Vascular Flashcards

1
Q

Aneurysm

A

Artery with dilatation >50% of original diameter

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2
Q

True vs false aneurysms

A

True: involve all layers of the arterial wall

False (pseudoaneurysms): collection of blood in adventitia which communicates with the lumen

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3
Q

Common aneurysm sites

A

Aorta (infrarenal most common)
Iliac
Femoral
Popliteal

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4
Q

Complications of aneurysm

A
Rupture
Thrombosis
Embolism
Fistulae
Pressure on other structures
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5
Q

Symptoms and signs of ruptured AAA

A

Intermittent or continuous abdominal pain, radiating through to back, iliac fossae or groin
Syncope
Expansile abdominal mass
Haemodynamic instability and shock

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6
Q

Symptoms and signs of unruptured AAA

A

Often no symptoms but may cause abdominal/back pain

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7
Q

RFs for AAA rupture

A

HTN
Smoking
Female
Strong FHx

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8
Q

Mx of ruptured AAA

A

Contact vascular surgeon and experienced anaesthetist, advice theatre
IV access with 2 large-bore cannulae
ECG, bloods (lipase, Hb, crossmatch)
Keep SBP

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9
Q

Features of polymyalgia rheumatica (PMR)

A

Age >50 years
Subacute onset (less than 2 weeks) of bilateral aching, tenderness and morning stiffness in shoulders and proximal limb muscles +/- mild polyarthritis, tenosynovitis and CTS
May be associated with fatigue, fever, LOW, anorexia, depression
NOT associated with true weakness

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10
Q

Ix in PMR

A

CRP
ESR >40 but may be normal
CK normal (cf myositis, myopathy)

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11
Q

Mx of PMR

A

Prednisolone 15mg/day (wean over months, according to symptoms and ESR; most need steroids for >2 years so give gastric and bone protection)
Expect a dramatic response within 1 week

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12
Q

Steroid SEs

A

GIT: pancreatitis, candidiasis, ulceration
MSK: myopathy, OP, #, growth suppression
Endocrine: adrenal suppression, Cushing’s syndrome (HTN, hyperglycaemia)
CNS: aggravated epilepsy, depression, psychosis
Eye: cataracts, glaucoma, papilloedema
Immune: increased susceptibility to and severity of infections
Fever, increased WCC (rarely cause leucopenia)

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13
Q

DDx for PMR

A
Recent onset RA
Polymyositis
Hypothyroidism
Primary muscle disease
Occult malignancy or infection
OA (esp cervical spondylosis, shoulder OA)
Neck lesions
Bilateral subacromial impingement
Spinal stenosis
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14
Q

What is vasculitis?

A

Inflammatory disorder of blood vessel walls resulting in destruction (aneurysm/rupture) or stenosis
May be primary or secondary
Classified according to main size of blood vessel affected

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15
Q

Causes of secondary vasculitis

A

SLE
RA
Hepatitis B and C
HIV

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16
Q

Large vessel vasculitis

A

GCA

Takayasu’s arteritis

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17
Q

Medium vessel vasculitis

A

Polyarteritis nodosa

Kawasaki disease

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18
Q

ANCA+ small vessel vasculitis

A

p-ANCA associated microscopic polyangiitis
Churg-Strauss syndrome
c-ANCA associated with Wegener’s granulomatosis

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19
Q

ANCA- small vessel vasculitis

A

Henoch-Schonlein purpura
Goodpasture’s syndrome
Cryoglobulinaemia

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20
Q

Other causes of vasculitis

A

Malignancy-associated vasculitis

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21
Q

Sx of vasculitis

A

Differs depending on affected organs; should be considered in any unidentified multisystem disorder
May presents just as overwhelming fatigue with increased ESR or CRP

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22
Q

Is a severe vasculitis flare a medical emergency? Why/why not?

A

Yes

Organ damage may occur rapidly (e.g. critical renal failure within 24 hrs)

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23
Q

Epidemiology of GCA

A

Elderly (if under 55 consider Takayasu’s)

Associated with PMR in 50%

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24
Q

Sx of GCA

A

Headache
Temporal artery and scalp tenderness (e.g. when combing hair)
Jaw claudication
Amaurosis fugax or sudden blindness (typically unilateral)
Extracranial Sx: dyspnoea, morning stiffness, unequal or weak pulses

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25
Q

Mx of suspected GCA

A

Order ESR and commence prednisolone 60mg/day PO IMMEDIATELY
Risk is irreversible bilateral vision loss which can occur suddenly (some advocate IV methylpred for 3 days if there are visual Sx)

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26
Q

Ix findings in GCA

A

Increased ESR and CRP
Increased platelets, decreased Hb
Increased ALP
Definitive: temporal artery biopsy (within 7 days of starting steroids; skip lesions occur so don’t be put off by negative biopsy)

27
Q

Prognosis of GCA

A

Typically a 2 year course then complete remission
Reduce prednisolone once Sx have resolved and ESR has decreased (increase if Sx recur)
Main cause of death and morbidity is long-term steroid treatment so consider risks and benefits, provide gastric and bone protection (PPI and bisphosphonate)

28
Q

What is polyarteritis nodosa (PAN)?

A

Necrotising vasculitis that causes aneurysms and thrombosis in medium-sized arteries, leading to infarction in affected organs and severe systemic symptoms

29
Q

Epidemiology of PAN

A

More common in males

May be associated with hepatitis B

30
Q

Sx of PAN

A

Typically systemic
Predominantly skin: rash and “punched out” ulcers
Renal, cardiac, GI and GU involvement

31
Q

Kawasaki disease

A

Childhood PAN variant (may get coronary aneurysms)

32
Q

Ix findings in PAN

A

Increased WCC, mild eosinophilia, anaemia
Increased ESR/CRP
ANCA -ive
Renal or mesenteric angiography (showing multiple aneurysms) or renal biopsy can be diagnostic

33
Q

Mx of PAN

A

Control BP meticulously
Specialist r/v
Most respond to corticosteroids and cyclophosphamide
Any HBV should be managed with an antiviral after initial treatment with steroids

34
Q

What is microscopic polyangiitis?

A

Necrotising vasculitis affecting small- and medium-sized vessels

35
Q

Sx of microscopic polyangiitis

A

Rapidly progressive glomerulonephritis (RPGN) usually features
Pulmonary haemorrhage in up to 30%
Other features rare

36
Q

Ix findings in microscopic polyangiitis

A

p-ANCA (MPO) positive

37
Q

Mx of microscopic polyangiitis

A

As for PAN (specialist involvement; most respond to corticosteroids and cyclophosphamide)

38
Q

Features of vasculitis by organ system

A

Systemic: fever, malaise, LOW, arthralgia, myalgia
Skin: purpura, ulcers, livedo reticularis, nailbed infarcts, digital gangrene
Eyes: episcleritis, scleritis, visual loss
ENT: epistaxis, nasal crusting, stridor, deafness
Pulmonary: haemoptysis and dyspnoea secondary to pulmonary haemorrhage
Cardiac: angina or MI (due to coronary arteritis), HF, pericarditis
GI: pain or perforation (infarcted viscus), malabsorption (chronic ischaemia)
Renal: HTN, haematuria, proteinuria, casts, renal failure (renal cortical infarcts; glomerulonephritis in ANCA +ive vasculitis)
Neurological: stroke, fits, chorea, psychosis, confusion, impaired cognition, altered mood, arteritis of vasa nervorum (arterial supply to peripheral nerves) may cause mononeuritis multiplex or sensorimotor polyneuropathy
GU: orchitis (testicular pain or tenderness)

39
Q

What is Takayasu’s arteritis?

A

AKA aortic arch syndrome, pulseless disease
Systemic vasculitis affecting the aorta and its major branches
Granulomatous inflammation causes stenosis, thrombosis and aneurysms

40
Q

Epidemiology of Takayasu’s arteritis

A

Rare outside of Japan!

Often affects women aged 20-40 years

41
Q

Sx of Takayasu’s arteritis

A

Dependent on arteritis involved
Aortic arch often involved, with cerebral, opthalmological and upper limb Sx (e.g. dizziness, visual changes, weak arm pulses)
Systemic features common: fever, LOW, malaise
HTN often a feature due to renal artery stenosis

42
Q

Complications of Takayasu’s arteritis

A

Aortic valve regurgitation
Aortic aneurysm and dissection
Ischaemic stroke (due to HTN or thrombus)
IHD

43
Q

Ix findings in Takayasu’s arteritis

A

Increased ESR and CRP

MRI/PET allows earlier Dx than standard angiography

44
Q

Mx of Takayasu’s arteritis

A

Predinisolone (1mg/kg/day PO)
Methotrexate or cyclophosphamide have been used in resistant cases
Angioplasty +/- stenting or CABG is performed for critical stenosis

45
Q

What is Henoch-Schonlein purpura (HSP)? Epidemiology, presentation, complications, Mx

A

Small vessel vasculitis, presenting with purpura often over buttocks and extensor surfaces, typically affecting young males
Complications: glomerulonephritis, arthritis, abdominal pain +/- intussusception (which may mimic “acute abdomen”)
Mx: mostly supportive

46
Q

What are purpura?

A

Non-blanching purple papules due to intradermal bleeding

47
Q

What is Churg-Strauss syndrome?

A

Triad of adult-onset asthma, eosinophilia and vasculitis (+/- vasospasm +/- MI +/- DVT) affecting lungs, nerves, heart and skin

48
Q

Complications of Churg-Strauss syndrome

A

Can get septic-shock picture (systemic inflammatory response syndrome, SIRS), may be accompanied by glomerulonephritis/renal failure (esp ANCA +ive)

49
Q

Mx of Churg-Strauss syndrome

A

Steroids

Biological agents if refractory disease (e.g. rituximab)

50
Q

What is Wegener’s granulomatosis?

A

Granulomatosis with polyangiitis (GPA)
Multisystem disorder of unknown cause characterised by necrotising granulomatous inflammation and vasculitis of small and medium vessels
Has a predilection for the upper respiratory tract, lungs and kidneys

51
Q

Sx of Wegener’s granulomatosis

A

Upper airways disease: nasal obstruction, ulcers, epistaxis, destruction of the nasal septum causing characteristic “saddle-nose” deformity, sinusitis
Renal disease: RPGN with crescent formation, haematuria and proteinuria
Pulmonary involvement: cough, haemoptysis, pleuritis
Others: skin purpura or nodules, peripheral neuropathy, mononeuritis multiplex, arthritis/arthralgia, ocular involvement

52
Q

Ix for Wegener’s granulomatosis

A

c-ANCA directed against PR3 is most specific
Increased ESR/CRP
Urinalysis: proteinuria, haematuria
CXR: nodules +/- fluffy infiltrate of pulmonary haemorrhage

53
Q

Mx for Wegener’s granulomatosis

A

Severe: corticosteroids and cyclophosphamide (or rituximab) to induce remission
Maintenance: azothioprine, methotrexate
Co-trimoxazole for prophylaxis against PJP and staphylococcal colonisation

54
Q

General principles of vasculitis Mx

A

Large vessels: steroids in most cases
Medium/small: steroids and IV cyclophosphamide (15mg/kg)
Azathioprine may be useful as steroid-sparing maintenance treatment

55
Q

Goodpasture’s syndrome

A

Pulmonary-renal syndrome
Characterised by acute glomerulonephritis + lung symptoms (haemoptysis/diffuse pulmonary haemorrhage) caused by anti-GBM Abs binding the kidney’s BM and alveolar membrane

56
Q

Ix findings in Goodpasture’s syndrome

A

CXR: infiltrates due to pulmonary haemorrhage, often in lower zones
Renal biopsy: crescenteric GN

57
Q

Mx of Goodpasture’s syndrome

A

Treat shock

Vigorous immunosuppressive treatment and plasmapheresis

58
Q

Raynaud’s syndrome

A

Peripheral digital ischaemia due to paroxysmal vasospasm, precipitated by cold or emotion
Fingers or toes ache and change colour: pale (ischaemia) to blue (deoxygenation) to red (reactive hyperaemia)

59
Q

Raynaud’s disease vs Raynaud’s phenomenon

A

Raynaud’s disease: idiopathic

Raynaud’s phenomenon: underlying cause

60
Q

Mx of Raynaud’s syndrome

A

Keep warm (gloves)
Stop smoking
Nifedipine
Evening primrose oil
Sildenafil
Prostacyclin for severe attacks/digital gangrene
In severe disease, consider chemical or surgical (lumbar or digital) sympathectomy

61
Q

Conditions in which Raynaud’s phenomenon may be exhibited

A

CTDs: systemic sclerosis, SLE, RA, dermatomyositis/polymyositis
Occupational: using vibrating tools
Obstructive: thoracic outlet obstruction, Buerger’s disease, atheroma
Blood: thrombocytosis, cold agglutinin disease, polycythaemia rubra vera, monoclonal gammopathies
Drugs: B-blockers
Endocrine: hypothyroidism

62
Q

Behcet’s disease

A

Systemic inflammatory disorder of unknown aetiology, common in Mediterranean and Chinese

63
Q

Sx of Behcet’s disease

A
Recurrent oral and genital ulceration
Uveitis
Skin lesions (e.g. erythema nodosum)
Arthritis (non-erosive large joint oligoarthropathy)
Thrombophlebitis
Vasculitis
Myo/pericarditis
CNS involvement (pyramidal signs)
Colitis
64
Q

Mx of Behcet’s disease

A

Colchicine for orogenital ulceration

Azathioprine or cyclophosphamide