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Vasculitis Flashcards

1
Q

What is vasculitis?

A

Vasculitis is inflammation of the blood vessel, often leading to ischaemia and necrosis of the tissue

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2
Q

What are the 3 main sub-types of vasculitis?

A

Large vessel
Medium vessel
Small vessel

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3
Q

What are the 3 sub-groups of small-vessel vasculitis?

A

Immune complex small-vessel vasculitis
Anti-GBM disease
ANCA-associated small-vessel vasculitis

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4
Q

What are some examples of large-vessel vasculitides?

A

Takayasu’s arteritis
Giant cell arteritis

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5
Q

What are some examples of medium-vessel vasculitides?

A

Polyarteritis nodosa
Kawasaki disease

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6
Q

What are some examples of immune complex small-vessel vasculitides?

A

Henoch-Schönlein
Hypocomplementemic urticarial vasculitis (Anti-C1q vasculitis)

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7
Q

What are some examples of ANCA-associated small-vessel vasculitides?

A

Microscopic polyangiitis
Granulomatosis with polyangiitis (Wegener)
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)

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8
Q

What are some factors that can cause secondary vasculitis?

A

Infection
Drugs
Toxins
Other inflammatory disorders
Cancer

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9
Q

What are some common features of all vasculitides?

A

Fever
Malaise
Weight loss
Fatigue

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10
Q

What is Takayasu’s arteritis?

A

This is a large cell vasculitis, most commonly affecting the aortic arch

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11
Q

Who is most at risk of Takayasu’s arteritis?

A

This is most commonly found in those under 40 years and in females

It is also more prevalent in Asian populations

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12
Q

What are some non-conventional features of Takayasu’s arteritis?

A

Claudication in arms
Blood pressure differences in extremities
Bruit (Most commonly in carotids)

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13
Q

What investigations are required in Takayasu’s arteritis?

A

Blood tests - Raised inflammatory markers
CT or MR angiography - Stenosis and vessel wall thickening

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14
Q

How is Takayasu’s arteritis usually managed?

A

Initial management of large vessel vasculitis is 40-60mg prednisolone, with steroid sparing agents given in Takayasu’s arteritis

These include leflunamide and methotrexate

Tocilizumab is a biologic that can be given

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15
Q

What is another name given to giant cell arteritis?

A

temporal arteritis

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16
Q

What is giant cell arteritis?

A

A type of systemic vasculitis affecting the large and medium arteries

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17
Q

Who is most at risk of Giant cell arteritis?

A

It is more commonly found in those over 50, and has a strong link with polymyalgia rheumatica and white ethnicity

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18
Q

What are some un-conventional symptoms of giant cell arteritis?

A
  • Unilateral acute temporal headache (Temporal artery)
  • Scalp tenderness
  • Temporary visual disturbances (Ophthalmic artery)
  • Blindness (Ophthalmic artery)
  • Jaw claudication
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19
Q

What are some features of giant cell arteritis not affecting the head?

A

Carpel tunnel syndrome
Peripheral oedema

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20
Q

What is the main clinical sign of giant cell arteritis?

A

Inflamed temporal artery

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21
Q

What investigations are required in giant cell arteritis?

A

Bloods - Raised ESR, CRP
USS
Temporal artery biopsy
PET, CT or CT angiogram

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22
Q

Why might a temporal artery biopsy be negative in giant cell arteritis?

A

Giant cell arteritis causes skip lesions

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23
Q

How is giant cell arteritis managed?

A

Initial management of large vessel vasculitis is 40-60mg prednisolone, with steroid sparing agents considered in GCA
These include leflunamide and methotrexate
This dose is then reduced over 18 -24 months

Tocilizumab is a biologic that can be given

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24
Q

What medication is given in giant cell arteritis, in cases of jaw claudication or visual symptoms?

A

In cases of visual symptoms or jaw claudication, 500-1000mg of methylprednisolone is given daily

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25
Q

What drugs can be given to counteract steroid side effects in giant cell arteritis?

A

PPIs, bisphosphonates, calcium and vitamin D can be given to counteract side effects of steroids (Gastric ulceration and bone destruction)

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26
Q

What is polyarteritis nodosa?

A

This is a systemic medium vessel condition occurring mostly in middle age to older patients

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27
Q

What are some causes of secondary polyarteritis nodosa?

A

Hepatitis B
Hepatitis C

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28
Q

What are some renal symptoms of polyarteritis nodosa?

A

Renal hypertension
Renal function impairment

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29
Q

What are some cutaneous presentations of polyarteritis nodosa?

A

Purpura
Livido reticularis
Ulcers

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30
Q

What is a common musculoskeletal symptoms of polyarteritis nodosa?

A

Muscle pain

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31
Q

What are some neurological presentations of polyarteritis nodosa?

A

Mononeuritis
Polyneuropathy

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32
Q

What are some gastrointestinal presentations of polyarteritis nodosa?

A

Abdominal pain
Diarrhoea (±blood)
Bowel perforation

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33
Q

What is livido reticularis?

A

A transient or persistent, blotchy, reddish-blue to purple, net-like cyanotic pattern that occurs in polyarteritis nodosa

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34
Q

What investigations are required in polyarteritis nodosa?

A

Biopsy of affected tissue
Angiogram
There are no specific blood tests

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35
Q

How is non-organ threatening polyarteritis nodosa treated?

A

In cases of non-organ threatening disease steroids are given with an immunosuppressant, such as azathioprine, methotrexate or mycophenolate

36
Q

How is organ threatening polyarterits nodosa treated?

A

Steroids are given with cyclophosphamide

37
Q

What is Kawasaki disease?

A

This is a very rare, medium cell vasculitis, also known as mucocutaneous lymph node syndrome, occurring mostly in children under 5

38
Q

Who is most at risk of Kawasaki disease?

A

Children under 5
Children from Northeastern Asia, especially Japan and Korea

39
Q

How does Kawasaki disease present?

A

Initially it presents as a normal infection, however, it then goes on to cause symptoms such as:
- High fever
- Widespread rash
- Bilateral conjunctivitis
- Strawberry tongue
- Coronary artery aneurysm

40
Q

What are the 2 main treatments of Kawasaki disease?

A

Aspirin
IV immunoglobulin

41
Q

What is used in Kawasaki disease that does not respond to IV immunoglobulin therapy?

A

Corticosteroids

42
Q

What are some general MSK and cutaneous symptoms of small vessel vasculitides?

A

Palpable purpura
Cutaneous ulcers
Arthrlagia
Myalgia/Myositis

43
Q

What are some common ENT presentations in small vessel vasculitides?

A

Sinusitis
Nasal crusting
Epistaxes
Mouth ulceration
Otitis media and deafness
Saddle nose (Cartilage damage)
Sub-glottic inflammation

44
Q

What are some respiratory symptoms of small vessel vasculitides?

A

Cough
haemoptysis
Pulmonary infiltrates
Diffuse alveolar haemorrhage
Cavitating nodules
Asthma

45
Q

What are some ocular symptoms of small vessel vasculitides?

A

Conjunctivitis
Episcleritis
Uveitis
Optic nerve artery vasculitis
Retinal artery occlusion
Proptosis-pseudotumour

46
Q

What are some neurological symptoms of small vessel vasculitides?

A

mononeuritis multiplex
Sensorimotor polyneuropathy
Cranial nerve palsy

47
Q

What is ANCA?

A

Anti-Neutrophil Cytoplasmic Antibodies

A form of auto-antibodies against the cytoplasms of neutrophils within the blood vessels

48
Q

What are the 2 forms of ANCA antibodies?

A

P-ANCA - MPO antibody - Against nucleus cytoplasm (P = Perinuclear)
C-ANCA - PR2 antibody - Against all cytoplasm (C= Cytoplasmic)

49
Q

What is Granulomatosis with polyangiitis (Wegener’s)

A

This is a vasculitis characterised by granulomatous inflammation, affecting the small and medium sized vessels of the lungs, eyes or kidneys

50
Q

Who is most at risk of developing GPA?

A

Northern Europeans
Males (Slightly)
35-55 years old

51
Q

What types of symptoms will occur in GPA?

A

Respiratory symptoms
Necrotising glomerulonephritis
Granulomatous inflammation
Nasal symptoms
Ocular features

52
Q

What respiratory symptoms are most common in GPA?

A

Upper airways disease
Pulmonary parenchymal disease

53
Q

What investigations are required in small vessel vasculitides?

A

Bloods
urine dipstick testing
Immunofluorescence
Biopsy

54
Q

What will blood testing show in small vessel vasculitides?

A

Raised ESR, PV and CRP
Anaemia in chronic disease
Complement activation
Abnormal U+E in renal involvement

55
Q

What will be seen on urine dipstick testing in small vessel vasculitides?

A

Haematuria

56
Q

What is the predominant antibody in GPA?

A

P-ANCA

57
Q

What further tests can be performed in small vessel vasculitis to show organ involvement?

A

CT chest scan
Nerve conduction testing
Muscle MRI
Tissue biopsy

58
Q

How is remission induced in organ threatening GPA?

A
  • Glucocorticoids + Rituximab/Cyclophosphamide
  • Avocopan - C5 inhibitor may be added
  • Plasma exchange when creatinine >300umol
59
Q

How is remission maintained in organ threatening GPA?

A
  • Tituximab or azathioprine/methotrexate
  • Mycophenolate or leflunamide
60
Q

How is resistant disease managed in organ threatening GPA?

A
  • Rituximab + Cyclophosphamide
  • IV immunoglobulin therapy
61
Q

How is remission induced in non-organ threatening GPA?

A

Glucocorticoids + Rituximab/Methotrexate/Mycophenolate

62
Q

How is remission maintained in non-organ threatening GPA?

A
  • Rituximab/Azathioprine/Methotrexate
  • Mycophenolate or Leflunamide
63
Q

What is microscopic polyangiitis?

A

Microscopic polyangiitis is a necrotising vasculitis of the small vessels, with few immune deposits, typically with pulmonary, renal and skin involvement

64
Q

What are the most common presentations of microscopic polyangiitis?

A

Glomerulonephritis
Nervous system dysfunction
Diffuse alveolar haemorrhage

65
Q

What is the predominant antibody found in microscopic polyangiitis?

A

C-ANCA

66
Q

How is remission induced in organ threatening microscopic polyangiitis?

A
  • Glucocorticoids + Rituximab/Cyclophosphamide
  • Avocopan - C5 inhibitor may be added
  • Plasma exchange when creatinine >300umol
67
Q

How is remission maintained in organ threatening microscopic polyangiitis?

A
  • Tituximab or azathioprine/methotrexate
  • Mycophenolate or leflunamide
68
Q

How is resistant organ threatening microscopic polyangiitis managed?

A
  • Rituximab + Cyclophosphamide
  • IV immunoglobulin therapy
69
Q

How is remission induced in non-organ threatening microscopic polyangiitis?

A

Glucocorticoids + Rituximab/Methotrexate/Mycophenolate

70
Q

How is remission maintained in non-organ threatening microscopic polyangiitis?

A
  • Rituximab/Azathioprine/Methotrexate
  • Mycophenolate or Leflunamide
71
Q

What is eosinophilic granulomatosis with polyangiitis (Churg-Strauss)?

A

Eosinophilic granulomatosis with polyangiitis is an aesinophilic inflammation affecting small and medium sized vessels, most commonly in the respiratory tract and skin

72
Q

How will EGPA most commonly present?

A
  • Nervous system dysfunction
  • Skin irritation
  • Late onset asthma
  • Granulomatous inflammation
73
Q

How can EGPA be distinguished from GPA?

A

EGPA will have a high eosinophil count and is a C-ANCA predominant condition

74
Q

What is the predominant antibody in EGPA?

A

C-ANCA

75
Q

How is remission induced in organ threatening EGPA?

A

Steroids + Cyclophosphamide

76
Q

How is remission maintained in organ threatening EGPA?

A

Azathioprine/Methotrexate/Mepolizumab/ Rituximab

77
Q

How is remission induced in non-organ threatening EGPA?

A

Steroids

78
Q

How is resistant, non-organ threatening EGPA managed?

A

Mepolizumab - IL5 inhibitor

79
Q

What is Henoch-Schönlein purpura (IgA Vasculitis)?

A

This is an acute IgA-mediated generalised vasculitis involving the small vessels of the skin, the GI tract, the kidneys, the joints, and rarely, the lungs and rarely, the CNS

80
Q

Who is most likely to get Henoch-Schönlein purpura?

A

HSP occurs mostly in children aged 2-11

81
Q

What is thought to cause HSP?

A

It is thought to be caused by a preceding URT infection, pharyngeal infection or GI infection, with group A streptococcus being the most common causative infection, occurring 1-3 weeks before HSP develops

82
Q

How does HSP usually present?

A
  • Purpuric rash, typically on the buttocks and lower limbs
  • Colicky abdominal pain
  • Bloody diarrhoea
  • Joint pain ± Swelling
  • Renal involvement (50%)
83
Q

How is HSP usually managed?

A

HSP is usually self limiting and symptoms tend to resolve within 8 weeks, however, relapses may occur for months to years

84
Q

How is resistant HSP treated?

A

Steroids and immunosuppressive drugs
urinalysis for renal involvement

85
Q
A

Musculoskeletal (123 decks)

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