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MSK + Rheumatology > Vasculitis > Flashcards

Vasculitis Flashcards

1
Q

What is vasculitis?

A

An inflammatory disorder of blood vessel walls.
- inflammation & necrosis of blood vessel walls with subsequent impaired blood flow.

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2
Q

Briefly describe the pathophysiology of vasculitis.

A

Inflammation and necrosis of blood vessel walls with subsequent impaired blood flow resulting in:

  1. Vessel wall destruction - aneurysm, rupture and stenosis:
    * Resulting in perforation and haemorrhage into tissues
  2. Endothelial injury:
    * Resulting in thrombosis + ischaemia/infarction of dependent tissues
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3
Q

According to which 2 factors is vasculitis classified?

A
  1. Size of the blood vessel involved.
  2. Presence or absence of anti-neutrophil cytoplasmic antibodies (ANCA).
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4
Q

What does ANCA stand for?

A

Anti-neutrophil cytoplasmic antibodies.

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5
Q

What are the 3 categories of vasculitis classified according to size?

A
  1. Large-vessel vasculitis:
    - Refers to the aorta and its major tributaries
  2. Medium-vessel vasculitis:
    - Refers to medium and small-sized arteries and arterioles
  3. Small-vessel vasculitis:
    - Refers to small arteries, arterioles, VENULES and capillaries
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6
Q

Give 2 examples of medium-vessel vasculitis.

A
  1. Classical polyarteritis nodosa (PAN)
  2. Kawasaki’s disease
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7
Q

Give 2 examples of ANCA-associated small-vessel vasculitis.

A
  1. Microscopic polyangitis
  2. Granulomatosis with polyangitis
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8
Q

Give 2 examples of ANCA-negative small-vessel vasculitis.

A
  1. Essential cryoglobulinaemia
  2. Cutaneous leucocytoclastic vasculitis
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9
Q

Which 2 features are found in ALL forms of vasculitis?

A
  1. Raised ESR
  2. Anaemia
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10
Q

Are the types of vasculitis common?

A

ALL RARE except giant cell (temporal) arteritis.

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11
Q

Give an infective condition associated with vasculitis (risk factor).

A

Subacute infective endocarditis

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12
Q

Giv 3 non-infective conditions associated with vasculitis (risk factors).

A

Non-infective:
1. Vasculitis with RA
2. SLE
3. Scleroderma
4. Polymyositis/dermatomyositis
5. Good pasture syndrome and Inflammatory bowel disease (UC/Crohn’s)

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13
Q

Give 2 examples of large-vessel vasculitis.

A
  1. Giant cell arteritis/polymyalgia rheumatic
  2. Takayasu’s arteritis
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14
Q

Describe the epidemiology of large-vessel vasculitis.

A
  1. Affects those > 50 YO.
  2. More common in FEMALES than males
  3. Systemic disease of the elderly - incidence increases with age
  4. Associated with polymyalgia & RA
  5. In general - it’s rare; GCA is the most common type
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15
Q

What is Polymyalgia Rheumatica (PMR)?

A

A condition that causes pain, stiffness and inflammation in the muscles around the shoulders, neck and hips.

Separate condition to GCA - but usually co-exist

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16
Q

Give 2 risk factors for PMR.

A
  1. SLE
  2. Polymyositis/dermatomyositis
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17
Q

Describe the clinical presentation of polymyalgia rheumatica (PMR).

A

Sudden onset of severe pain and stiffness of the shoulders
and neck, and of the hips and lumbar spine; a limb girdle
pattern.

Symptoms are worse in the morning, lasting from 30 mins -
several hours

Mild polyarthritis of peripheral joints.

1/3rd experience: fatigue, fever, weight loss, depression.

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18
Q

Investigations for Polymyalgia Rheumatica (PMR).

A
  1. Clinical history is usually diagnostic and the patient is ALWAYS OVER 50
  2. BOTH ESR & CRP RAISED - diagnostic
  3. ANCA negative
  4. Serum alkaline phosphatase raised
  5. Mild normochromic, normocytic anaemia may be present
  6. Temporal artery biopsy:
    * Shows giant cell arteritis in 10-30% cases
  • Note: creatinine kinase is normal - helps to distinguish from myositis / myopathies
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19
Q

Treatment for Polymyalgia Rheumatica (PMR).

A
  1. Corticosteroids with PPI + Alendronate + Ca2+ + Vit. D
    - e.g. Oral Prednisolone
    - Give a dramatic reduction of symptoms of PMR within
    24-48 hours of starting treatment
  • PPI e.g. lansoprazole = GI protection due to long-term use of steroids
  • Alendronate = bisphophonate for osteroporosis prevention dye to steroids
  • Ca2+ and Vit. D = bone protection
  • If improvement doesn’t occur: diagnosis should be questioned
  • Decrease dose slowly
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20
Q

Define giant cell arteritis (GCA).

A

Inflammatory granulomatous arteritis of large CEREBRAL ARTERIES as well as other large vessels e.g aorta, which occurs in association with PMR

*Arteritis = inflammation of the lining of the arteries

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21
Q

Pathophysiology of GCA:
In GCA, which layers of the artery are affected?
What is the net effect of this?

A

Tunica media + interna.

Arteries become inflamed, thickened, cause narrowing of the lumen and can obstruct blood flow.

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22
Q

Which arteries are commonly affected in GCA?

A
  1. Cerebral arteries
    - Common temporal (splits into frontal + temporal)
    - Linguinal / facial
  2. Opthalmic arteries
    - Cilliary (to retina)
23
Q

Give 5 cranial-related symptoms of GCA.

A
  1. Severe headaches
    - Abrupt temporal unilateral headaches
  2. Scalp tenderness
  3. Jaw claudication (when eating)
  4. Tenderness + swelling of one or more temporal or occipital arteries
    - Visible dilation of temporal artery on side of face
  5. SUDDEN PAINLESS VISION LOSS - EMERGENCY
    - Arteritic anterior ischaemic optic neuropathy - optic disc is very pale/swollen
24
Q

Give 3 non-cranial-related symptoms of GCA.

A
  1. Malaise, lethargy, chronic low grade fever
  2. Associated symptoms of PMR
  3. Dyspnoea, morning stiffness and unequal or weak pulses
25
What might you find on clinical investigation in someone with giant cell arteritis?
1. Palpable and tender temporal arteries with reduced pulsation. 2. Sudden monocular visual loss, the optic disc is pale and swollen.
26
What is the diagnostic criteria for GCA?
Diagnostic criteria - 3 or more of: 1. Age > 50 2. New headache 3. Temporal artery tenderness or decreased pulsation 4. ESR raised 5. Abnormal artery biopsy - inflammatory infiltrates present
27
What investigations might you do in someone who you suspect has giant cell arteritis?
1. Bloods: - Normochromic, normocytic anaemia - HIGH inflammatory markers - ESR and CRP - ANCA negative - Serum alkaline phosphatase may be raised 2. Temporal artery biopsy - DIAGNOSTIC!! - Should be taken BEFORE or within 7 days of starting high dose corticosteroids * Lesions are patchy so take a big chunk! 3. Ultrasound - Halo sign on US of temporal and axillary artery
28
Investigations for GCA: Temporal Artery Biopsy - what would you observe?
Lesions are patchy so take a big chunk! * Histological features: 1. Cellular infiltrates of CD4+ T lymphocytes, macrophages and giant cells (may not be visible in all cases) in the vessel wall = tightly-packed as if 1 giant cell 2. Granulomatous inflammation of the intima & media 3. Breaking up of the internal elastic lamina
29
What cells might you see on a histological slide taken from someone with GCA?
Neutrophils and giant cells.
30
Describe the treatment for GCA.
1. High-dose Corticosteroids RAPIDLY with PPI + Alendronate + Ca2+ + Vit. D e.g. PREDNISOLONE to stop vision loss - Gradual reduction of steroids over 12-18 months - PPI e.g. lansoprazole = GI protection due to long-term use of steroids - Alendronate = bisphophonate for osteroporosis prevention/prophylaxis due to steroids - Ca2+ and Vit. D = bone protection 2. Immunosuppressants that are used include: - Cyclophosphamide - Methotrexate - Azathioprine - Rituximab and other monoclonal antibodies 3. Monitor treatment progress by looking at ESR/CRP (should fall).
31
Define Polyarteritis nodosa (PAN).
A rare multi-system disorder characterised by widespread inflammation, weakening, and damage to small and medium-sized arteries.
32
Pathophysiology of Polyarteritis nodosa: what is the underlying pathology of PAN?
A vasculitis - fibrinoid necrosis of vessel walls with microaneurysm formation, thrombosis and infarction in medium sized arteries.
33
Give 3 risk factors for PAN.
1. Male 2. Hepatitis B 3. RA, SLE, scleroderma
34
Which vasculitis is most associated with Hep. B?
Polyarteritis nodosa (PAN).
35
List some general + systemic features of polyarteritis nodosa (PAN).
General - fever, malaise, weight loss, myalgia. Skin - skin lesions, purpura, livedo reticularis (a mottled, purplish, lace like rash), ulcers, gangrene. Cardiac - angina, HF, pericarditis. Renal - hypertension, haematuria, renal failure. GI - pain or perforation, malabsorption. GU - orchitis. Neuro - Mononeuritis multiple (Numbness, tingling, abnormal / lack of sensation and inability to move part of the body)
36
What investigations would you carry out in polyarteritis nodosa (PAN)?
1. Bloods: - Anaemia - WCC raised - ESR + CRP raised - ANCA negative (it's very rarely positive) 2. Angiography: * Demonstrates micro-aneurysms in hepatic, intestinal or renal vessels - "String of beads" pattern along the artery 3. Biopsy, of kidney in particular - To look for hypertension and other damage - can be diagnostic
37
How would you treat polyarteritis nodosa (PAN)?
1. BP control - ACEi e.g. Ramipril 2. Corticosteroids with Immunosuppressants - Prednisolone with Azethioprine / Cyclophosphamide 3. Hep. B should be treated with an antiviral after initial treatment with steroids
38
what size vessels does ANCA vasculitis affect?
small
39
what are the two ANCA associated vasculitides?
p-ANCA: microscopic polyangiitis, eosinophillic, UC, primary schlerosing cholangitis c-ANCA: granulomatosis with polyangiitis (aka wegeners)
40
eosinophilic granulomatosis presents similarly to
allergy | asthma
41
What is Henoch-Schoenlein purpura?
IgA vasculitis (small-vessel vasculitis) 1. Rash 2. Abdominal pain 3. Glomerulonephritis 4. Arthritis/arthralgia
42
Microscopic polyangiitis affects only the?
Kidney and lung
43
What is Granulomatosis with polyangitis (Wegener's granulomatosis)?
Granulomatosis with polyangiitis is a small vessel vasculitis. It was previously known as Wegener’s granulomatosis.
44
Is granulomatosis with polyangitis associated with c-ANCA or p-ANCA?
c-ANCA.
45
What organ systems can be affected by granulomatosis with polyangitis?
1. URT. 2. Lungs. 3. Kidneys. 4. Skin. 5. Eyes.
46
What is the affect of granulomatosis with polyangitis on the URT?
- Sinusitis. - Otitis. - Nasal crusting.
47
What is the affect of granulomatosis with polyangitis on the lungs?
- Pulmonary haemorrhage/nodules. - Inflammatory infiltrates are seen on X-ray.
48
What is the affect of granulomatosis with polyangitis on the kidney?
Glomerulonephritis.
49
What is the affect of granulomatosis with polyangitis on the skin?
Ulcers.
50
What is the affect of granulomatosis with polyangitis on the eyes?
- Uveitis. - Scleritis. - Episcleritis.
51
Describe the clinical presentation of granulomatosis with polyangitis.
Classic sign on exams: saddle shaped nose Epistaxis Crusty nasal/ ear secretions 🡪 hearing loss Sinusitis Cough, wheeze, haemoptysis
52
Diagnosis of granulomatosis with polyangitis.
High eosinophils on FBC. Histology shows granulomas. Presence of c-ANCA.
53
What is the treatment for granulomatosis with polyangitis?
- If severe: high dose steroids with immunosuppressants e.g. cyclophosphamide - If non-end organ threatening: moderate steroids.

MSK + Rheumatology (22 decks)

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