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4th Year Surgery Block > Vascular > Flashcards

Vascular Flashcards

1
Q

What is peripheral arterial disease? What is it caused by?

A
  • Describes narrowing or occlusion of the peripheral arteries, affecting the blood supply to the lower limbs
  • Peripheral arterial disease of the lower limbs is most commonly caused by atherosclerosis which narrows the affected arteries limiting blood flow to the affected limb
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2
Q

Risk factors for peripheral arterial disease?

A
  • Same as those for atherosclerosis
  • Main ones are smoking and diabetes
  • Others: hyperlipidaemia, hypertension, obesity, diet high in fats, age, family history
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3
Q

3 presentation of peripheral arterial disease?

A

acute limb ischaemia, chronic limb ischaemia, chronic limb threatening ischaemia

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4
Q

What is acute limb ischaemia, what is the cause of most?

A
  • Sudden decrease in limb perfusion that threatens limb viability (develops over less than 2 weeks)
  • 80% are due to embolic events
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5
Q

Presentation of acute limb ischaemia? Describe the colours the legs go?

A
  • 6Ps: pain, pallor, paraesthesia, paralysis, perishingly cold and pulselessness
  • Legs will first be white, then capillaries fill with stagnant cyanotic blood (mottling) which blanches on pressure, if reperfusion is not achieved arteries thrombose and capillaries rupture so there is fixed blue staining of the skin which does not blanch on pressure
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6
Q

Investigations for acute limb ischaemia?

A
  • Investigations: FBC, UandE, coag screen, ECG, imaging for all patients in which amputation is not inevitable – CTA first line
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7
Q

Management of acute limb ischaemia?

A
  • Management: O2, IV and fluid resus, foot down tilt, unfractionated heparin, revascularisation surgery
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8
Q

Presentation of chronic limb ischaemia?

A
  • This presents as intermittent claudication (diminished circulation leads to pain in the lower limb on walking or exercise that is relieved by rest
  • May also have non healing wounds on the lower limb
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9
Q

Diagnosis of chronic limb ischaemia?

A
  • Diagnosis is made on presence of clinical features and ABPI
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10
Q

Management of chronic limb ischaemia?

A

manage CV risk, advice on smoking cessation, supervised exercise programme, referral for consideration of angioplasty/ bypass, consideration of naftidrofuryl oxalate if not been satisfactory improvement and doesn’t want referral for surgery

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11
Q

What is meant by chronic limb threatening ischaemia?

A
  • Chronic inadequate tissue perfusion at rest, ischaemic rest pain, with or without tissue loss
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12
Q

Management of chronic limb threatening ischaemia?

A
  • These people need urgent referral to vascular MDT
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13
Q

Vascular claudication vs neurogenic claudication?

A
  • Neurogenic claudication can also be relieved by leaning forward
  • Vascular pain tends to be more predictable, a patient can walk x distance before the pain comes on, neurogenic is more random
  • vascular pain tends to be more of a crampy pain, neuorgenic is more burning/ shooting (not always though)
  • vascular pain is more distributed in the calves, neurogenic pain distribution will depend on nerve roots affected
  • Vascular claudication will have signs like potential pallor, unhealing wounds
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14
Q

What is naftidrofuryl ?

A
  • This is a vasodilator and also enhances cellular oxidative capacity
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15
Q

What is an aneurysm

A
  • Aneurysm can be defined as focal dilatation of a blood vessel > 1.5x its normal diameter
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16
Q

Explain what is meant by true and false aneurysm

A
  • A true aneurysm involves all three vessel wall layers
  • False aneurysms or pseudoaneurysms occur when the intimal and medial layers are disrupted and the dilated segment is surrounded by the adventitia only
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17
Q

Are AAA aneurysms usually true or false

A

usually true - * AAA is the most common true arterial aneurysm, false aneurysms of the abdominal aorta are usually due to trauma or infection

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18
Q

Risk factors/ what groups get AAA?

A
  • More common in older men
  • 1 in 70 men over 65 yrs have a AAA
    aetiology is largely unknown
  • Risk factors include smoking, hypertension, hyperlipidaemia, FH, male gender and increasing age
  • Diabetes decreases risk but mechanism is poorly understood
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19
Q

Are AAA usually symptomatic?

A
  • Unruptured aneurysms are generally asymptomatic and may only be an incidental finding or detected on screening
  • Small subset present with triad of lower back pain, weight loss and raised ESR
  • Most people are symptomatic because they have had a rupture or distal embolisation
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20
Q

Rupture AAA presentation?

A
  • Classic triad of a ruptured aneurysm is abdominal/ back pain, hypovolaemia and pulsatile abdominal mass but this triad is relatively rare
  • May be groin pain/ syncope/ paralysis/ flank mass
  • Can get rupture into the vena cava or iliac vein, this leads to tachycardia, CHF, leg swelling, abdominal thrill, abdominal bruit, renal failure and peripheral ischaemia
  • Can also cause a GI bleed
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21
Q

Embolism AAA presentation?

A
  • AAA can through off embolisms
  • These people may develop acute limb ischaemia or “blue toe syndrome”
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22
Q

Explain management of unruptured AAA?

A
  • Any AAA less than 5.5cm can be monitored via Duplex USS as surgery prior to this diameter provides no survival benefit, cardiovascular risk factors should be modified as appropriate
  • Surgery in unruptured should be considered in those who are: symptomatic, asymptomatic but it’s larger than 4.0 cm and grown by more than 1cm in 1 year or in those where it is asymptomatic and 5.5cm or larger
  • Aneurysms can either be repaired by open repair (cut open and the aneurysm part removed and replaced with a prosthetic graft) or by endovascular repair (introduce a graft via the femoral arteries and fixing the stent across the aneurysm)
  • Both have good long term outcomes but endovascular has better hospital stay outcomes, although endovascular repair may need more reinterventions and have more ruptures
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23
Q

Management of ruptured AAA?

A
  • ABCDE
  • If patient unstable they get immediate transfer to theatre for open surgical repair
  • If they are stable they get a CT angiogram to determine whether the aneurysm is suitable for endovascular repair
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24
Q

Explain screening for AAA?

A
  • Men in their 65th year are invited to be screened by ultrasound of abdomen
  • If no aneurysm men are not invited back for further screening
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25
Q

What are 3 acute aortic conditions affecting the thoracic aorta?

A
  • Aortic dissection
  • Intramural haematoma (IMH)
  • Penetrating aortic ulcer (PAU)
    All three conditions may co-exist and IMH and PAU may lead to dissection
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26
Q

What is an aortic dissection?

A
  • Overall rare
  • This is a tear in the intima of the aorta that allows blood to tunnel between the intima and media
  • As the blood is at a high pressure it sheers more of the intima off the media and get a false lumen forming
27
Q

Risk factors for aortic dissection?

A

uncontrolled hypertension, atherosclerosis, weakened aorta e.g. Marfans, Ehlers Danlos or aneurysm already present, coarctation of the aorta also increases risk of dissection

28
Q

Explain why an aortic dissection causes problems?

A
  • Blood in the false lumen can cause a re-entry tear (because pressure in false lumen is higher than true lumen), this can then lead to compression of the true lumen which results in visceral/ limb malperfusion or rupture of the false lumen
  • Blood in the false lumen may flow back up into the pericardial space causing pericardial tamponade
  • Blood can also track down in the false lumen until it reaches branches coming off the aorta e.g. renal arteries, the false lumen can then compress these arteries and cause ischaemia
  • If the false lumen ruptures there will be bleeding into the mediastinum which can result in rapid deterioration and death
29
Q

Explain type an and type b dissections? Which is more worrying?

A
  • Aortic dissection can be classed as Type A (in the ascending aorta and 2/3 cases) or Type B (in the descending aorta)
  • Type A dissections are more likely to be acute which makes them more worrying because there is higher risk of rupture
30
Q

Presentation of an aortic dissection?

A
  • Classic presentation = sudden onset severe chest pain with radiation to neck or back and migration of pain as the dissection progresses
  • May have weak pulses in downstream arteries from the dissection
  • May have differences in BP between left and right arms
  • Hypotension or shocked patient
31
Q

Investigations for an aortic dissection?

A
  • FBC, U and E, d-dimer, LFTS, lactate, coagulation, troponin, group and save
  • CXR may show a widened aorta
  • ECG may show myocardial ischaemia or LV strain/ hypertrophy
  • Transoesophageal echo has 90% sensitivity and 95% specificity
  • CTA has 100% sensitivity and 98% specificity
32
Q

Management of a type A aortic dissection?

A
  • Cardiothoracic emergency – need referred to surgery as an emergency
  • Urgent surgery is always indicated
  • Surgery usually involves sealing the entry point to decompress the lumen then replacing the dissected part of the aorta and reconstructing the aorta
33
Q

Management of a type b aortic dissection?

A
  • Early outcomes are more favourable vs type A
  • Patients may develop type A in years to come though
  • First line treatment is IV beta blockage
  • Peripherally acting CCBs e.g. nicardipine may be added as second line agent
  • Hydralazine can be added as an additional agent
34
Q

Explain what an intramural haematoma is?

A
  • This is clotted blood in the intramural space without an obvious intimal tear
  • Typically associated with hypertension and is initiated by aortic wall infarction
  • Often regarded as a precursor to dissection
  • Can present similarly to a dissection and management is pretty much the same (surgery for type A, medication for type B)
35
Q

Explain what a penetrating aortic ulcer is?

A
  • Focal ulceration of an atherosclerotic plaque into the media
  • May be associated with intramural haematoma
  • Poorer prognosis than a dissection
36
Q

5 reasons diabetics are particularly prone to foot ulcers?

A
  1. Diabetic peripheral sensory neuropathy – loss of sensation in lower extremities
  2. Autonomic neuropathy – leads to reduced sweating, dry fragile skin, more risk of fissuring
  3. Motor neuropathy – wasting of intrinsic muscles of the foot, altered foot shape results in altered pressures
  4. Infections – diabetics have impaired immune response, more likely to get infections
  5. Ischaemia – may have diabetic arterial disease
37
Q

Time lengths for monitoring a diabetic foot?

A
  • Patients need regular foot reviews
  • Those at low risk (i.e. no risk factors and callus alone) receive an annual review
  • Those at medium risk (deformity or neuropathy or absent pulses) receive a 3-6 month review
  • Those at high risk (previous ulcer, amputation, on dialysis, have more than one medium risk e.g. ischaemia plus neuropathy) receive a 1-2 month review
38
Q

Diabetic foot reviews should assess?

A
  • 10g monofilament testing
  • Foot pulses
  • Skin for callus, fissuring, tinea
  • Shoe examination
  • Symptoms of neuropathy
39
Q

Describe a neuropathic diabetic ulcer?

A
  • A warm, well perfused foot with bounding pulses and distended veins
  • Ulcer is typically at a site of repetitive trauma
40
Q

Management of a neuropathic diabetic ulcer?

A
  • Key is pressure relief and off-loading
  • Orthotic footwear should be provided
  • Total contact cast is superior to other forms of offloading
  • Debridement of callus is important as it prevents migration of epidermal cells from the wound margin
41
Q

Describe ischaemic and neuro-ischaemic diabetic ulcers?

A
  • Typical sites include the toes, heel and medial aspect of the 1st MT head
  • Callus typically absent and may have necrotic centre
  • Often precipitated by minor infection
42
Q

Management of ischaemic and neuro-ischaemic diabetic ulcers?

A
  • Should ensure patient is on secondary prevention e.g. statin, antiplatelet, smoking cessation, BP control, good glycaemic control
  • May measure ABPI and suggest revascularisation depending on results
43
Q

Describe infection of diabetic ulcers?

A
  • Mild infection of superficial ulcers usually due to Staph A or strep
  • Deep ulcers with ischaemia or that have been present for a long time are likely to be multimicrobial and more likely to be infected by gram negative organisms and anaerobes

osteomyelitis can occur as a complication

44
Q

Management of diabetic ulcer infection?

A

antibiotic treatment needs to reflect that it is likely polymicrobial
iv antibiotics in severe
Abscesses or collection need surgically drained within 24 hours

45
Q

What is charcot neuro-osteoarthropathy?

A
  • Bone and joint changes that occur secondary to loss of sensation, most commonly associated with diabetes but can be associated with other conditions
  • There is inflammation, bone and joint destruction, fragmentation and remodelling
  • It may be triggered by trauma
46
Q

Presentation of charcot neuro-osteoarthropathy?

A
  • Classically presents with oedema, skin erythema and calor with fractures/ dislocations across the joints of the foot and ankle
  • Midfoot is the commonest site in diabetes
47
Q

Treatment of charcot neuro-osteoarthropathy?

A
  • Mainstay of treatment is a total contact cast, when skin temperature has normalised weaning can be performed to orthotic footwear
48
Q

What are varicose veins?

A
  • These are abnormally dilated, elongated tortuous veins > 3mm in diameter
  • Due to venous hypertension and failure of valves as superficial veins cannot stand high pressure and backflow can cause the whole superficial network to become varicosed
  • Usually the legs that are involved as more likely to come under hydrostatic pressure due to gravity
49
Q

Risk factors for varicose veins?

A
  • Risk factors include pregnancy, female sex, obesity and older age, not entirely sure why some people get varicose veins
50
Q

Presentation of varicose veins?

A
  • May present purely with cosmetic complaint or due to sequalae of itching, discomfort, heaviness of legs, night cramps, oedema, burning sensations, paraesthesiae, exercise intolerance or restless legs
  • Need to examine for signs of chronic venous insufficiency e.g. ulcers, lipodermatitis, pigmentation, telangiectasia or venous eczema
51
Q

Management of varicose veins?

A
  • Not many primary care options, need to determine if symptoms actually related to varicose veins
  • People should only be referred if they are symptomatic, have lower limb skin changes due to chronic venous insufficiency, have superficial vein thrombosis or have or have had a venous ulcer
  • In secondary care can do different procedures such as radiofrequency ablation, endovenous laser therapy or foam sclerotherapy
52
Q

Describe how venous ulcers develop?

A
  • These are due to venous insufficiency (improper functioning of the one way valves). This results in pooling of blood around lower part of the leg to just below the ankle, increased venous pressure causes fibrin deposits around the capillaries which then act as a barrier to the flow of oxygen and nutrients to the muscle and skin tissue, death of tissue leads to ulceration
53
Q

Presentation of venous ulcers?

A
  • These are generally found below the knee in the gaiter area (inner aspects of legs)
  • Usually relatively painless unless infected
  • There may be oedema of the lower leg, varicose veins, venous eczema, brown pigmentation from haemosiderin staining and lipodermatosclerosis (inflammation of fat under the epidermis)
54
Q

Management of venous ulcers?

A
  • Management: Non-adherent dressing, De-sloughing agent, 4 layer compression bandaging, may need to increase pressure gradually if pain is a problem, Leg elevation, Once the ulcer has healed prevention needs to be done with continual wearing of compression stockings
55
Q

What is deep venous insufficiency?

A
  • Chronic disease that is either caused by deep vein thrombosis or valvular insufficiency
  • Deep venous insufficiency occurs as a result of a failure of the venous system characterised by valvular reflux, venous hypertension and obstruction
  • Pathophysiology is similar to varicose veins but just affects the deep veins
56
Q

Risk factors for deep venous insufficiency?

A
  • Increasing age
  • Female
  • Pregnancy
  • Previous DVT or phlebitis
  • Obesity
  • Smoking
57
Q

Presentation of deep venous insufficiency?

A
  • Chronically swollen lower limbs which can become aching, pruritic and painful
  • May get venous claudication, pain and tightness on walking that resolves with leg elevation
  • Can have varicose eczema, thrombophlebitis, haemosiderin skin staining, lipodermatosclerosis, atrophie blanche
58
Q

Investigations for deep venous insufficiency?

A
  • Doppler US to assess extent of venous reflux
  • Routine blood to exclude other aetiologies
  • ABPI to determine if suitable for compression
59
Q

Management of deep venous insufficiency?

A
  • Conservative management involves compression stockings and suitable analgesic control
  • Surgical management does not have good evidence
60
Q

Why may drug users be susceptible to acute limb ischaemia?

A

Heroin use may precede the development of an arterial thrombus if it is accidentally injected into an artery instead of a vein

61
Q

Should consider acute limb ischaemia in ________

A

in anyone presenting with acute onset pain in lower limb with sensory and motor dysfunction

62
Q

What medication can be given in someone in acute limb ischaemia? What is the purpose?

A

Unfractionated heparin is given in everyone to prevent further thrombus formation from the static blood that can’t move around the thrombus

63
Q

Why may you need to do fasciotomy after reperfusion surgery in acute limb ischaemia?

A
  • Fasciotomy may need to be done in anyone who has had significant limb ischaemia because if they had muscle ischaemia will get oedema then compartment syndrome
  • Can test for potential muscle ischaemia by seeing if patient has calf tenderness

4th Year Surgery Block (11 decks)

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