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Cardiovascular Diseases > Peripheral Vascular Disease > Flashcards

Peripheral Vascular Disease Flashcards

1
Q

What is intermittent claudication?

A
  • Intermittent muscle ischaemia
  • Where insufficient blood reaches an exercising muscle.
  • Patient pain free at rest, develops ischaemic pain in affected limb with exercise, but relieved at rest
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2
Q

What two large complications can arise from PVD?

A
  • Stroke
  • MI (coronary ischaemia)
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3
Q

What are the Fontaine stages of peripheral vascular disease?

A
  • I - Normal, no change
  • IIa - IC when walking over 200m
  • IIb - IC when walking under 200m
  • III - pain at rest
  • IV - tissue loss
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4
Q

What kind of people are more at risk of IC?

A
  • Male
  • Age (older = higher risk)
  • Classic CV risk dactors
  • Fibrinogen
  • ALCOHOL IS PROTECTIVE
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5
Q

What are the non-invasive investigations of lower limb ischaemia?

A
  • ABPI (ankle brachial pressure index - ratio of BP in ankle to BP of arm) - can be done with or without exercise
  • Duplex ultrasound scanning (structure and flow)
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6
Q

What are the invasive investigations of lower limb ischaemia?

A
  • Magnetic resonance angiography
  • CT angiography
  • Catheter angiography
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7
Q

What are the ABPI ranges?

A
  • Normal = 0.9 - 1.2
  • Claudication = 0.4 - 0.85
  • Severe = 0 -4.5
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8
Q

What is the “guardian” therapy of LLI?

A
  • Slow progression
    • Smoking cessation
    • Lipid lowering
    • Antiplatelets
    • Treat hypertension / diabetes
    • Walk to develop collateral circulation
  • INFORMATION
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9
Q

How can you improve claudication symptoms?

A
  • Exercise training
  • Drugs (cliostozol)
  • Angioplasty/stenting
  • Surgery
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10
Q

When do you use vasodilator therapy for someone with IC?

A
  • If exercise not led to satisfactory improvement
  • The person does not wish to undergo surgery
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11
Q

Where does critical limb ischaemic pain normally first present?

A

Toes and forefoot

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12
Q

What are the levels of lower limb amputation?

A
  • Hip disarticulation
  • Transfemoral
  • Through knee
  • Transtibial
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13
Q

What is the main factor that influences whether or not a limb will be lost with IC/CLI?

A

Smoking

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14
Q

What is the definition of a DVT?

A
  • Formation of thrombi within the lumen of the vessels that make up the deep venous system
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15
Q

What is meant by distal and proximal vein thrombosis?

A
  • Distal - DVT of the calves
  • Proximal - DVT of popliteal/femoral vein
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16
Q

What are the three parts of Virchow’s triad?

A

PREDISPOSE TO THROMBUS FORMATION

  • Endothelial Injury
  • Circulatory status
  • Hypercoagulable state
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17
Q

What are the two groups of risk factors for DVT?

A
  • Exposing risk factors (acute conditions or trauma, surgery)
  • Predisposing risk factors (patient characteristics)
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18
Q

What is VTE and what factors can cause it?

A
  • Venous thromboembolism
  • Provoked - Surgery, hospitalisation, cancer…
  • Unprovoked - No identifyable cause
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19
Q

What are the 5 known consequences of VTE?

A
  • Fatal Pulmonary Embolism
  • Risk of recurrent VTE
  • Post-thrombotic syndrome (PTS)
  • Chronic thromboembolic pulmonary hypertension (CTEPH)
  • Reduced quality of life
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20
Q

What do venous blood clots contain?

A
  • RBCs
  • Fibrin
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21
Q

What characterises PTS?

A
  • Pain
  • Oedema
  • Hyperpigmentation
  • Eczema
  • Varicose collateral veins
  • Venous ulceration
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22
Q

What is the progression of symptoms in CTEPH?

A
  • Asymptomatic initially
  • Followed by progressive dyspnoea and hypoxaemia
  • RHF can occure
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23
Q

What do you test for in blood if suspected VTE?

A
  • D-dimer - breakdown product of cross linked fibrin
  • 25-50% of patients require no further investigations
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24
Q

What score do you calculate if there is a suspected DVT? What are the ranges?

A
  • Wells score
  • 0 or less = low
  • 1-2 = moderate
  • 3+ = high
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25
Q

What do you do if there is a low Wells score and what do you do if there’s a moderate/high Wells score?

A
  • Low - D-dimer, no imaging if -ve
  • Mod/High - Need imaging regardless of D-dimer, if negative imagining and positive D-dimer, repeat imaging
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26
Q

What is the score used for identifying PE and what are the ranges?

A
  • Modified wells score
  • ≤4 - PE unlikely
  • >4 PE likely
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27
Q

What score can be used as an alternative to Wells?

A

Geneva

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28
Q

What two other imaging techniques can be used in a suspected PE?

A

CTPA (CT pulmonary angiography) gold standard

CXR - can show pleural effusion and occasionaly infarct

V/Q scan

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29
Q

What are the three types of pharmacological intervention against DVT/PE?

A
  • Anticoagulation
  • Thrombolysis
  • Analgesia
30
Q

What are the two main types of mechanical interventions against DVT/PE?

A
  • Graduated compression stockings
  • IVC filters
31
Q

What are the two conditions that lead to screeing for DVT/PE?

A
  • Cancer
  • Thrombophilia
32
Q

What are compression stockings used for, what class are used and how long are they worn for?

A
  • To prevent PTS
  • Class 2 European standard used
  • Worn as soon as possible after diagnosis and worn for at least 2 years post thrombosis
33
Q

When are IVC filters used?

A
  • Temporarily in patients with DVT or PE who cannot have anticoagulation treatment
  • Recurrent proximal DVT or PE despite adequate anticoagulation
34
Q

What is the pharmacological treatment of proximal DVT/PE?

A
  • LMWH/fondaparinux
  • Vitamin K antagonists for 3 months
  • Can use edoxaban, apixaban, rivaroxaban or dabigatran etexilate
35
Q

When do you thrombolyse (and what method) for DVT/PE?

A
  • DVT - consider catheter-directed thrombolytic therapy if no contraindications
  • PE - consider pharmacological systemic thrombolytic therapy if PE and haemodynamic instability
36
Q

When do you use balloon pulmonary angioplasty?

A

For chronic thromboembolic pulmonary hypertension

37
Q

When do you test for thrombophilia?

A
  • Consider testing for antiphospholipid antibodies in patients who have had unprovoked DVT or PE if it is planned to stop anticoagulation treatment.
  • Consider testing for hereditary thrombophilia in patients who have had unprovoked DVT or PE and who have a first-degree relative who has had DVT or PE if it is planned to stop anticoagulation treatment.
38
Q

What is an aneurysm?

A

Dilatation of a vessel by more than 50% of its normal diameter

39
Q

What is the normal aortic diameter?

A

1.2-2cm

40
Q

What is the difference between a true and a false aneurysm?

A
  • True - all 3 layers of the vessel wall intact
  • False - breach in vessel wall but surroundin g structures are acting as a vessel wall
41
Q

What is a saccular and fusiform morphology? Which is more common?

A

Fusiform

42
Q

What is a mycotic aneurysm?

A

An aneurysm secondary to an infection process, involving all 3 layers of the artery?

43
Q

What is the pathogenesis of an AAA?

A
  • Medial degeration
    • Regulation of elastin/collagen in aortic wall
    • Aneurysmal dilatation
    • Increase in aortic wall stress
    • Progressive dilatation
44
Q

What gender is more likely to have an AAA, what happens with age and what aneurysm is highly related?

A
  • Male:Female = 6:1
  • Increases with age
  • 25% with AAA have popliteal also
45
Q

How does AAA typically present? What symptoms?

A
  • 75% asymptomatic - found on imaging of other pathology
  • Symptoms
    • Pain (may mimic renal colic)
    • “Trashing”
    • Rupture
46
Q

What are the symptoms of an AAA rupture?

A
  • Sudden onset of epigastric/central pain
  • May radiate through back
  • May mimic renal colic
  • Collapse
47
Q

What are the signs of a rupture AAA?

A
  • May look “well”
  • Hypo/hypertensive
  • Pulsatile, expansile mass +/- tender
  • Transmitted pulse
  • Peripheral pulses
48
Q

What are the outcomes of a rupture AAA? What type is rapidly fatal? What is the operative mortality?

A
  • 75% don’t make it to hospital
  • Most retroperitoneal, contained rupture
  • Free intraperitoneal rupture is rapidly fatal
  • 50% operative mortality
49
Q

When do you intervene with an AAA?

A
  • Symptomatic
  • Asymptomatice wit >5.5cm AP diameter or >0.5cm growth / 6 months (watch even if not)
50
Q

What is the preferred imaging technique for AAAs? What does it show? What is the other technique and what can it uniquely identify?

A
  • Duplex ultrasound
  • AP diameter and involvement or iliac arteries
  • Other = IV contrast CT
  • Only imaging method to identify ruptured AAA
51
Q
A
52
Q

What is the surgical management of an AAA

A
  • Laparotomy
  • Clamp aorta and iliacs
  • Can use Dacron (synthetic tube) graft
53
Q

What is EVAR?

A
  • Endovascular Aneurysm Repair
  • Exclude AAA from inside the vessel
  • Inserted via peripheral artery, x-ray guided
54
Q

What is the mortality of (in respect to AAA):

  1. Elective repair
  2. Rupture repair
  3. Overall with rupture
A
  1. 2-5%
  2. 30-50%
  3. 75-90%
55
Q

What is acute limb ischaemia?

A

Sudden loss of blood supply to a limb - usually due to occlusion of native artery / bypass graft

56
Q

What are the 5 causes of sudden occlusion?

A
  • Embolism
  • Atheroembolism
  • Arterial dissection
  • Trauma
  • Extrinsic compression
57
Q
A
58
Q

What are the 6 Ps of Acute Limb Ischaemia?

A
  • Pain
  • Pallor
  • Pulseless
  • Perishingly cold
  • Paraesthesia (tingling)
  • Paralysis
59
Q

What is the clinical sign of necrosis?

A
  • Tenderness with tight “woody” compartments
60
Q

What is mottling?

A
  • Clinical appearance of stagnant, de-oxygenated blood
  • Blanching = salvagable, Non-blanching = irreversible
61
Q

What are the feaures of acute limb ischaemia over time?

A
  • 0-4hrs - white foot, painful, sensorimotor deficit (salvageable)
  • 4-12hrs - mottled, blanches on pressure (partly reversible)
  • >12hrs - fixed mottling, non-blanching, compartments tender/red, paralysis (non salvageable)
62
Q

What is the management of ALI? (bar surgery)

A
  • ABC - resuscitate and investigate
  • FBC, U/Es, CK, Coag (+/- troponins)
  • ECG - MI / arrhythmia
  • CXR - underlying malignancy
  • Anticoagulate - stops propagation of thrombus, may improve perfusion
  • Arterial imaging if no prior history / cause unknown
63
Q

What is the method of treatment if the limb is salvageable (with ALI)?

A

Embolectomy +/- fasciotomies +/- thrombolysis

64
Q

What long term complication of diabetes leads to the most hospital admissions?

A

Foot issues

65
Q

What does diabetic foot problems triad encompass and what does it lead to?

A
  • Diabetic neuropathy
  • PVD
  • Infection
  • Can lead to tissue ulceration, necrosis and gangrene which can result in limb amputation
66
Q

What are 3 potential sources of diabetic foot sepsis?

A
  • Simple puncture would
  • infection from the nail plate or interdigital space
  • From a neuro-ischaemic ulcer (occurs on areas of increased pressure i.e. under metatarsal heads)
67
Q

Where does infection leading to diabetic foot sepsis travel to?

A

Tracks in the soft tissue into the rigid compartment of the intrinsic muscles of the digits

68
Q

What is the problem of infection of digital compartments?

A
  1. Pus cannot escape
  2. Pressure builds up rapidly leading to impairment of capillary blood flow
  3. Causes further ischaemia and tissue damage
  4. Can rapidly progress to sepsis and ultimately limb loss
69
Q

What are the systemic clinical findings of DFS?

A
  • Pyrexia
  • Tachycardia
  • Tachypnoeia (hyperventilation)
  • Confusion
  • Kussmaul’s breathing (deep and labored breathing pattern often associated with severe metabolic acidosis)
70
Q

What are the local clinical findings of DFS?

A
  • Swollen affected digit and forefoot
  • Tenderness
  • Ulcer with pus
  • Erythema (may track up limb)
  • Patches of rapidly developing necrosis
  • Crepitus in the soft tissues of the foot
  • May or may not be pedal pulses
71
Q

What is the treatment of DFS?

A
  • Vascular surgical emergency - contact vascular team asap
  • Appropriate antibiotic asap
72
Q

What surgically goes on in the treatment of DFS?

A
  • Removal of infected tissue
  • Wound open to encourage drainage

Cardiovascular Diseases (9 decks)

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