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MSK > Vasculitis > Flashcards

Vasculitis Flashcards

1
Q

Vasculitis

A

Inflammation of blood vessels

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2
Q

Vasculitis Pathogenesis

A

An inflammatory process causes transcription factor and collagen to be exposed.
Leads to the formation of a thrombosis.
The vessel wall becomes leaky.
Leading to aneurysm.
Fibrosis occurs due to fibrin deposition.
Thrombosis and fibrosis narrow the vessel.
Leading to Reduced Blood Flow.

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3
Q

Vasculitis Vessel Changes

A

Vessel Wall thickening.
Vessel Stenosis
Occlusion of vessels with subsequent infarction.

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4
Q

Large Vessel Vasculitis Types (2)

A

Giant cell arteritis

Takayasu Arteritis

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5
Q

Large Vessel Vasculitis Early Features

A 
Malaise
night Sweats
Weight loss 
Arthralgia
Fatigue
Claudicant Symptoms
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6
Q

Large Vessel Vasculitis Late Features

A

Vascular Stenosis
Aneurysms
Reduced pulses and bruit.

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7
Q

Large Vessel Vasculitis possible signs

A

Reduced pulses

Carotid Bruit

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8
Q

Giant Cell Arteritis - Arteries affected (3)

A

Temporal Artery
Opthalmis Artery
Facial Arteries
- jaw claudication if in facial arteries

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9
Q

Giant Cell Arteritis Epidemiology

A

Most common in women >50

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10
Q

Giant Cell Arteritis Histology

A

Granulomas are present in the elastic lamina

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11
Q

Takayasu Arteritis - Arteries affected

A

Affects the arteries off off the aortic arch

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12
Q

Takayasu Arteritis Epidemiology

A

Most common in Asian Women <40

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13
Q

Large Vessel Vasculitis Treatment

A

Treatment with 40-60mg Prednisolone

-Gradually reduced

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14
Q

Medium Vessel Vasculitis Types (3)

A

Kawasaki Disease
Polyarteritis Nodosa
Buerger’s Disease

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15
Q

Kawasaki Disease Features

A 
Conjunctivitis
Rash over body
Adenopathy
Strawberry Tongue
Hands and feet swelling 
Fever
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16
Q

Kawasaki Disease Treatment

A

Self-limiting.

Can be treated with IV Ig and Aspirin

17
Q

Polyarteritis Nodosa Pathology

A

Immune cells directly attack the endothelial cells.

Causes transmural necrosis. Leaves vessels prone to aneurysm.

18
Q

Polyarthritis Nodosa Investigations

A

Angiogram

-‘string of beads’

19
Q

Polyarthritis Nodosa Features

A

Can affect renal. lung and GI

  • If renal, can lead to hypertension
  • If GI, can lead to abdominal pain and GI bleeding
20
Q

Buerger’s Disease

A

Affecting vessels in fingers and toes

21
Q

Buerger’s Disease Risk Factor

A

Tobacco Use

22
Q

Buerger’s Disease Features

A

Blood clots occur.

Cause ulceration, auto-amputation and necrosis

23
Q

Small Vessel Vasculitis Types (4)

A
  1. Granulomatosis with Polyangiitis (GPA)
  2. Microscopic Polyangiitis (MPA)
  3. Eosinophilic granulomatosis with polyangiitis (EGPA)
  4. Henloch Schonlein Purpur
24
Q

Granulomatosis with Polyangiitis (GPA) Epidemiology

A

More common in men

Typical age 35-55

25
Q

Granulomatosis with Polyangiitis (GPA) Pathology

A

Granulomatous Inflammation of respiratory tract, small and medium vessels.

26
Q

Granulomatosis with Polyangiitis (GPA) Features

A 
Affects nasopharynx, lungs and kidneys 
Sinusitis 
Bloody mucus
Saddle Nose Deformities
Difficulty Breathing 
Relapse is common
27
Q

Granulomatosis with Polyangiitis (GPA) Investigations

A

cANCA +ve

anti-PR3

28
Q

Granulomatosis with Polyangiitis (GPA) Treatment

A

ANCA +ve vasculitis treated with IV steroids and cyclophosphamide

29
Q

Microscopic Polyangiitis (MPA)

A

necrotising vasculitis with few immune deposits.

30
Q

Microscopic Polyangiitis (MPA) Features

A

Doesn’t affect nasopharynx
No granulomas present
Can cause glomerulonephritis

31
Q

Microscopic Polyangiitis (MPA) Investigations

A

pANCA +ve

High eosinophil count.

32
Q

Eosinophilic granulomatosis with polyangiitis (EGPA)

A

Eosinophilic granulomatous inflammation of respiratory tract, small and medium vessels.

33
Q

Eosinophilic granulomatosis with polyangiitis (EGPA) Affected Sites

A 
Sinuses
Lungs
GI
Kidneys
Skin
nerve
Heart
34
Q

Eosinophilic granulomatosis with polyangiitis (EGPA) Features

A

Granulomas are present

Associated with asthma

35
Q

Eosinophilic granulomatosis with polyangiitis (EGPA) Investigations

A

Anti-MPO
anti-PR3
Increased eosinophils
No ANCA

36
Q

Henloch Schonlein Purpura

A

Non-ANCA Vasculitis

Acute IgA mediated disorder

Often past history of URTI

37
Q

Henloch Schonlein Purpura Pathology

A

IgA targets endothelial cells via molecular mimicry

38
Q

Henloch Schonlein Purpur Features

A

palpable purpura due to fibrosis occurring in affected vessel

  • over buttocks and lower legs
  • abdominal pain
  • vomiting
  • joint pain

Can occur in GI tract and kidneys
GI- Haematuria
Renal- IgA Nephropathy

39
Q

Henloch Schonlein Purpura Treatment

A

Can spontaneously resolve
Self limiting
Does not require treatment

MSK (35 decks)

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