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Clinical lectures: Yr1 > Large-vessel vasculitis: Takayasu arteritis, Giant Cell Arteritis > Flashcards

Large-vessel vasculitis: Takayasu arteritis, Giant Cell Arteritis Flashcards

1
Q

Define vasculitis?

A

Heterogeneous group of conditions characterised by blood vessel wall inflammation

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2
Q

What are the 2 most common pathophysiologies of vasculitis?

A

Immune-mediated inflammation

Direct vascular pathogenic invasion

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3
Q

Apart from immune inflammation and pathogenic invasion, how can physical and chemical injuries to vessel walls cause vasculitis?

A

Factors such as mechanical trauma, toxins, radiation

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4
Q

Give the 3 primary ways of classifying vasculitides?

A

Vessel diameter

Involvement of immune complexes

ANCA-associated or not

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5
Q

Define granulomatous vasculitis?

A

Pathological process due to the destruction of vessels by a granulomatous infiltrate which contains different immune cell lines

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6
Q

Is Takayasu arteritis a type of granulomatous or non-granulomatous vasculitis?

A

Granulomatous

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7
Q

Which 3 blood vessels are characteristically inflamed in Takayasu arteritis?

A

Aorta

Major aortic branches

Medium-sized pulmonary arteries

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8
Q

How does Takayasu arteritis characteristically affect the upper extremities?

A

Causes weak pulse and bp

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9
Q

Which facial feature does Takayasu arteritis characteristically affect?

A

Eyes

Causes ocular disturbances

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10
Q

What is the ratio of females to males who develop Takayasu arteritis?

A

8:1

Much more prevalent in females

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11
Q

Which continent has the highest prevalence and incidence of Takayasu arteritis?

A

Asia

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12
Q

What is the typical onset age range for Takayasu arteritis?

A

25-40

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13
Q

In Takayasu arteritis, what is the first stage of progression, and which vessel does it occur in?

A

Scarring and thickening of aorta, arch branches due to granulomatous inflammation causes significant lumen narrowing

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14
Q

In the pre-pulseless/early symptoms of Takayasu arteritis, are symptoms specific or systemic?

A

Systemic symptoms

eg. weight loss, arthragia, fever, fatigue, claudication (muscle pain due to lack of oxygen that’s triggered by activity and relieved by rest)

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15
Q

Define claudication, and in which phase of Takayasu arteritis does it occur?

A

Muscle pain due to lack of oxygen that’s triggered by activity and relieved by rest

Early symptom/pre-pulseless phase

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16
Q

In which phase of Takayasu arteritis do ocular disturbances occur, and give 3 common examples?

A

Late symptom/pulseless phase

eg. visual field defects, retinal defects, blindness

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17
Q

In which phase of Takayasu arteritis does weak pulse and bp in upper extremities occur?

A

Late symptoms/pulseless phase

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18
Q

Give 2 common symptoms of pulmonary artery involvement in Takayasu arteritis, and which phase does this occur in?

A

Pulmonary hypertension

Bruits/vascular murmurs (sound caused by turbulent blood flow of blood in artery, possibly due to partial obstruction)

Occur in late symptoms/pulseless phase

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19
Q

What type of x-ray is done to investigate Takayasu arteritis?

A

Angiography: X-ray of blood vessels

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20
Q

What is meant by occlusion?

A

complete/partial blockage of blood vessel

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21
Q

Define aneurysmal dilation, and what is the other name for this?

A

Aortic root aneurysm

enlargement/bulging near aortic valve due to weakened vessel walls

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22
Q

Define coarctation?

A

Narrowing in aortic arch

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23
Q

What are the 3 characteristic radiological findings on an angiogram, in Takayasu arteritis?

A

Coarctation (narrowing in aortic arch)

Aortic root aneurysm (Bulging near aortic valve due to weakened walls)

Occlusion (complete/partial blockage of blood vessel)

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24
Q

What lab test is done to diagnose Takayasu arteritis, and what is the characteristic finding?

A

FBC

Normocytic normochromic anaemia: Low number of normal-sized (normocytic) and normal red-coloured (normochromic) RBCs

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25
Q

Define normocytic normochromic anaemia?

A

Low number of normal-sized (normocytic) and normal red-coloured (normochromic) RBCs

26
Q

How is Takayasu arteritis generally managed?

A

High-dose glucocorticoids and immunosuppressants

27
Q

Do people with Takayasu arteritis have a high or low 5-year survival rate?

A

High (83%)

28
Q

Are people with Takayasu arteritis likely to make a full recovery in the long-term?

A

No, they are more likely to have visual, neurological deficits

29
Q

What are the other 2 names for Giant Cell Arteritis (GCA)?

A

Temporal arteritis

Cranial arteritis

30
Q

Is GCA a type of granulomatous or non-granulomatous vasculitis?

A

Granulomatous

31
Q

Which arteries are characteristically inflamed in GCA?

A

Arteries in head, mostly temporal arteries (around temples) and occipital arteries (posterior portion of neck and back of head)

32
Q

Which other rheumatological condition is GCA commonly associated with?

A

Polymyalgia rheumatica

33
Q

Give 2 of the largest risk factors for developing GCA?

A

Old age

North-European descent

34
Q

How does age affect risk of developing GCA?

A

Risk increases with age

35
Q

How does ethnic descent affect risk of developing GCA?

A

North-European descent is at higher risk

36
Q

What is the typical onset age for GCA?

A

Over 50 yrs old

37
Q

In GCA presentation, describe the person’s energy level?

A

Low energy, feel fatigued

38
Q

In GCA presentation, where does facial pain tend to occur and which 2 movements exacerbate it?

A

Jaw claudication

Worsened by chewing and talking

39
Q

In GCA presentation, where are headaches most intense and tender upon palpation and why?

A

Around temples

Because temporal arteries are there

40
Q

How does GCA commonly affect the scalp in 3 ways?

A

Tender scalp

Hair loss

Red, shiny ulcers

41
Q

How does GCA commonly cause temporal and occipital arteries to look and feel?

A

Thickened and bulging from skin

Tender, low pulsation

42
Q

Is GCA due to immune-mediated inflammation or vascular pathogenic invasion?

A

T-cell mediated immune response to antigen found in vessel wall leads to granulomatous inflammation and high interleukin levels

43
Q

Which artery is affected in GCA, to cause ocular problems?

A

Ophthalmic artery

44
Q

Is vision loss or vision disturbance more common in GCA?

A

Vision disturbance in 25-50% cases

Vision loss in 6-10% cases

45
Q

Give 4 examples of ocular problems that occur due to ophthalmic artery involvement in GCA?

A

Diplopia (double vision)

Visual hallucinations

Temporary monocular blindness

Complete blindness

46
Q

How does GCA affect the risk of aneurysms, and where are they most likely to occur?

A

Increases risk of aneurysms

Most likely to be aortic aneurysms

47
Q

Give 2 ways in which GCA can cause serious heart complications?

A

Aortic aneurysm

Myocardial infarction

48
Q

How does GCA affects the risk of strokes?

A

Increases risk of cerebral vascular accidents (strokes)

49
Q

What used to be the first-line investigation for diagnosing GCA, and why is it not first-line anymore?

A

Temporal artery biopsy

Negative biopsy result doesn’t rule out GCA as vascular inflammation is patchy and the non-inflamed tissue area could have been obtained for the sample instead

50
Q

Why does a single negative temporal artery biopsy not rule out GCA, and how can you be more sure to rule out GCA using this investigation?

A

Negative biopsy result doesn’t rule out GCA as vascular inflammation is patchy and the non-inflamed tissue area could have been obtained for the sample instead

Should obtain multiple samples to biopsy

51
Q

What is the current gold-standard for investigating GCA, and what is the characteristic sign?

A

Ultrasound imaging shows ‘halo’ sign

‘halo’ sign: dark thick border (edema/swelling in thickened vessel wall) surrounding narrowed arterial lumen

52
Q

When would you use PET scan to investigate GCA, and what is the main disadvantage?

A

When GCA affects deep vessels

Uses large amount of radiation

53
Q

Describe the CRP and ESR levels, in GCA?

A

Elevated

54
Q

Describe the 2 main findings of a FBC, in GCA?

A

Elevated platelet count

Normochromic normocytic anaemia

55
Q

Why is GCA a medical and ophthalmic emergency?

A

Causes complete blindness (as ophthalmic artery vasculitis can lead to sudden and permanent blindness)

Other life-threatening complications due to occlusion/rupture of arteries

56
Q

If someone has GCA and suspected blindness, what medication should you prescribe to have an effect within 48-72 hrs, and what is the starting dose?

A

Prednisolone

60-80 mg (weight-dependent)

57
Q

In GCA treatment, what should the dose of prednisolone ideally be after 8 weeks of administration?

A

Should be tapered down from 60-80mg to 10-15mg, after 8 weeks

58
Q

After the prednisolone dose has been reduced to 10-15 mg, how should it be further tapered and adjusted if there is a flare up, in GCA?

A

Now rate of reduction should decrease by 1 mg per month, if flare occurs then increase dosage again and try tapering in few weeks time

59
Q

To treat resistant cases of GCA, what medication is now used and for how long?

A

Tocilizumab can be used for resistant cases for 12 months

60
Q

When can bisphosphonates be taken to help treat GCA?

A

After assessing risk of osteoporosis and vitamin D sufficiency

Clinical lectures: Yr1 (28 decks)

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