneously over time. b. Tarsal tunnel syndrome: may need surgical release

257
Q
  1. Presentation of Morton Neuroma?
A

a. Painful Burning sensation in the interdigital webspace between the third and fourth toes. b. Tenderness when pressure is applied to tween the heads of the third and fourth metatarsals. c. Sharp, intermittent pain, radiating into the toes that feels better when shoes are taken off.

rheumatology (2 decks)

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