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Senoir 21-2 > VASCULITIS > Flashcards

VASCULITIS Flashcards

1
Q

What is the vasculitis most common to Turkey

A

Behcets

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2
Q

What is the vasculitits most common to japan

A

Kawasakis syndrome

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3
Q

What vasculitis is most common with Hep C

A

Cryoglobulinemia

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4
Q

What vasculitis is most common with Hep B

A

Polyarteritis Nodosa

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5
Q

What separates Giant Cell and Takayasu

A

If older than 50 = giant cell

If younger than 50= takayasu

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6
Q

50 % of Giant cell pts present with what other vasculitis

A

Polymyalgia Rheumatica : Aching and stiffness of the shoulders, neck and hip-girdle area

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7
Q

When should Bx be done for Giant Cell arteritis

A

Needs to be done within 2 weeks of steroids before biopsy results will be altered

Consider second biopsy if clinical suspicion is high after initial negative biopsy

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8
Q

If a pt with Giant cell arteritis develops transient vision loss

What should be done

A

Patients with suspected GCA who have experienced transient visual loss for a few hours should be admitted and given high-dose intravenous methylprednisolone (eg, 1000 mg/day) for 3–5 days.

Then transitioned to oral prednisone 40-60mg daily.

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9
Q

If a pt has giant cell without vision loss

What is the Tx?

A

Prednisone 1mg/kg max;60mg/ day

X 1 year

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10
Q

When can steroid taper start in pts with giant cell

A

After the first month of treatment, almost all patients will have a normal ESR

  • At this point, the prednisone can begin to be tapered by 10% every week or two
  • When patients reach 10 mg, decrements of 1 mg every 2 or so weeks may reduce the chance of flare

Consideration of addition of low dose aspirin 81mg may reduce chance of associated visual loss or stroke

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11
Q

How old is the Dx for Polymyalgia Rheumatica

A

50 and older

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12
Q

A 50 year old pt report morning MUSCLE stiffness and aching that last longer than 30 minutes (not in the joint)

Think

A

Polymyalgia Rheumatica

Stiffness involves at least two of the following three areas:

  • Neck or torso
  • Shoulders or proximal regions of the arms
  • Hips or proximal aspects of the thighs
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13
Q

What is the treatment appraoch to polymaylagia Rheumatica

A

PMR alone is usually treated with 10–20 mg/day of prednisone.
-If the patient does not improve within the first week, doubt should be cast on the diagnosis of PMR.

Prolonged corticosteroid taper. Most patients require treatment for 1-2 years.

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14
Q

What are the important late complications of giant cell arteritis

A

Thoracic aortic aneurysms and aortic dissection are important late complications

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15
Q

Define Takayasu’s Arteritis

A

Granulomatous Vasculitis of the Aorta and its major branches

Preferentially affects young women

Distinguishing characteristics related to aorta/branch involvement

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16
Q

A 20 year old woman presents with absent pulse or bruit, Claudication, or HTN +/- fever of unknown origin

Think what vasculitis

A

Takayasu’s

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17
Q

A 20 year old woman that complains of Claudication while drying her hair
.. think

A

Takayasus

Look for abNML pulses or unequal BP
Bruits, or HTN

Murmurs: AR
Or Angina from stenosis of the ostia of the coronary arteries

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18
Q

What is the tx approach to Takayasu’s

A

High dose prednisone 1mg/kg/day x 1 month -> Taper to 10mg/day over 4-6 months
-Very effective but relapse is common

Addition of Methotrexate or Mycophenolate Mofetil to prednisone may provide added benefit

May require Surgical intervention for heart conditions

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19
Q

What is the vasculitis associated with HLA B51

A

Behcets

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20
Q

What types of vessels does Behcets affect?

A

Inflammatory vasculitis that affects large, medium, and small blood vessels.

Affects both arteries and veins

Arterial inflammation leads to occlusion, aneurysm, or rupture

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21
Q

What is the hallmark sign of Behcets

A

painful aphthous ulcers in the mouth and genitalia

  • Tongue, gums, oral cavity
  • Genital lesions –similar, but don’t occur in all pts
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22
Q

What is the major difference in the lesions of Behcets and sarcoidosis or IBD ?

A

Erythema nodosum–like lesions that tend to ulcerate

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23
Q

What are the 4 major S/s of Behcets

A

Painful apthous ulcers

Erythema Nodusom like lesions that then ulcerate

Anterior or posterior Uvetitis

And neurologic lesions than mimic MS

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24
Q

Define Polyartetits Nodosa

A

Necrotizing inflammatory vasculitis of medium arteries and muscular arterioles

Spares venous circulation and capillaries (confined to arterial circulation)

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25
Q

What is required for Dx of Polyartertis Nodosa

A

Angiogram or biopsy of involved organ required for diagnosis

  • Lung is usually spared
  • Granulomatous inflammation absent
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26
Q

What is the onset of PAN following HEP B infection

A

Within 6 months

27
Q

A pt presents with severe abdominal pain + peripheral neuropathy and mononerutitis multiplex (wrist/foot drop), Palpable purpura, lívido reticularis, and skin ulcers

Think of what condition that is assoc with HEP B infection

A

PAN

28
Q

What separates polyangitis nodosa from microscopic polyangitis

A

PAN does not involve the lungs/ Pulm

29
Q

What are the key Lab tests for PAN

A

HBV testing at time of initial diagnosis

True PAN is ANCA-negative

And Bx: Characteristic transmural necrosis and a homogeneous, eosinophilic appearance of the blood vessel wall (fibrinoid necrosis)

30
Q

What is the Tx approach to PAN

A

Prolonged high dosed corticosteroids

Cyclophosphamide (Cytoxan)
-For patients whose disease is refractory to glucocorticoids
or
-who have serious involvement of major organs (GI; mononeuritis multiplex)

31
Q

What are the 4 keys to Dx buergers

A

recognition of clinical findings-digital ischemia without other organ involvement

identification of typical pattern in angiography

exclusion of diseases that may mimic Buerger

confirmation that ongoing tobacco exposure is present

32
Q

What is the age of onset for Kawasakis

A

Most commonly in kids 3 months to 5 years old

-Typically Asians or native Pacific Islanders

33
Q

A 4 year old pt presents with a fever for 5 days!, with bilateral non exudative conjunctivitis, strawberry tongue/ cracked lips, with erythema to the hands and feet, + a polymorphous rash

Think

A

Kawasaki’s

34
Q

What is the treatment for a child with kawasakis

A

IVIG within the first 10 days of illness!
-Dramatically reduce risk of cardiac morbidity (coronary aneurysms)

+Aspirin (low-dose as effective as high-dose)

If unresponsive to IVIG, can use cyclosporine

Glucocorticoids reserved for salvage therapy in which IVIG and ASA failed

35
Q

What is the classic finding for small vessel vasculitis

A

Palpable purpura

36
Q

What is the most common vasculitis in children

A

HENOCH-SCHONLEIN PURPURA

37
Q

What are the hallmarks of HENOCH-SCHONLEIN PURPURA

A

Pathologic hallmarks of HSP are a leukocytoclastic (neutrophil debris) vasculitis and deposition of IgA in the walls of involved blood vessels.

Onset typically ~10 days after a URI

38
Q

What is the tetrad of henoch schonlein purpura

A

The tetrad of purpura, arthritis, glomerulonephritis, and abdominal pain is often observed.

However, this is not required for Dx

39
Q

A child (less than 20 yo) presents with palpable purpura, bowel angina, and vessel wall granuloctyes on BX

Think

A

Henoch Scholein

40
Q

HENOCH-SCHONLEIN PURPURA Tx

A

NSAIDs
-can aggravate GI symptoms and should be avoided with renal disease

Dapsone
-Antibiotic & anti-inflammatory

Glucocorticoids

Hospitalization
-Severe cases (Renal Failure)

41
Q

What are cryoglobulins

A

Immunoglobulins (antibodies IgG, IgM) that precipitate out of blood at low temperatures (< 37oC)

42
Q

What is the most common involved organ for Cryoglobulinemia

A

The skin

Other frequently affected organs include the joints, peripheral nerves, and kidneys.

43
Q

What is the most common serum marker found in Cryoglobulinemia

A

RF postive

44
Q

What is the pt demographic that has the worst prognosis with Cryoglobulinemia

A

Lower survival rates are observed with age over 60 years, male sex, and renal involvement.

45
Q

What are the diseases that are assoc with Cryoglobulinemia

A

Associated with malignancy (multiple myeloma), Hepatitis C, Sjogren and systemic lupus erythematosus

46
Q

What are the labs for Cryoglobulinemia

A

RF present in Types II & III
ESR/CRP elevated
Complement is decreased (just like in Sjogren)

47
Q

What is the tx for Cryoglobulinemia

A

Usually focused on the underlying cause (usually hepatitis C)

  • Ledipasvir/sofosbuvir (Harvoni)
  • Ribavarin (Copegus)

Antiviral strategies are commonly combined with B cell depletion approaches
-Rituximab (Rituxan)

Some cases can evolve to malignant B cell lymphoma

48
Q

A pt that presents iwth necrotizing vasculitis + upper/ lower resp and renal manifestations

Think

A

GRANULOMATOSIS WITH POLYANGIITIS

49
Q

What is the hallmark of GRANULOMATOSIS WITH POLYANGIITIS

A

Hallmarks: Granulomatous inflammation, vasculitis, and necrosis

Age onset; 50

50
Q

What are the key findings in Granuloatousus with polyangitis

A

ANCA positive

+ saddle nose (sinus: rhino, epistaxis)
Normochromic normocytic anemia

Must get cANCA and BX ( Lung>kidneys>URI)
(CT>CXR)

51
Q

What is the most common CXR finding in GPA

A

Pulm infiltrates and nodules

52
Q

What is the treatment for GPA (severe and Limited)

A

Severe: life threatening: Rituxiab and steroids
Or Cyclophosphamide and steroids

Limited: Methotrexate and steroids

All should receive Pneumocystis jiroveci pneumonia prophylaxis
-Sulfamethoxazole-trimethoprim, Dapsone

53
Q

What are the hallmarks of eosinophila granulomatous polyangitis

A

Asthma, eosinophilia, and systemic vasculitis are the hallmarks of eosinophilic granulomatosis with polyangitis

54
Q

What are the classic necrotizing features of EGPA

A 
Allergic rhinitis and nasal polyposis
Reactive airway disease
Peripheral eosinophilia
Fleeting pulmonary infiltrates and occasional alveolar hemorrhage
Vasculitic neuropathy
Congestive heart failure
55
Q

What is the serum marker for EGPA

A

Approximately 50% of patients with EGPA have antineutrophil cytoplasmic antibodies (ANCAs), usually with a specificity for myeloperoxidase (MPO).

MPO-ANCAs usually produce a perinuclear-ANCA (P-ANCA) pattern on serum immunofluorescence testing

56
Q

What are the three phases of EGPA

A

Prodromal phase: characterized by allergic disease, (allergic rhinitis, or asthma)

Eosinophilic phase: peripheral blood eosinophilia and eosinophilic infiltration of multiple organs, heart, lung, GI tract and others.

Vasculitic phase: a life-threatening systemic necrotizing vasculitis of small & medium vessels – wide range of organs including heart, lungs, peripheral nerves and skin

57
Q

What is the key differnce in GPA vs EGPA

A

ASTHA in EGPA

58
Q

What is the most common cardiac manifestation of EGPA

A

CHF

59
Q

What is the treatment for EGPA

A

Steroids to induce remission

Azathioprine, methotrexate, or mycophenolate can be added to corticosteroids for moderate cases

60
Q

What is the most common cause of pulmonary renal syndomre of alveolar hemorrhage and Glomerulonephritis

A

Microscopic polyangitis

61
Q

What are the main differences in microscopic polyangitis and polyarteritis nodosa

A

Main differences: ANCA positivity, vein AND artery involvement, glomerulonephritis & lung involvement

62
Q

If a pt is on PTU for hyperthyroidism

What is the vasculitis d/o that is an increased risk

A

Microscopic polyangitis

63
Q

What is the treatment of choice in microscopic polyangitis

A

Traditionally combo therapy with glucocorticoids and cytotoxic agents (cyclophosphamide)

Rituximab now preferred over cyclophosphamide due to superior long-term side effect profile.

If rituximab cannot be given or if the patient does not respond to regimen, cyclophosphamide is treatment of choice.

Senoir 21-2 (77 decks)

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