Rheumatology Flashcards

1
Q

What is the next step in the management of chronic monoarthritis in a pt that has a joint drained twice and bloodwork is unrevealing?

A

Synovial Biopsy

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2
Q

What is this? What systemic disease is it ass’d with?

A

enthesitis (where the tendon inserts to bone)

Spondyloarthritis (ankylosing spondylitis, psoriatic arthritis, inflammatory bowel disease–associated arthritis, and reactive arthritis)

Spondyloarthritis refers to a group of disorders that share an overlapping set of features, including inflammation of the axial skeleton, tendons, and entheses (insertion of tendon to bone); tendon and enthesis calcification; an association with HLA-B27; and mucocutaneous, gastrointestinal, and ocular inflammation.

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3
Q

What are the 4 spondyloarthritis? What are the characteristic features of this group of disorders?

A
  1. ankylosing spondylitis
  2. psoriatic arthritis
  3. inflammatory bowel disease–associated arthritis
  4. reactive arthritis

Spondyloarthritis refers to a group of disorders that share an overlapping set of features, including inflammation of the axial skeleton, tendons, and entheses (insertion of tendon to bone); tendon and enthesis calcification; an association with HLA-B27; and mucocutaneous, gastrointestinal, and ocular inflammation.

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4
Q

65F with PMH Giant Cell Arteritis. On 60mg Prednisone and ASA81. DEXA 6mo ago based upon the results of the Fracture Risk Assessment Tool, the patient was classified as medium risk (10%-20%) for a major osteoporotic fracture in the next 10 years.

How do you interpret this and what is the mgmt?

A

10 year risk >20% need to be treated with bisphosphonates.

Especially this woman who is still on steroids.

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5
Q

What is the treatment for mono osteo-arthritis in an elederly patient with CAD and CKD3 on ASA81?

A

Topical NSAIDs

PO NSAIDs are first line, but they are not reccomended in patients >75 y/o d/t potential toxicity (age, CKD, CAD, and ASA intake)

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6
Q

What medications need to be avoided in a pt who is on colchicine?

A

CYP3A4 inhibitors

  • clarithromycin
  • fluconazole

This can cause a potentially fatal colchicine toxicity with kidney failure, rhabdo, BM suppression

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7
Q

78M PMH HTN and Gout (on lisinopril, colchicine and febuxostat) dx with CAP started on Clarithromycin 5d ago. Yesterday he developed generalized weakness and diarrhea.

On physical examination, temperature is 36.9 °C (98.4 °F), blood pressure is 104/60 mm Hg, pulse rate is 112/min, respiration rate is 18/min, and oxygen saturation is 98% breathing ambient air. There is no rash. The oropharynx appears dry. The chest is clear to auscultation. Tophi are noted at the olecranon processes. There are no swollen or tender joints. Neurologic examination is normal.

Laboratory studies;

  • Absolute neutrophil count: 1300/µL (1.3 × 109/L)
  • Hemoglobin: 9.8 g/dL (98 g/L)
  • Leukocyte count: 2700/µL (2.7 × 109/L)
  • Platelet count: 96,000/µL (96 × 109/L)
  • Reticulocyte count (corrected): 1.2%
  • Creatine kinase: 8433 U/L
  • Creatinine: 1.7 mg/dL (150.1 µmol/L)
  • Urinalysis: 4+ blood; 0-1 erythrocytes/hpf; 0-2 leukocytes/hpf

There are no schistocytes seen on peripheral blood smear.

What is this?

A

Colchicine toxicity 2/2 Clarithromycin initiation

  • Both meds need to be discontinued
  • Pathophys: CYP3A4 inhibition by clarithromycin -> colchicine toxicity
  • Presenation is kidney failure, rhabdo, BM suppression
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8
Q

What are the ADRs of pregabalin?

A

Weight gain, peripheral edema, lethargy, dizziness.

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9
Q

What ADRs of MTX do you need to monitor?

A

Megaloblastic anemia or Pancytopenia

Periodic CBC is reccomended

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10
Q

What is leflunomide used to treat?

What are the ADRs?

A

RA & Psoriatic Arthritis

Uncommon ADR: Peripheral neuropathy (goes away when discontinued)

Common ADR: nausea, HA, rash, diarrhea, transaminitis

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11
Q

53M PMH CKD3 with 5y h/o recurrent gout attacks that are becoming more frequent and severe. Serum Urate is 9.2. He is of Thai descent. What is the next step in management?

A

HLA-B*5801 allele testing

This patient given his Asian background and CKD is at high risk for allopurinol hypersensitivity

Allopurinol hypersensitivity is characterized by DRESS (drug reaction, eosinophilia, and systemic symptoms) syndrome and can result in kidney failure and death; allopurinol should be discontinued at the first sign of a rash. The presence of the HLA-B*5801 allele is a contraindication to prescribing allopurinol

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12
Q

What are the risk factors for allopurinol hypersensitivity?

What test do you do to help evaluate risk?

A

CKD, Asian, Diuretic use

The presence of the HLA-B*5801 allele is a contraindication to prescribing allopurinol

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13
Q

What RA meds are CI during pregnancy?

A

MTX and Leflunomide

Note: Hydroxychloroquine is safe

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14
Q

What is the most helpful AB used to dx RA?

A

Anti-cyclic citrullinated AB

Note: you would also get RF and inflammatory markers

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15
Q

53F with 15y h/o RA who presents with intermittent sensory loss in the hands and an occasional shock-like sensation from the neck down the back with neck flexion. She has not noted any weakness. Medications are methotrexate, etanercept, and folic acid.

Neck flexion triggers her symptoms. There is no muscle atrophy at the hands. Tinel and Phalen signs at the wrist are negative. Reflexes, strength, and sensation of the upper and lower extremities are normal.

What is this? What is the next step in mgmt?

A

C1-C2 Subluxation

Flexion/extensoin radiography of the cervical spine

Patients with long-standing (>10y) RA are at risk. nflammation from RA can lead to attenuation of the transverse ligament that normally limits the posterior motion of the odontoid process of the C2 vertebrae.

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16
Q

What eye disease is ass’d with RA?

A

Scleritis

Typical features include eye pain, pain with gentle palpation of the globe, and photophobia. The deep scleral vessels are involved and may lead to scleromalacia, which is characterized by thinning of the sclera and is seen as a dark area in the white sclera

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17
Q

What is the difference between scleritis and episcleritis?

A

Scleritis: eye pain, pain with gentle palpation of the globe, and photophobia. Scleritis can be vision-threatening and lead to blindness; it is therefore important to urgently refer the patient to an ophthalmologist for care. Ass’d with autoimmune diseases.

Episcleritis is an abrupt inflammation of the superficial vessels of the episclera, a thin membrane that lies just beneath the conjunctiva. Not ass’d with autoimmune diseases. Patients with episcleritis frequently present without pain or decreased visual acuity. On examination, the inflammation appears localized. White sclera can be seen between superficial dilated blood vessels. Episcleritis typically resolves spontaneously.

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18
Q

What type of pleural effusion is ass’d with RA?

A

Exudative

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19
Q

What is Light’s Criteria? Which type of pleural effusion is ass’d with RA?

A

Exudative

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20
Q

50M with 15y h/o worsening arthritis which has not been worked up. He has a lower extremity ulcer.

On physical examination, vital signs are normal. The spleen tip is palpable. There is swelling of multiple small joints at the hands, knees, and metatarsophalangeal (MTP) joints. There is ulnar deviation and subluxation of the metacarpophalangeal joints. Subcutaneous nodules are present at the elbows bilaterally. There is a 2- × 2-cm shallow ulcer at the medial left lower extremity just above the ankle.

Laboratory studies:

  • Hematocrit: 33%
  • Leukocyte count: 2100/µL (2.1 × 109/L), with 900 neutrophils
  • Platelet count: 276,000/µL (276 × 109/L)
  • Urinalysis: Normal

What is the most likely dx?

A

Felty syndrome

  • Long-standing aggressive RA
  • Neutropenia
  • Splenomegaly
  • Ass’d with the risk for serious infections, lower extremity ulcers, and vasculitis.
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21
Q

What is the initial monotherapy for RA?

A

Methotrexate

Methotrexate is an anchor drug in RA and is the preferred initial monotherapy, as it both controls symptoms and prevents joint damage. Clinical trials have demonstrated that 30% to 50% of patients treated with methotrexate monotherapy will show no disease progression as measured by hand and foot radiographs.

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22
Q

What is the main modifiable risk factor for OA?

A

Weight

patient’s with higher BMI have proprotionally higher risk of getting OA.

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23
Q

74M with pain and stiffness in the mid and lower spine that has progressively worsened over the past 10 years. The pain is worse with activity.

Limited range of motion and pain on motion of thoracic and lumbar spine are noted. There is no peripheral joint swelling or tenderness and no sacroiliac tenderness. The FABER test of the hip is normal.

Laboratory studies show a normal erythrocyte sedimentation rate.

Thoracolumbar spine radiographs reveal bridging ossification on the right side along the anterolateral aspects of the vertebral bodies of T9-L2. Radiographs of the sacroiliac joints are normal.
What is the dx?

A

Diffuse Idiopathic Skeletal Hyperostosis (DISH)

Diffuse idiopathic skeletal hyperostosis is a noninflammatory condition that involves ossification of spinal ligaments and entheses and usually presents as back pain and stiffness; characteristic radiographic changes include confluent ossification of at least four contiguous vertebral levels, usually on the right side of the spine.

Ankylosing spondylitis is characterized by bilateral sacroiliac joint abnormalities on spinal radiographs. Other spinal sections may also be involved, but sacroiliac joint involvement is cardinal for diagnosis. Inflammatory back pain is the most common symptom and is usually comprised of four of five of the following features: onset of back discomfort before the age of 40 years; insidious onset; improvement with exercise; no improvement with rest; and pain at night (with improvement upon arising).

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24
Q

50F with 1mo h/o pain on the inner L knee. The pain is aggravated by ascending stairs and rising from a seated position. This is different than her OA knee pain.

Tenderness to palpation and slight swelling over the proximal medial tibia about 6 cm below the anteromedial joint margin of the knee are noted. Examination of the knee shows no crepitus, minimal pain along the medial joint line, and no pain on valgus stress; anterior and posterior drawer signs are negative.

What is this?

A

Pes anserine bursitis

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25
Q

How would you treat knee OA and low back pain in a 73F who has tried nonpharmacologic interventons, had minimal benefit from intra-articular glucocorticoid and hyaluronic acid injections and was recently dx with PUD?

A

Duloxetine

Note: Topical Capsaicin or NSAIDs would be an option if it was just her knee.

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26
Q

What ADR should you counsel your patient’s on when rx topical NSAIDs?

A

Localized skin rash

Note: they provide similar pain relief as oral medications with less risk for GIB

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27
Q

What are the 3 drugs used to treat fibromyalgia?

A

Pregabalin

Duloxetine

Milnacipran

Each drug has about a 30% reduction in pain. Note: NSAIDs are not part of the treatment. The above meds can be used in combination.

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28
Q

Do you need HLA-B27 testing to confirm AS?

A

No, it does not need to be checked if they have;

  • Inflammatory back pain for 3 or more mo
  • <45 y/o
  • Limited lumbar spine motion
  • Elevated inflammatory markers
  • Bilateral sacroilitis on imaging

The only time it would be helpful if the case is less clear.

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29
Q

What is the MCC of reactive arthritis? What test would you do to confirm?

A

Chlamydia trachomatis

Nucleic acid amplification urine test

30
Q

What imaging modality should you do to dx AS?

A

AP Radiograph of the pelvis and SI joint first. However, this may be unremarkable early in the course of the diesease. Then you would…

MRI of the SI joint

31
Q

What is the first line therapy for AS?

A

NSAIDs

Ex: Diclofenac

32
Q

What disorders does Hydroxychlorquine treat?

A

RA, SLE and Dermatomyositis

33
Q

What is first and 2nd line treatment for Psoriatic Arthritis?

A

1st: MTX
2nd: TNF-a inhibitor (Infliximab, Ustekinumab, Secukinumab)

34
Q

What is the difference between acute cutaneous lupus eythematosis (ACLE) and subacute cutaneous lupus erythematous (SCLE)?

A

ACLE:

  • Almost 100% of these patients have SLE
  • Most commonly presents as malar rash

SCLE:

  • anti-Ro/SSA antibodies in 75% of cases
  • 50% have SLE
  • More mild symptoms
  • Photosensitive rash that is most commonly on forearms, chest, upper back
35
Q

34F w 2y h/o Lupus Nephritis on hydroxychloroquine, mycophenolate mofetil, and prednisone. She has had 6mo of worsening pain in the L groin and radiation to the L buttock, particularly with stair climbing.

She has weakness of the left hip flexors. Decreased passive range of motion of the left hip in both external and internal rotation with pain is noted.

What is the most likely dx? What is the next step in mgmt?

A

Glucocorticoid-induced osteonecrosis of the L hip

Mgmt: Plain radiography of the L hip. MRI only if plian radiograph is wnl.

Note: Both steroids and SLE itself are risk factors for osteonecrosis

36
Q

What are the 2 life threatening pulmonary diseases ass’d with SLE? How do you differentiate?

A

Lupus Pneumonitis: SOB, Hypoxia, diffuse pulmonary infiltrates

DAH: Hemoptysis, anemia, BAL showing blood

Note: It can be difficult to differentiate bilateral infiltrates in an SLE patient

37
Q

What AB is used to help dx an SLE flare?

A

anti-dsDNA

38
Q

What is the treatment for isolated class V lupus nephritis without evidency of kidney dysfunction?

A

Mycophenolate mofetil

Note: it is teratogenic and must be stopped 3mo before pregancy

Cyclophosphamide is used for severe organ disease ass’d with SLE but it has terrible side effects (reduces fertility, premature menopause). It may be used to induce remission in severe active nephritis but not for maintenance therapty

39
Q

What is the treatment for SLE with persistent mild to moderate active disease already on hydroxychloroquine, mycophenolate and prednisone and could not tolerate leflunomide?

A

Belimumab

Belimumab is designed to inhibit B-lymphocyte stimulator (BLyS) protein. BLyS plays a key role in the selection, maturation, and survival of B cells, and it has a significant role in the pathogenesis of SLE.

40
Q

What would be the next step in the workup of a patient with signs of Sjogren (dry eyes and mouth), but serologies are negative?

A

Lip Biopsy

41
Q

What is the Schirmer test and what does it help dx?

A

It confirms dry eyes (not dry mouth) in a pt you’re evaluating for Sjogren Syndrome

42
Q

What is the treatment for Sicca symptoms of Sjogren?

A

Artificial tears and sugar free candies.

Note: Even if they’ve lost teeth d/t dental caries

MTX is used to treat the joint disease related to Sjogren if it does not respond to NSAIDs, not the sicca symptoms

43
Q

47F with onset over 2 to 3 weeks of low-grade, intermittent fever; blanching of the second and third right fingertips in response to cold exposure; cracking and peeling of the skin on the sides of the second digits and palms; and pain and swelling of the second and fourth proximal interphalangeal joints bilaterally. She does not take any medications.

Erythema of the malar area, forehead, and chin is present. Pulmonary examination reveals crackles at the lung bases.

Skin findings are shown.

Laboratory studies:

  • Creatine kinase: 115 U/L
  • Antinuclear antibodies: Titer: 1:1280
  • Anti–double-stranded DNA antibodies: Negative
  • Anti–Jo-1 antibodies: Positive
  • Anti-Smith antibodies: Negative

What is this?

A

Antisynthetase syndrome

  • ILD
  • Myositis
  • Raynaud
  • Arthritis
  • Mechanic’s hands
  • +Anti-Jo-1
44
Q

How do you differentiate Inclusion body myositis from polymyositis?

A

Inclusion Body Myositis

  • Proximal OR Distal muscle
  • Elderly
  • Men>Women
  • CKD 10-12x ULN
  • Muscle biopsy showed muscle fibers containing multiple rimmed vacuoles

Polymyositis

  • Women>Men
  • <50 y/o
  • Proximal
  • CK more like 50x ULN

Note: it is important to differentiate becuase they have different treatments

45
Q

Antinuclear ABs in a centromere pattern

A

Limited Cutaneous Systemic Sclerosis

46
Q

43M with GIB. PMH diffuse cutaneous systemic sclerosis with Raynauds and GERD.

Upper gastrointestinal endoscopy demonstrates linear ectatic vessels resembling the stripes found on a watermelon that arise from the pylorus.

What is this?

A

Gastric Antral Vascular Ectasia

Proliferation of blood vessels typically in the stomach antrum. 60% of people with this finding have an underlying autoimmune disease.

47
Q

How do you differential ILD and PAH in a pt with systemic slcerosis when they both present with gradual worsening of dyspnea on exertion?

A

PAH: Normal CXR and lung exam. Increased pulmonic sound and widened split of S2.

ILD: Abnormal lung exam (“Velcro” like inspiratory crackles at the bases) and abnormal CXR

48
Q

What is the treatment for ILD in a pt with systemic sclerosis?

A

Mycophenolate Mofetil

It works better than cyclophosphomide

49
Q

anti-Scl-70

A

Systemic Sclerosis, with increased risk for ILD

Note: AKA DNA topoisomerase-1

50
Q

DNA topoisomerase-1

A

anti-Scl-70

Systemic Sclerosis with increased risk for ILD

51
Q

32F PMH Raynaud and GERD who presented to the ED with 2d h/o HA and vomiting.

BP is 240/140. Skin findings are digital pitting at the ends of the fingers, thickening of the skin over the fingers and dorsum of the hands, and thickening with poikilodermic changes over the skin of the anterior chest.

HCT 32%, Platelets 75, Cr 1.5, UA 2+ protein. Peripheral smear shows diminshed platelet numbers and schistocytes.

What is the dx? tx?

A

Scleroderma Renal Crisis

  • HTN Emergency
  • HA
  • Microangiopathic hemolytic anemia
  • Thrombocytopenia
  • Elevated Cr
  • Proteinuria

Tx: ACEI (Captopril)

52
Q

anti-U1-ribonucleoprotein (RNP) antibodies

A

MCTD

53
Q

What is the treatment for severe acute refractory gout?

A

Off label treatment with IL-1 inhibitor

Anakinra or canakinumab

54
Q

When is the best time to use cholchicine for an acute gout flare?

A

Within 24h

Any longer than that and it will be ineffective

55
Q

What are the serum urate goals in patients with gout?

A

<6

<5 if they have tophi

56
Q

What is the max dose of Allopurinol?

A

800mg and the dose should be this high if the patient can tolerate it before adding on more therapy.

57
Q

What serum lab values would help differentiate gout from pseudogout?

A

Gout: Serum urate will be high

Pseudogout: Ca level will be high

58
Q

82F with 3y h/o joint pain and stiffness presents with 3d h/o L wrist pain and swelling. She does not have RA. She has CKD3 and HTN on HCTZ, BB and Losartan.

Decreased range of motion of both wrists and a few metacarpophalangeal (MCP) joints is noted, and shoulder abduction is limited to 90 degrees passively. The left wrist is swollen and tender. There are no subcutaneous nodules at the elbows, hands, or heels.

Laboratory studies:

  • Erythrocyte sedimentation rate: 51 mm/h
  • Urate: 4.3 mg/dL (0.25 mmol/L)
  • Rheumatoid factor: 15 U/mL (15 kU/L)

Anti–cyclic citrullinated peptide antibodies: Negative

Radiographs show osteoarthritic changes at the second through fourth MCP joints bilaterally, both wrists, and glenohumeral joints. Chondrocalcinosis is seen in the knees and both wrists. There are no periarticular erosions in the wrists or hands.

What is the dx? Tx?

A

Chronic calcium pyrophosphate arthropathy is a “pseudo-rheumatoid arthritis”

Tx: low dose steroids. low dose colchicine or NSAIDs would be an option. Allopurinol wont work with pseudogout because it’s not a uric acid issue. NSAIDs wouldn’t work for this patient with CKD and HTN.

59
Q

26F with 3d h/o fatigue, chills, and joint pain in the fingers of the left hand, left wrist, and right ankle. There is no travel history. She is currently taking ibuprofen for her symptoms; she also takes an oral contraceptive pill.

temperature is 39.0 °C (102.2 °F), blood pressure is 114/72 mm Hg, and pulse rate is 106/min. Fusiform enlargement of the second and fourth digits of the left hand with pain on extension is noted. Tenosynovitis over the dorsum of the left wrist and at the right ankle is present.

A painless lesion on the palm is shown.

What is this?

A

Disseminated gonococcal infection

Triad of;

  1. Tenosynovitis
  2. Dermatitis (usually painless pustular or vesiculopustular lesion)
  3. Polyarthralgia without frank arthris
  • Fever, chills, malaise
60
Q

How do you treat PMR? How do you treat relapses?

A

PMR is characteristic in that it responds dramatically to low-dose prednisone (12.5-20mg/d).

Taper after 1-2mo

Relapse: Go back to last dose patient was doing well at.

Note: If they do not respond to low dose prednisone, you should consider an alternative dx

61
Q

What other rheumatologic diseaes is ass’d with giant cell arteritis?

A

Polymyalgia rheumatica

Note: PMR is not a vasculitis, but it’s ass’d with one.

62
Q

What is the vasculitis ass’d with young women with BP discrepancies in arms and reduced pulses?

A

Takayasu Arteritis

  • Granulomatous vasculitis
  • Young, Asian women
  • Aorta and major branches
  • Claudication, cardiac ischemia, AR or MR, Dissection and renal artery stenosis
63
Q

65M with 1mo h/o malaise, fatigue, 8lb weight loss, R foot weakness and numbness, testicular pain, and a painful rash on his legs.

2mo was dx with HTN, started on HCTZ.

165/90. The left testicle is tender. Small necrotic ulcers are noted on the legs. Numbness of the right lateral ankle and calf is noted, as well as weakness of right foot plantar flexion.

Laboratory studies:

  • Erythrocyte sedimentation rate: 100 mm/h
  • Hemoglobin: 10 g/dL (100 g/L)
  • Leukocyte count: 13,000/µL (13 × 109/L)
  • Platelet count: 430,000/µL (430 × 109/L)
  • Creatinine: 1.7 mg/dL (150.3 µmol/L)
  • ANCA: Negative
  • Urinalysis: Normal

Renal angiogram shows microaneurysms of the renal arteries. A deep skin biopsy (deep dermis and subcutis) shows panmural inflammation with necrosis of a medium-sized artery.

What is this?

A

Polyarteritis Nodosa

  • Medium sized vasculitis
  • Hep B/HIV/Hairy Cel Leukemia
  • Symptoms: constitutional and neurological (mononeuritis mulitplex)
  • Skin rash
  • Kidney involvement (HTN d/t renal artery vasculitis with infarction)
64
Q

What is the treatment for primary angiitis of the CNS?

A

Cyclophosphamide and high dose glucocorticoids

Most of these patients will have permanent neurological impairment and 27% recurrence.

65
Q

What is the treatment for relapse of granulomatosis with polyangiitis?

A

Rituximab

66
Q

Biopsy of a skin ulcer shows nongranulomatous, necrotizing small-vessel vasculitis with immunofluorescence negative for immune complexes.

Whta is this in a patient intubated with DAH?

A

Microscopic polyangiitis.

Gold standard of dx is nongranulomatous, necrotizing pauci-immune vasculitis of small vessels.

67
Q

How do you make the dx of IgA Vasculitis (Henoch-Schonlein purpura)?

A

Biopsy of the affected organ

Typically the skin as this organ is always affected.

Biopsy will show a leukocytoclastic vasculitis with predominace of IgA depositis on immunofluorescence.

Note: Measuring IgA levels is not helpful.

68
Q

35F with L sided pleuritic chest pain and SOB for 1d. 4 weeks ago she started spiking fevers 1-2 times/day with pharyngitis, intermittent rash on the trunk and proximal extremities when the fevers spiked, severe joint pain, and myalgia. She had a baby 10 weeks ago.

Fever 102.2. She has cervical lymphadenopathy and hepatosplenomegaly. Pleural friction rub is present. She has a pink maculopapular rash on her trunk. She has tenderness and swelilng on her wrists, knees and ankles.

Labs;

  • ESR: 90
  • Hb: 10
  • WBC: 20
  • ALT: 80
  • AST: 70
  • Ferritin: 6000
  • UA: wnl

What is the dx?

A

Adult onselt Still disease (AOSD)

  • Spiking fever
  • Evanescent salmon-colored rash
  • Arthritis
  • Lymphadenopathy
  • extremely high ferritin
  • may be seen during pregancy or post-partum
69
Q

55M with joint pain and swelling, erythema nodosum, and hilar lymphadneopathy on CXR. What is the dx and what is the next step in management?

A

Lofgren syndrome: Acute arthritis, hilar lymphadenopathy, and erythema nodosum. This is a rheumatologic manifestation of Sarcoidosis.

Mgmt: No further management if all 3 of the above criteria are met

70
Q
A