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Cardiovascular Module > Vasculitis > Flashcards

Vasculitis Flashcards

1
Q

Vasculitis

A

Group of conditions where there is focal inflammation of blood vessels

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2
Q

Main type of vessel mostly affected by vasculitis

A

Arterial system

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3
Q

Arteritis

A

Inflammatory diseases that are primary lesions of arteries

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4
Q

Can necrosis occur in severe cases of arteritis ?

If yes what is the consequence of necrosis

A

Yes

superimposed occlusive thrombosis , Rupture of vessel and aneurysm

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5
Q

During healing of arteritis, can permanent stenosis of lumen occur ?

A

Yes

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6
Q

Pheblitis

A

Inflammation of vein with infiltration of layers of the veins and formation of thrombus

Edema , stiffness , pain, red cord formation

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7
Q

Is there etiologic or morphological classification of vasculitis

A

Not really , diseases overlap too much

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8
Q

Pathogenic classification of vasculitis

A

Direct infection

Immunologic - immune complex mediated

Immunologic - antineutrophil cytoplasmic autoAntibody mediated

Immunologic - direct antibody attack

Immunologic - cell mediated

Immunologic- unknown

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9
Q

Direct infection category

A

Bacterial

Rickettsial

Spirochetal

Fungal

Viral

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10
Q

Immune complex mediated classification

A

Infection

Henoch schonlein purpura

SLE & rheumatoid arthritis

Drug induced

Serum sickness

Cryoglobulinaemia

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11
Q

Immunologic - antineutrophil cytoplasmic autoAntibody mediated category

A

Wegeners granulomatosis

Microscopic polyarteritis nodosa

Churg strauss syndrome

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12
Q

direct antibody attack category

A

Good pasture syndrome

Kawasaki disease

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13
Q

cell mediated Category

A

Allograft organ rejection

Paraneoplastic vasculitis

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14
Q

Unknown immunological category

A

Giant cell

Takayasu

PAN Classic

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15
Q

Classification based on vessel size

A

Large vessel ( giant cell arteritis, takayasu arteritis )

Medium sized vessel ( pan classic , kawasaki, thromboangitis obliterans)

Small vessel ( wegener granulomatosis, churg Strauss, micro PAN, henoch schonlen purpura, essential cryoglobulinaemia, cutaneous leucocytoclastic)

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16
Q

2 main common mechanisms

A

Immune mediated

Direct invasion by microorganisms

17
Q

Can physical agents cause vascular inflammation

A

Yes

18
Q

Between directly induced infectious vasculitis and infection triggered immune vasculitis which one will respond to immunosuppressive therapy and which one will be worsen

A

infection triggered immune vasculitis will respond to immunosuppressive therapy

Devastating consequences if immunosuppressive therapy is administered in directly induced infectious vasculitis

19
Q

Immune mediated vasculitis pathogenesis ( Immune complexes)

A

Immune reactants & complements present in the serum
( In SLE => DNA-antiDNA complex)
( in cryoglobulinaemia => ig-complement complex)

10% from drug hypersensitivity ( drugs ( act like hapten)-serum protein complex)) penicillin or gold

After infectious agents => HBsAg & HBsAg-anti HBsAg complexes accumulate ( seen in pan , membrane-proliferative glomerulonephritis)

20
Q

Immune mediated vasculitis pathogenesis ( antineutrophil cytoplasmic autoantibodies)

A

Cytoplasmic ANCA

Perimuclear ANCA

21
Q

C-ANCA

A

Bind Proteinase 3

Associated with wegeners granulomatosis

22
Q

P ANCA

A

Specific for myeloperoxidase

Found in microscopic polyarteritis and churg strauss syndrome

23
Q

Polyarteritis nodosa

A

Group of systemic necrotizing vasculitides and usually thrombosis

Widespread distribution of arterial lesions
Medium sized and small muscular arteries
Multiple organ systems
Widespread ischemic tissue injury
Focal random and episodic

24
Q

What vasculature is spared in polyarteritis nodosa

A

Pulmonary vasculature

25
Q

Polyarteritis nodosa pathology

A

Lesions ( mostly in kidneys, heart, skeletal muscle, gi, NS) - affect whole circumference of smaller arteries or segment of large artery

Acute phase - whole thickness necrotic , neutrophils and eosinophils infiltration, intense inflammation in adventitia

Chronic phase- fibrosis , chronic inflammatory cell infiltration, thrombus organisation.

Possible formation of micro aneurysm

26
Q

Percentage of patient with polyarteritis nodosa that have HBsAg in serum

A

30%

27
Q

Clinical features of polyarteritis nodosa

A

Disease of young

Variation depending on organs

Severe cases have fever, leucocytosis, high ESR, prostration

Symptoms from ischemia in affected organs :
Paresthesia with nerves 
Angina and cardiac failure in heart 
Stroke from cerebral 
Acute abdomen , intestinal infarction

Severe and rapidly fatal
Can be prolonged over years with remission and relapse
Death from lesions in kidney, heart , other organs and hypertension

28
Q

Prognosis of polyarteritis nodosa

A

Poor

29
Q

Treatment of polyarteritis nodosa

A

Corticosteroids
Cytotoxic drugs
Treatment of HPT

30
Q

Giant cell arteritis ( temporal or cranial arteritis)

A

Acute and chronic , often granulomatous, inflammation of large and medium arteries

Can be systemic

31
Q

Commonest form of vasculitis

A

Giant cell arteritis

32
Q

Arteries involved in giant cell arteritis

A

Carotid Especially temporal artery

33
Q

Cause of giant cell arteritis

A

Unknown

34
Q

Pathology of giant cell arteritis

A

Partial destruction of artery wall due to inflammation of whole thickness

Infiltration in wall by multinucleate langhans, foreign body giant cells , phagocytosis of elastic lamina

Begin in media

Often involves long segment of artery with skip areas

Fibrous thickening at end stage of intima
Scaring of media
Thrombotic occlusion of lumen

35
Q

Clinical features of giant cells arteritis

A

Variable symptoms

Could just manifest as weakness , malaise , low grade fever , weight loss

More Specific symptoms: 
Headache 
Pain radiating into jaws, neck, tongue 
Facial pain
Visual disturbance and blindness 
Cerebral infarction 
Intermittent claudication of jaw
Localized reddening 
Tenderness 
Pain
Nodularity of arteries 
Scalp sensitive to pressure
36
Q

Treatment of giant cells arteritis

A

Steroid therapy

Cardiovascular Module (21 decks)

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