Vascular Flashcards

1
Q

What is peripheral arterial disease?

A

Narrowing of arteries supplying limbs and periphery, reducing blood supply to these areas. Usually lower limb claudication.

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2
Q

What is intermittent claudication?

A

Cramping leg pain due to ischaemia in a limb, occurring during exertion and relieved by rest.

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3
Q

What is critical limb ischemia?

A

End-stage of peripheral arterial disease, where there is an inadequate supply of blood to a limb to allow it to function normally at rest. The features are pain at rest, non-healing ulcers and gangrene. There is a significant risk of losing the limb.
6Ps:
pain, pallor, pulseless, paralysis, parasethesia, perishing cold

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4
Q

What is acute limb ischemia?

A

Rapid onset limb ischemia - usually a clot in the arterial supply of the distal limb

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5
Q

Define necrosis and gangrene.

A

Necrosis = tissue death

Gangrene - due to inadequate blood supply

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6
Q

What is atherosclerosis?

A

Atheromas (fatty deposits in artery walls) and hardening and stiffening of the blood vessel walls (sclerosis). Caused by chronic inflammation and activation of immune system in artery wall. Lipids deposited first followed by fibrous atheromatous plaques. These cause stiffening, hypertension, heart strain; stenosis, and can rupture –> ischemia.

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7
Q

What is Leriche syndrome?

A

Leriche syndrome occurs with occlusion in the distal aorta or proximal common iliac artery. There is a clinical triad of:

Thigh/buttock claudication
Absent femoral pulses
Male impotence

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8
Q

How can you differentiate arterial and venous ulcers?

A

Arterial ulcers are caused by ischaemia secondary to an inadequate blood supply. They are painful, esp at night when elevated; peripheral, punched out, smaller, deeper, well defined borders, “punched-out”, reduced bleeding
Venous ulcers are caused by impaired drainage and pooling of blood in the legs.
Occur after a minor injury to the leg. Larger, superficial, irregular, gently sloping borders, gaiter area - mid-calf to ankle (more proximal),
signs of chronic venous insufficiency (e.g., haemosiderin staining and venous eczema), less painful and pain is worse on lowering the leg

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9
Q

How is peripheral arterial disease diagnosed?

A

Ankle-brachial pressure index (ABPI) = ratio of systolic blood pressure (SBP) in the ankle (around the lower calf) compared with the systolic blood pressure in the arm, taken manually using a Doppler probe.

0.9 – 1.3 = normal
0.6 – 0.9 = mild PAD
0.3 – 0.6 = moderate to severe PAD
< 0.3 = severe disease to critical ischaemic

An ABPI above 1.3 can indicate calcification of the arteries, making them difficult to compress. This is more common in diabetic patients.

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10
Q

What is the management for intermittent claudication?

A

Lifestyle change to manage modifiable risk factors for atherosclerosis - stop smoking, diet
Optimise medical treatment of comorbidities
Exercise training
Medical - atorvastatin 80mg, clopidogrel 75mg OD, naftidrofuryl oxalate (5-HT2 antagonist that dilates peripheral blood vessels)
Surgical - Endovascular angioplasty and stenting. Endarterectomy (cutting vessel open and removing plaque), bypass surgery. Think similar to cath lab

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11
Q

How is critical limb ischemia managed?

A

Urgent referral to vasc team, analgesia, revascularisation with EVAS, endarterectomy, bypass or amputation if unable to revascularise

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12
Q

How is acute limb ischemia managed?

A

Urgent referral to vascular.
Endovascular thrombolysis, endovascular thrombectomy, surgical thrombectomy, endarterectomy, bypass surgery, amputation if unable to revascularise.

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13
Q

What can cause stroke in someone with a DVT?

A

Septal defect (VSD, ASD)

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14
Q

What are thrombophilias? Give 5 examples

A
Thrombophilias are conditions that predispose patients to develop blood clots. Eg:
Antiphospholipid syndrome
Factor V Leiden 
Antithrombin deficiency
Protein C or S deficiency
Hyperhomocysteinaemia
Prothombin gene variant
Activated protein C resistance
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15
Q

How is VTE prevented?

A

Every patient admitted to hosp is assessed for risk, receive prophylaxis unless contraindicated (eg already on anticoags). This is usually with LMWH. Anti-embolic compression stocking are also used, contraindicated in significant peripheral artery disease.

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16
Q

How does a DVT present? Where do you measure the leg?

A

Calf or leg swelling 10cm below the tibial tuberosily, >3cm difference
Dilated superficial veins
Tenderness to the calf (particularly over the site of the deep veins)
Oedema
Colour changes to the leg

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17
Q

How is VTE diagnosed?

A
  1. D Dimer - exclude VTE where there is low suspicion. Raised in pneumonia, malignancy, HF, surgery, pregnancy
  2. Doppler - repeat in 1 week if negative but likely DVT
  3. CTPA or VQ for PE (eg CTPA CI in significant kidney impairment so cant have contrast)
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18
Q

How is VTE managed?

A

DOAC eg apixaban. Guideline change in 2020 from using LMWH.
Catheter directed thrombolysis for iliofemoral DVT.
Long term anticoag eg with DOAC:
3 months if reversible cause then review
6 months if uprovoked OR irreversible underlying cause eg APLS, cancer
IVC filter in rare cases of recurrent PE or unsuitable for anticoagulation.

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19
Q

How do you investigate an unprovoked DVT?

A

Review medical history, physical exam, baseliine blood results. Ask about FHx of VTE - hereditary thrombophilia. We no longer routinely do imaging.
If not continuing on anticoagulation, consider APLS antibodies

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20
Q

What are varicose veins?

A

Distended superficial veins measuring more than 3mm in diameter. Caused by valve incompetency from DVT, obesity, pregnancy, increasing age
May present with heavy sensation in legs, aching, oedema, cramps, restless legs, CVI

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21
Q

What are reticular veins?

A

Dilated blood vessels in the skin measuring less than 1-3mm in diameter

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22
Q

What is telangiectasia?

A

Dilated blood vessels in the skin measuring less than 1mm in diameter, also known as spider veins or thread veins.

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23
Q

What is chronic venous insufficiency and what are 3 signs?

A

When blood pools in the distal veins, the pressure (venous hypertension) causes the veins to leak small amounts of blood into the nearby tissues. The haemoglobin in this leaked blood breaks down to haemosiderin, which is deposited around the shins in the legs. This gives a brown discolouration to the lower legs.
Pooling of blood in the distal tissues results in inflammation –> dry, inflamed skin aka venous eczema.
The skin and soft tissues become fibrotic and tight, causing the lower legs to become narrow and hard, referred to as lipodermatosclerosis.
Inflammation of sc fat - panniculitis
Inverted champagne bottle appearance
Atrophie blanche - smooth white tissue

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24
Q

What is a saphenous varix? How can you diagnose it?

A

Dilated vein at saphenofemoral junction. Cough test - apply pressure at the SFJ and ask patient to cough, feel for thrill

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25
Q

What is the Trendelenburg’s test?

A

With the patient lying down, lift the affected leg to drain the veins completely. Then apply a tourniquet to the thigh and stand the patient up. The tourniquet should prevent the varicose veins from reappearing if it is placed distally to the incompetent valve. If the varicose veins appear, the incompetent valve is below the level of the tourniquet. Repeat the test with the tourniquet at different levels to assess the location of the incompetent valves.

26
Q

What is Perthes test?

A

Apply a tourniquet to the thigh and ask the patient to pump their calf muscles by performing heel raises whilst standing. If the superficial veins disappear, the deep veins are functioning. Increased dilation of the superficial veins indicates a problem in the deep veins, such as deep vein thrombosis

27
Q

What is the management for varicose veins?

A

Varicose veins in pregnancy often improve after delivery.

Conservative:
Weight loss if appropriate
Staying physically active
Keeping the leg elevated when possible to help drainage
Compression stockings (exclude arterial disease first with an ankle-brachial pressure index)

Surgical:
Endothermal ablation – inserting a catheter into the vein to apply radiofrequency ablation
Sclerotherapy – injecting the vein with an irritant foam that causes closure of the vein
Stripping – the veins are ligated and pulled out of the leg

28
Q

Give 3 complications of varicose veins.

A
Prolonged and heavy bleeding after trauma
Superficial thrombophlebitis (thrombosis and inflammation in the superficial veins)
Deep vein thrombosis
All the issues of chronic venous insufficiency (e.g., skin changes and ulcers)
29
Q

What is the management of chronic venous insufficiency?

A

Keep skin healthy - monitor, emollients eg diprobase, topical steroids for venous eczema, potent topical steroids for lipodermatosclerosis flares.
Improve venous drainage - wt loss, activity, elevation, compression stockings (exclude PAS with ABPI first)
Manage complications - cellulitis, pain, ulceration

30
Q

What is an ulcer? Give 4 types.

A

Wound/break in skin that does not heal or heals slowly due to underlying pathology.
Venous, arterial, diabetic foot, pressure.

31
Q

What is a diabetic foot ulcer?Why do they occur and what is an important complication?

A

Diabetic neuropathy –> injury to foot and don’t notice.
Vascular damage –> impaired blood supply and wound healing
Hyperglycemia, immune suppression and autonomic neuropathy –> poor healing.
Risk of osteomyelitis (bone infection)

32
Q

What causes pressure ulcer? What scoring system is used to assess risk of pressure ulcer?

A

Pressure ulcers typically occur in patients with reduced mobility, where prolonged pressure on particular areas (e.g., the sacrum whilst sitting) lead to the skin breaking down. This happens due to a combination of reduced blood supply and localised ischaemia, reduced lymph drainage and an abnormal change in shape (deformation) of the tissues under pressure.The Waterlow Score is a commonly used risk assessment tool for estimating an individual patient’s risk of developing a pressure ulcer.

33
Q

How are ulcers diagnosed and investigated?

A

ABPI
Bloods - infection, co-morbidity, albumin for malnutrition
Charcoal swab for infection
Skin biopsy for cancer eg SCC –> 2ww

34
Q

How are arterial ulcers managed?

A

Same as PAD - urgent referral to vasc for surgical revascularisation. Should heal after that.

35
Q

How are venous ulcers managed?

A

Vasc surgery if suspected arterial component
Tissue viability/specialist leg ulcer clinics in complex or non-healing ulcers. Wound care - cleaning, debridement (removing dead tissue), dressing
Derm where alternative diagnosis suspected
Pain clinic if pain difficult to manage. NSAIDS can worsen
Diabetic ulcer service if diabetic ulcer
Compression therapy (exclude PAD)
Pentoxifylline PO can help but not licensed
Abx for infection

36
Q

What is lymphoedema?

A

Chronic condition caused by impaired lymphatic drainage. Tissues in areas affected become swollen with excess, protein-rich fluid. These areas are prone to infection.
Primary - rare, genetic, early onset
Secondary - eg to breast cancer surgery due to axillary lymph node clearance

37
Q

What is lipoedema?

A

Abnormal build-up of fat tissue in the limbs, often the legs. The feet are spared in lipoedema, unlike lymphoedema. This affects women more often than men. It can cause pain, psychological distress and significantly affect the patient’s quality of life.

38
Q

How is lymphoedema diagnosed and assessed?

A

Stemmer’s sign - pinch skin at toe/finger, if you can’t make a little tent, it is positive for lymphoedema.
Limb volume calculated using circumferential measurements, water displacement, and perometry (square frame with perpendicular light beams moved along the limb, measuring outline and volume)
Bioelectric impedance spectrometry - measures electrical resistance through the tissues
Lymphoscintigraphy - nuclear medicine - radioactive tracer injected, gamma camera used to assess structure of lymphatic system

39
Q

What is the management for lymphoedema?

A

Specialist service
Conservative:
Manual lymphatic drainage (massage),
Compression bandages, lymphoedema exercises to improve drainage, wt loss, skin care
Surgical - lymphatricovenular anastamosis. Connect lymph vessels to veins to allow drainage.
Abx for cellulitis
CBT and antidepressants if indicated
DONT take blood/insert cannula/do BP or give any injections into a limb with lymphoedema!!

40
Q

What is lymphatic filariasis?

A

Infection from parasitic worms spread by mosquitos. The worms live in the lymphatic system and cause severe lymphoedema ‘elephantiasis’. Afria, Asia.

41
Q

What is an AAA?

A

Abdominal aortic aneurysm -= dilation of abdominal aorta >3cm in diameter.

42
Q

Give 4 risk factors for AAA.

A

Male, increased age, smoking, hypertension, family history, CVD

43
Q

Describe the screening process for AAA.

A

Males age 65 and women >70 with risk factors have ultrasound.
Normal = <3cm
3-4.4 = small, refer to vasc (routine), follow up yearly
4.5-5.5 = medium, refer to vasc (routine), follow up 3-monthly.
>5.5 = large, urgent referral to vasc

44
Q

How does AAA present?

A

Aysmptomatic until rupture

May have non specific abdo pain, pulsative and expansile mass

45
Q

What is the management of AAA?

A

Manage RFs - smoking, diet, exercise, optimise management of comorbidities
3-4.4 = small, refer to vasc (routine), follow up yearly
4.5-5.5 = medium, refer to vasc (routine), follow up 3-monthly.
>5.5 = large, urgent referral to vasc
Elective repair if large, symptomatic or growing more than 1cm per year. This can be done with open repair or EVAR.
DRIVING - inform DVLA is >6cm, stop driving if >6.5cm, stricter if HGV

46
Q

How does AAA rupture present?

A

Haemodynamic instability, pain radiating to back or groin, collapse, pulsatile expansile mass in abdomen.
Risk of rupture 5% for 5cm, 40% for 8cm.
Mortality 80% in rupture.

47
Q

What is the management for ruptured AAA?

A

Surgical emergency
Permissive hypotension to reduce blood loss
Theatre is haem unstable
CT angio if haem stable

48
Q

What is aortic dissection?

A

Break or tear in the tunica intima of aorta allowing blood to enter between tunica intima and tunica media (a false lumen). Most commonly affects the right lateral area of the ascending aorta, as this is under the most stress from blood exiting the heart.

49
Q

How is aortic dissection classified?

A

The Stanford system:
Type A – affects the ascending aorta, before the brachiocephalic artery
Type B – affects the descending aorta, after the left subclavian artery

The DeBakey system:
Type I – begins in the ascending aorta and involves at least the aortic arch, if not the whole aorta
Type II – isolated to the ascending aorta
Type IIIa – begins in the descending aorta and involves only the section above the diaphragm
Type IIIb – begins in the descending aorta and involves the aorta below the diaphragm

50
Q

Give 5 risk factors of aortic dissection.

A

Same as for PAD
Hypertension especially dramatic increase eg weightlifting and cocaine.
Bicuspid aortic valve, co-arctation of aorta, aortic valve replacement, CABG
CTDs: EDS, Marfan’s

51
Q

How does aortic dissection present?

A

Sudden onset severe tearing chest and/or abdo pain, anterior or posterior depending on where aorta affected, may radiate, may not have chest pain –> easily missed!
Htn, >20mmHg difference in BP between arms, radial pulse deficit - does not match apex beat in one arm, diastolic murmur, focal neurological deficit, collapse, hypotension (late)

52
Q

How is aortic dissection diagnosed?

A

ECG (exclude MI - may co-occur, thrombolysis could cause fatal progression of the AD)
CXR
CT angio first
MRI angio for more detail and to plan management

53
Q

What is the management of aortic dissection?

A

High mortality, surgical emergency
Analgesia
Control BP and HR eg with beta blockers
Surgical:
Type A –> open surgery (midline sternotomy)
Type B –> Transthoracic Endovascular Aortic Repair

54
Q

Give 4 complications of aortic dissection.

A

MI, Stroke, paraplegia, aortic regurg, cardiac tamponade, death

55
Q

What is carotid artery stenosis? How does it present?

A

Narrowing of carotid arteries in neck, usually due to atherosclerosis. Risk of embolic stroke. Patients with TIA/stroke are investigated for carotid artery stenosis with USS. Usually asymptomatic, may have carotid bruit during systole

56
Q

How is CAS categorised?

A

Mild - <50% reduction in diameter
Mod - 50-69%
Severe - >70%

57
Q

What is the management for carotid artery stenosis?

A

Conservative:
Reduce risk factors, manage co-morbidities, antiplatelets, statins
Surgery if severe:
Carotid endarterectomy (complications: stroke (2%), nerve injury (facial, glossopharyngeal, recurrent laryngeal)
Angioplasty and stenting

58
Q

What is Buerger disease?

A

Aka thromboangiitis obliterans
Inflammatory condition that causes thrombus formation in small and medium sized blood vessels in hands and feet. Causes painful, blue fingertips/toes, worse at night, risk of gangrene.
Affects young men (25-35) who smoke, without other RFs for atherosclerosis.

59
Q

How does Buerger disease present? How is it diagnosed?

A

Males under 50 with no other RFs for atherosclerosis, other than smoking
Angiogram - corkscrew collaterals

60
Q

How is Buerger disease managed?

A

STOP SMOKING including nicotine

IV iloprost = prostacyclin analogue, dilates blood vessels.