Rheumatology Flashcards

0
Q

What causes slapped cheek disease and childhood?

A

Fifth disease also known as slapped cheek disease is caused by an infection with parvovirus B 19. This infection is sometimes complicated by severe aplastic anemia caused by lysis of early erythroid precursors. The virus is primarily spread by infected respiratory droplets; blood-borne transmission, however, has been reported. The secondary attack risk for exposed household persons is about 50%, and about half of that for classroom contacts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Methotrexate is contraindicated to be used with sulfonamide antibiotics. True or false?

A

“Methotrexate is a folate antagonist. Antifolate medications, such as sulfonamide antibiotics, must be avoided in patients taking methotrexate; the combination “may result in pancytopenia. Supplemental folate, 1 mg daily, reduces the adverse effects of methotrexate. Patients with RA are often treated with aspirin or NSAIDs in combination with methotrexate. Penicillin antibiotics can be administered safely with methotrexate”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Children with fifths disease Are most infectious when they develop the characterstic rash of a slap cheek appearance. True or false?

A

False. Once infected, patients usually develop the illness after an incubation period of four to fourteen days. The disease commences with high fever and malaise, when the virus is most abundant in the bloodstream, and patients are usually no longer infectious once the characteristic rash of this disease has appeared

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the signs of fifths disease?

A

A usual brief viral prodrome with fever, headache, nausea, diarrhea.
As the fever breaks, a red rash of the cheeks forms, with relative pallor around the mouth (“slapped cheek rash”), sparing the nasolabial folds, forehead, and mouth.
“Lace-like,(reticular)” red rash on trunk or extremities then follows the facial rash. Infection in adults usually only involves the reticular rash, with multiple joint pain predominating.
Exacerbation of rash by sunlight, heat, stress.
Teenagers or young adults may develop the so-called “Papular Purpuric Gloves and Socks Syndrome”.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Does parvovirus affect joints?

A

In adults (and perhaps some children), parvovirus B19 can lead to a seronegative arthritis which is usually easily controlled with analgesics. Women are approximately twice as likely as men to experience arthritis after parvovirus infection. Possibly up to 15% of all new cases of arthritis are due to parvovirus, and a history of recent contact with a patient and positive serology generally confirms the diagnosis. This arthritis does not progress to other forms of arthritis. Typically joint symptoms last 1–3 weeks, but in 10–20% of those affected, it may last weeks to months.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the recommendations for a couple who wish to have a baby and one of them is taking methotrexate for RA?

A

“RA is an autoimmune disease, and it tends to remit during pregnancy when a woman is relatively immunosuppressed. Methotrexate is class X for pregnancy and is actually used in ectopic pregnancy to arrest fetal growth. Women and men on methotrexate should use an effective form of contraception, and continue contraception for 3 months after stopping methotrexate”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What can you tell a patient with RA about disease progression when well-managed?

A

90% of all joints involve will manifest in the first year. Early treatment with DMARDS has better outcome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the Jones criteria for rheumatoid fever?

A

“rheumatic fever, which is rare in developed countries, is recognized by the Jones criteria. The major Jones criteria consist of polyarthritis, carditis, Sydenham chorea, erythema marginatum, and subcutaneous nodules. (Here’s a fun mnemonic: “JONES” with a heart shape in place of the “O,” so that J = joints, O = carditis, N = nodules, E = erythema marginatum, and S = Sydenham chorea”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the diagnostic criteria for polymyalgia rheumatica?

A

“Age > 50 years
Pain/aching for at least 1 month involving 2 of the following areas: neck, shoulders/proximal arms, and pelvic girdle
Morning stiffness
ESR >40 mm/hr
Exclusion of other potential causes of the symptoms except giant cell arteritis”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the sensitivity of the ESR in giant cell arteritis?

A

Sensitivity = 85%. Up to 15% of patients with PMR or GCA (a closely related disorder—keep reading) have a false-negative ESR. Using ESR and CRP together is 97–99% sensitive for GCA. Double false negatives of ESR and CRP are uncommon, but do occur. Thus, in the patient in whom GCA is suspected but in whom there is a normal ESR and/or CRP, biopsy is still recommended. In those suspected of PMR, a trial of steroids is still recommended”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What causes polymyalgia rheumatica?

A

The cause of PMR is not well understood. The pain and stiffness result from the activity of inflammatory cells and proteins that are normally a part of the body’s disease-fighting immune system, and the inflammatory activity seems to be concentrated in tissues surrounding the affected joints.[8] During this disorder, the white blood cells in the body attack the lining of the joints, causing inflammation.[9] Recent studies have found that inherited factors also play a role in the probability that an individual will develop polymyalgia rheumatica. Several theories have included viral stimulation of the immune system in genetically susceptible individuals.[10]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the treatment of polymyalgia rheumatica?

A

“Steroids are the treatment of choice in PMR. The disease is usually self-limiting, lasting only 1-2 years. Doses of prednisone ranging from 10 to 20 mg QD usually control the disease. Higher doses (up to 30 mg/day) should be tried if there is no response in 1–2 weeks. If the patient fails to respond to low-dose steroids, the diagnosis of PMR should be reconsidered”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How should steroid management be utilized in the treatment of polymyalgia rheumatica?

A

The goal of treatment with PMR is to use the least amount of steroids possible. In order to do this, a taper of 10% should be done every 1 to weeks as soon as symptomatic control has been achieved. Monitor the ESR every 2 to 4 weeks. An asymptomatic patient with an ESR of 40 needs to be managed judicially. “However, an isolated elevation in ESR without symptoms is not a reason to increase the steroid dose.”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

During the course of treatment of PMR how often does a relapse occur?

A

“Relapses occur in 30–50% of patients after induction of a remission and should be treated by resuming or increasing prednisone. Usually, successful treatment of a relapse requires increasing the prednisone dose by a few milligrams.”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What’s the story with the relationship between giant cell arteritis and polymyalgia rheumatica?

A

Most experts agree that they are generally different presentations of the same disease. About 15% of people who are diagnosed with polymyalgia rheumatica also have temporal arteritis, and about 50% of people with temporal arteritis have polymyalgia rheumatica. Some symptoms of temporal arteritis include headaches, scalp tenderness, jaw or facial soreness, distorted vision or aching in the limbs caused by decreased blood flow, and fatigue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the visual loss pattern or giant cell arteritis compared to macular degeneration?

A

“The initial visual loss in temporal arteritis is peripheral, while the vision loss in macular degeneration is initially central. If you think about it, this makes sense. GCA basically causes an anterior ischemic optic neuropathy (AION) secondary to involvement of the retinal artery by vasculitis. The further you are from the artery, the poorer the perfusion”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

The patient presents with visual loss inspected giant cell arteritis, what is the treatment?

A

“When symptoms of vision loss occur, aspirin 81 mg daily and IV methylprednisolone 1 g daily for 3 days, followed by aspirin and prednisone 40–60 mg daily is the standard of care. Compared to PMR, higher doses of steroids are necessary to treat GCA. In the absence of vision loss, prednisone doses of 40–60 mg QD are usually required to relieve symptoms”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which life-threatening condition that presents with severe upper thoracic pain that feels like a ripping sensation is associated with polymyalgia rheumatica five years after its onset and how is it diagnosed?

A

“Thoracic aortic aneurysm is a late complication of GCA; aortic aneurysms generally occur an average of 6–7 years after the initial diagnosis of GCA. Thoracic aortic aneurysms occur 17 times more often in patients with GCA when compared to the general population. The diagnosis of thoracic aortic aneurysm is confirmed by CT scan of the chest”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

In the patient with suspected gonococcal arthritis how often is gonococcus aspirated and cultured from joint fluid?

A

“Gonococcus is cultured from the joint fluid only about 50% of the time in patients with gonococcal arthritis. Thus, a PCR of the joint fluid and urethral cultures should be done if the Gram stain is negative”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

The patient has a hot knee most likely from a joint infection. What is the recommended treatment?

A

“In order to ensure the best outcome, this patient should be admitted for monitoring and repeated joint aspiration. Purulent fluid tends to collect rapidly in the joint spaces in patients with septic arthritis, necessitating frequent drainage until antibiotics work and inflammation begins to subside. Most cases of gonococcal arthritis respond to needle aspiration, but arthroscopic or open debridement is occasionally necessary. Because IV antibiotics have good penetration into synovial fluid, intra-articular antibiotics are not recommended. When culture, PCR, and sensitivity results become available, antibiotic therapy should be tailored to the sensitivities”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

The patient has gonococcal joint infection what is the antibiotic regimen of choice?

A

“The initial antibiotic of choice in gonococcal arthritis is ceftriaxone, administered IV. In cases in which drug allergies or other contraindications prohibit the use of ceftriaxone, IV spectinomycin is an acceptable alternative. Remember that there is now fluoroquinolone-resistant gonococcus. Because of this, fluoroquinolones are no longer recommended as treatment of gonorrhea”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the treatment for gonococcal infection with suspected chlamydia too,.?

A

“cefixime 400 mg PO BID and doxycycline 100 mg b.i.d. for 7 to 14 days.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What kinds of joints does septic arthritis occur in and what are the predisposing factors?

A

“Septic arthritis occurs most often in large joints, such as the knee and hip. Factors that predispose a patient to septic arthritis include advancing age (especially >80 years), rheumatoid arthritis, joint prostheses, recent joint surgery, diabetes, and skin infection”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the mortality rate of septic arthritis?

A

“The mortality rate of septic arthritis is 10%, with up to one-third of survivors having persistent joint problems, such as limited range of motion, pain, and swelling. Note that the mortality is probably not due to the infection alone but rather to a combination of the underlying illness (e.g., immunosuppression) plus the infection.”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Name three diagnostic criteria for acute gout.

A

“Presence of characteristic urate crystals in the joint fluid or tophus proved to contain urate crystals by chemical means or polarized light microscopy or presence of 6 of the following 12 phenomena:

  1. More than 1 attack of acute arthritis
  2. Maximal inflammation developed within 1 day
  3. Attack of monoarticular arthritis
  4. Joint redness observed
  5. First MTP joint painful or swollen
  6. Unilateral attack involving first MTP joint
  7. Unilateral attack involving tarsal joint
  8. Suspected tophus
  9. Hyperuricemia
  10. Asymmetric swelling within a joint (radiograph)
  11. Subcortical cysts without erosion (radiograph)
  12. Negative joint fluid culture for microorganisms during attack of joint inflammation”
25
Q

What is the acute treatment of gout?

A

“An acute attack of gout should first be treated with NSAIDs, such as naproxen or indomethacin. The doses prescribed should be at the upper limit for the particular NSAID (e.g., naproxen 500 mg TID). Earlier treatment is associated with greater relief of symptoms and shorter duration of the acute event. Other potential first-line agents are steroids and colchicine. Narcotics may also be appropriate.

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
This material may be protected by copyright.

Check out this book on the iBooks Store: https://itun.es/us/vRMUI.l

26
Q

What is a maintenance therapy for gout?

A

“Allopurinol is indicated for prophylaxis of gout when hyperuricemia is documented, but its use in the acute setting is inappropriate. Initiation of allopurinol may actually cause or worsen exacerbations of gout.”

27
Q

What is the long-term management of acute gouty arthritis with hypeuricemia?

A

“Low doses of colchicine administered twice daily have been shown to reduce the frequency of gout attacks 75–85%. This patient also has hyperuricemia and is likely to benefit from lowering his uric acid level. Remember that the initiation of allopurinol may precipitate or worsen an acute attack of gout. Therefore, allopurinol should be initiated only with concurrent use of colchicine or an NSAID.
Probenecid is a uricosuric agent that also reduces the frequency and severity of acute gout attacks but has multiple drug interactions (including allopurinol) and contraindications (e.g., decreased renal function); however, it may well be indicated in the patient who does not achieve his target with allopurinol alone. An attempt should be made to lower uric acid to 6–7 mg/dL with one medication before considering a combination of drugs”

28
Q

What is the treatment of pseudogout?

A

“Although prophylaxis is more predictably successful in gout, colchicine 0.6 mg BID has been shown to reduce the frequency of pseudogout attacks in CPPD. NSAIDs or colchicine may be used in acute attacks”

29
Q

Name three diseases associated with pseudogout.

A

“Hypothyroidism, Hyperparathyroidism, Amyloidosis, Hemochromatosis. Additional associated conditions include hypophosphatemia and hypomagnesemia. For this reason, order the following studies in patients newly diagnosed with CPPD: thyroid-stimulating hormone (TSH), calcium, phosphate, magnesium, transferrin saturation, and alkaline phosphatase”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
This material may be protected by copyright.

Check out this book on the iBooks Store: https://itun.es/us/vRMUI.l

30
Q

“Cryoglobulinemia, a vasculitic disease caused by antibodies that precipitate in cold temperatures, is most often caused by which of the following viral infections?

A

“Hepatitis C is found in 80% of vasculitis cases associated with mixed cryoglobulinemia. Although up to 50% of patients with hepatitis C have cryoglobulins, only a minority of patients have clinical vasculitis. Because of the increasing prevalence of hepatitis C, cases of cryoglobulinemia will most likely increase as well.”

31
Q

What is a good diagnostic clue distinguishing JRA from Lyme disease?

A

“Neurologic symptoms, including Bell palsy (“A”) and even meningitis, may occur with Lyme disease but not JIA. Rash (“C”) is present in both diseases but differs substantially. The characteristic rash of Lyme disease is erythema migrans. The rash of JIA is macular, salmon-pink, and brought on by heat. Erythema migrans occurs in about 80% of patients with acute Lyme disease. The lesion is often described as “targetoid,” meant to convey a red circular rash with central clearing. However, most patients do not have the classic lesion. Instead, most patients present with a mildly to brightly erythematous patch in the axilla or belt line, where the tick bite occurs. The tick itself is rarely seen. Erythema migrans is usually not painful or pruritic. Both Lyme disease and JIA may have associated systemic findings, including fever and lymphadenopathy”

32
Q

What is most commonly found in the joint aspiration of a patient with Lyme disease?

A

“If synovial fluid is obtained in a patient with Lyme arthritis, analysis of the fluid reveals leukocytes, most commonly polymorphonuclear cells”

33
Q

What is arthralgia? Polyarthralgia?

A

The causes of arthralgia are varied and range, from a joints perspective, from degenerative and destructive processes such as osteoarthritis and sports injuries to inflammation of tissues surrounding the joints, such as bursitis.[6] These might be triggered by other things, such as infections or vaccinations. Polyarthralgia involves more than one joint.

34
Q

What is seborrheic dermatitis?

A

Seborrheic dermatitis is an inflammatory skin disorder affecting the scalp, face, and torso. Typically, seborrheic dermatitis presents with scaly, flaky, itchy, and red skin. It particularly affects the sebaceous-gland-rich areas of skin. In adolescents and adults, seborrhoeic dermatitis usually presents as scalp scaling similar to dandruff or as mild to marked erythema of the nasolabial fold.

35
Q

What population is at risk for SLE?

A

“Caucasians have a lower risk of SLE. The peak incidence of SLE occurs in the third to fifth decades of life. Women are 5-10 times more likely than men to be diagnosed with SLE. First-degree relatives of patients with SLE are at higher risk as well. Twin studies have shown a 25-50% concordance rate among monozygotic twins”

36
Q

What is drug related lupus? How is it distinguished from regular SLE?

A

“Patients with drug-induced lupus will generally have a positive ANA. However, it can be differentiated from SLE by a negative anti-dsDNA. Drug-related lupus presents with a lupus-like syndrome, with the most common features being arthralgias, myalgias, fatigue, malaise, and low-grade fever. Pericarditis and pleuritis are occasionally present. Skin, renal, and neurologic involvement are rare.”

37
Q

What is the diagnostic criteria for SLE?

A

“SLE requires the presence of 4 of the 11 findings below, not necessarily occurring at the same time.
1. Malar rash”
“2. Discoid rash
3. Photosensitivity
4. Oral ulcers (usually painless)
5. Arthritis (involving 2 or more peripheral joints)
6. Serositis (pericarditis or pleuritis)
7. Renal disorder (proteinuria >0.5 g/day or cellular casts)
8. Neurologic disorder (seizures or psychosis)
9. Hematologic disorder (hemolytic anemia, leukocyte count <100,000/mm3)
10. Positive ANA
11. Immunologic disorder (anti-DNA, anti-Smith, or antiphospholipid antibodies, or a false-positive serologic test for syphilis)”

38
Q

What is the treatment of SLE?

A

“NSAIDs, such as ibuprofen, are useful in treating arthralgias, mild arthritis, and mild pleurisy and pericarditis. In this case, oral (or perhaps intra-articular) steroids are indicated for immediate symptomatic relief of her arthritis, and a low-to-moderate oral dose should be used (20 mg rather than 60 mg). Vitamin D and calcium supplements should be prescribed with the steroids. Methotrexate can be used in recurrent, persistent arthritis. In the event of more serious renal, hematologic, or neurologic disease, high-dose steroids are employed. Hydroxychloroquine may provide relief of musculoskeletal and constitutional symptoms and may also have a steroid-sparing effect. Ideally, this patient should also be referred to a rheumatologist, but appropriate treatment should be started in a timely fashion. Close follow-up is necessary due to the potential adverse effects of these medications (e.g., diabetes with prednisone).”

39
Q

What can be expected for a patient with SLE during pregnancy?

A

“Women with SLE have a greater risk of premature birth, spontaneous abortion, and intrauterine fetal demise compared with otherwise healthy women. However, these patients appear to have comparable rates of fertility. Pregnancy outcomes are best when the patient is in remission 6-12 months before conception. Pregnancy appears to have a variable affect on SLE, with some patients experiencing exacerbations of the disease”

40
Q

What role does an aPTT play in diagnosing antiphospholipid antibody syndrome?

A

“Even though they are prone to clotting, patients with antiphospholipid antibody syndrome have a paradoxically elevated aPTT. If this abnormality does not correct in vitro with addition of normal serum, it is presumptive evidence of antiphospholipid antibody syndrome. Besides venous thrombus formation, “women with antiphospholipid antibody syndrome are more likely to have late fetal demise and multiple spontaneous abortions.”

41
Q

What is antphospholipid antibody syndrome?

A

The diagnostic criteria require one clinical event, i.e. thrombosis or pregnancy complication, and two positive blood tests spaced at least three months apart. These antibodies are: lupus anticoagulant, anti-cardiolipin and anti-β2-glycoprotein-I.[1]
Antiphospholipid syndrome can be primary or secondary. Primary antiphospholipid syndrome occurs in the absence of any other related disease. Secondary antiphospholipid syndrome occurs with other autoimmune diseases, such as systemic lupus erythematosus (SLE). In rare cases, APS leads to rapid organ failure due to generalised thrombosis; this is termed “catastrophic antiphospholipid syndrome” (CAPS) and is associated with a high risk of death.

42
Q

How do you treat antiphosphlipid antibody syndrome?

A

Antiphospholipid syndrome often requires treatment with anticoagulant medication such as heparin to reduce the risk of further episodes of thrombosis and improve the prognosis of pregnancy. Warfarin/Coumadin is not used during pregnancy because it can cross the placenta, unlike heparin, and is teratogenic.

43
Q

How does one monitor a patient with antiphosphlipid antibody syndrome who is on heparin?

A

“Since patients with antiphospholipid antibody syndrome have an elevated aPTT, this value cannot be used to monitor anticoagulation with standard heparin. Percent factor II activity is the most appropriate way to monitor these patients if they are on standard heparin. Antifactor Xa is used to monitor anticoagulation with enoxaparin”

44
Q

Name two meds used to treat lupus and their toxic side effects.

A

“NSAIDs: gastrointestinal bleeding, renal dysfunction, hypertension
Steroids: diabetes, hypertension, hyperlipidemia, osteoporosis, cataract formation, weight gain, infections
Hydroxychloroquine: macular damage, ciliary muscle dysfunction, corneal opacities, myopathy
Azathioprine: infections, myelosuppression, hepatotoxicity
Cyclophosphamide: infections, myelosuppression, hemorrhagic cystitis
Methotrexate: infections, myelosuppression, hepatic fibrosis”

45
Q

What is acrocyanosis?

A

“(a rare vasospastic disorder of persistent coldness and bluish discoloration of the hands and feet, not just fingers and toes, which may follow a viral infection”

46
Q

What are the most common causes of Reynaud’s syndrome?

A

“Over 80% of cases of Raynaud phenomenon that present to a primary care physician’s office are due to an exaggerated physiologic response to cold or emotional distress”

47
Q

What’s Buerger disease?

A

“Buerger disease (thromboangiitis obliterans) is strongly associated with tobacco abuse and presents with distal small vessel ischemia and symptoms that are similar to Raynaud phenomenon. It eventually progresses to infarction of tissue, frequently requiring digit amputation”

48
Q

What does the CREST syndrome stand for?

A

“calcinosis cutis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia”

49
Q

What medication is first line for Reynaud’s?

A

“Dihydropyridine calcium-channel blockers, like amlodipine, have been shown to reduce the frequency of attacks by about 50% compared with placebo. They must be scheduled, rather than used as needed”

“In systemic sclerosis, the benefit of calcium-channel blockers is often offset by their exacerbation of GERD. In these patients, ACE inhibitors or angiotensin receptor blockers (ARBs) are also beneficial for Raynaud phenomenon. Topical vasodilators like nitroglycerin have a role if calcium-channel blockers are not effective or the patient cannot tolerate them”

50
Q

How does determining the pattern of pain in a patient help make the diagnosis?

A

“Inflammatory causes of back pain are characterized by morning stiffness and improvement with activity. In contrast, degenerative back disease causes pain that is exacerbated by activity and relieved with rest. Inflammatory back pain typically presents in younger patients; degenerative back pain typically does not present before age 30 or 40. Acetaminophen and other analgesics may relieve pain from either category of disease and so will not help you narrow the diagnosis.”

“In a young patient with back pain, also consider fractures (e.g., spondylolysis, a bilateral pars defect), infection, disc disease, and osseous malignancies.”

51
Q

What is ankylosing spondylitis?

A

“ankylosing spondylitis, a seronegative (RF negative) spondyloarthropathy. Ankylosing spondylitis is the most common form of spondyloarthropathy and is thought to have a prevalence of 1% in Caucasian populations. Historically, there is a 5:1 male-to-female ratio (but this may also be because ankylosing spondylitis is less recognized in women). Studies based on radiographic appearance and human leukocyte antigen (HLA) B27 typing show a much lower ratio. In addition to the historical features mentioned in the answer to the previous question, there is often a family history of ankylosing spondylitis in patients ultimately diagnosed with the disease”

52
Q

What are 2 physical findings with sponyloarthopathies?

A

“Limited range of motion in the spine
Tenderness at the sacroiliac joints
Tenderness at tendon insertions, particularly the Achilles tendon and plantar fascia synovitis
Anterior eye symptoms (anterior uveitis in 30-40%)”

53
Q

What’s the best test to diagnose ankylosing spondylitis?

A

“The hallmark of anky-losing spondylitis is sacroiliitis on pelvic radiographs. Although there are no universally accepted criteria for diagnosing spondyloarthropathies, x-ray evidence of sacroiliitis in the setting of a consistent clinical picture is sufficient to diagnose ankylosing spondylitis. Unfortunately, in early ankylosing spondylitis, x-rays are often inconclusive. MRI is more sensitive for detecting early sacroiliitis, but the cost will be prohibitive in many cases”

54
Q

What’s the role of an HLA-B27 in diagnosing AS?

A

“HLAB 27, a class I HLA gene, is present in about 90% of white patients and 50-80% of nonwhite patients with ankylosing spondylitis and is generally associated with spondyloarthropathies. However, HLA-B27 is not specific. It is present in many normal individuals as well and is of very little diagnostic value (although it does have a good negative predictive value”

55
Q

What is the treatment of AS?

A

“NSAIDs are the mainstay of medical therapy for active phases of spondyloarthropathy. Patients generally experience significant relief from NSAIDs, and any additional benefit from systemic steroids is questionable. Sulfasalazine is a second-line drug. Interestingly, aspirin tends to be less effective in these patients. The management of ankylosing spondylitis should also include an exercise regimen designed specifically for the patient, and physical therapy may play a key role”

56
Q

In a patient with AS who is losing ROM despite NSAIDs, what is the next step?

A

“The patient is losing range of motion despite NSAID therapy. Referral to a rheumatologist to consider anti-TNF therapy (e.g., infliximab [Remicade]) is the best next step. Anti-TNF agents can halt disease progression and often improve range of motion in early disease.

57
Q

What is enteropathic arthritis?

A

Enteropathic arthropathy or arthritis refers to acute or subacute arthritis in association with or as a reaction to an enteric (usually colonic) inflammatory condition.
Causes/Associations:
Reactive arthritis (Reactive to enteric infection); Spondyloarthropathies associated with inflammatory bowel disease (Crohn disease and ulcerative colitis); Malabsorption related: Intestinal bypass (jejunoileal), Celiac disease, Whipple disease; Collagenous colitis.
Note that reactive arthritis can also occur secondary to urethral infection. In that case the term enteropathic arthropathy would not be used.
“Enteropathic arthritis occurs frequently in patients with inflammatory bowel disease, and has features in common with ankylosing spondylitis, including inflammatory back pain and sacroiliitis. However, it may also occur after a GI infection such as Salmonella, Yersinia, Shigella, or Campylobacter. Finally, other illnesses such as celiac disease may cause a reactive spondyloarthropathy.”

58
Q

Name two diseases associated with reactive arthritis.

A

“Reactive arthritis (formerly Reiter syndrome) is associated with HLA-B27 and not HLA-B8 (which is found in sclerosing cholangitis). Conjunctivitis. keratoderma blenorrhagicum, which is a rash found especially on the soles of patients with reactive arthritis. The urethritis is generally due to Chlamydia trachomatis”

59
Q

What’s the difference in onset of reactive arthritis versus AS?

A

“The onset of reactive arthritis is less insidious than that of ankylosing spondylitis, with some patients presenting with an acute illness that includes fever, acute joint swelling, and rash (keratoderma blenorrhagicum). Generally, reactive arthritis resolves within 12 months. Antibiotics are not effective as treatment of reactive arthritis (although may be indicated for the underlying infection”

60
Q

What are the diagnostic criteria for dermatomyositis and poly Myosotis?

A

“Three of four are required:
Elevated muscle enzymes (CPK and aldolase)
Symmetrical proximal muscle weakness Abnormal EMG
Consistent findings on muscle biopsy
Note: Skin findings must be present in order to diagnose dermatomyositis.”
“Violaceous plaques on the knuckles are commonly called Gottron papules. Similar lesions are often observed over pressure points (e.g., elbows).

61
Q

Name two screening tests that should be ordered with adult onset dermatomyositis.

A

“Adult onset dermatomyositis has a particularly strong association with malignancy; the risk is up to six times greater than in the general population. Therefore, upon diagnosing dermatomyositis, a thorough history and physical exam must be performed. All patients should undergo age-appropriate cancer screening tests (e.g., Pap smear, fecal occult blood testing, and mammography). Also, other tests generally recommended include CBC, metabolic profile, liver function tests, urinalysis, and chest x-ray—especially important in smokers. Since the patient is over age 50, colonoscopy is indicated.
The association of dermatomyositis with GI malignancy, especially colon cancer, is particularly strong. You may consider an alpha-fetoprotein, given this association. Some suggest CA-125 in all women with dermatomyositis, as well as a pelvic ultrasound or CT of the abdomen and pelvis to rule out ovarian cancer”