Vascular

Question 1

Pathophysiology of atherosclerosis

Answer 1

1. Endothelial injury
2. Inflammation and formation of fatty streaks
3. Plaque formation
4. ECM degradation
5. Development of stenosis
   - Turbulent flow and pressure drop
   - Impaired endothelial function post stenosis
   - Impaired ability to increase flow, leading to mismatch of supply and demant,
   - Reduced ABPI
6. Development of collateral flow with chronicity

Question 2

Rutherford categories of acute limb ischaemia

Answer 2

I - Viable
Mild pain, normal CRT, no motor or sensory deficit. Dopplers audible. Mx: urgent evaluation.
IIa - marginally threatened
Moderate pain, delayed CRT, No motor or sensory loss. No arterial doppler. Mx: Urgent revascularisation
IIb - Immediately threatened
Severe pain, delayed CRT, Partial motor and sensory loss, No arterial doppler. Mx: Emergency revascularisation.
III - Nonviable
Variable pain, absent CRT, Complete paralysis and anaesthetic, no arterial or venous dopplers. Mx: Amputation

Question 3

Management of acute critical limb ischaemia

Answer 3

Medical
- Heparin infusion
Radiological/ Endovascular
- Thrombolysis (tPA)
- Embolectomy
- Angioplasty
Surgical
- Embolectomy
- Bypass

Subsequent followup/ Ix
- Echocardiogram
Full vascular imaging
Oral anticoag for at least 3m
Risk reduction/ lifestyle modification for PVD

Question 4

Pathophys of aneurysms

Answer 4

Embryological development
- Mesodermal somites
- Decreased number and thickness of elastic layers and less collagen

Inflammation
- Th2 cells produce cytokines, degrading collagen, elastin and ECM proteins
- ROS breakdown collageb, elastin, ECM and SM cells

Increased hemodynamic stress
- Particularly at bifurcation of aorta, leading to dilatation

Question 5

Risk of rupture of AAA by size (yearly risk)

Answer 5

<5cm - 1%
5-6cm up to 10%
6-7cm up to 20%
>7cm up to 35%

Question 6

Indications for treatment of superficial vein thrombosis

Answer 6

Prophylactic clexane 45 days
- SVT within 3-5cm of SFJ or SPJ
- SVT > 5cm long in GSV, AASV, SSV
- SVT that propagates despite symptomatic treatment

Treatment clexane 3 months
- SVT within 3cm of deep system or involving SPJ or SFJ
Recurrent SVT after cessation of anticoagulation
- Propagation despite prophylactic clexane

Question 7

Pathophysiology of venous insuffiency

Answer 7

1. Venous hypertension caused by obstruction, valvular incompetence, increased central venous pressure or inadequate muscle contraction
2. Anatomical, histological and phsyiological changes
   - Anatomical: Loss of valvular competence causing inflammatory changes in the vessel wall and deterioration of soft tissues
   - Histological: Decreased collagen type I fibres, increased collagen type III, ECM and SM degradation.
   - Physiological: Endothelial cell dysfunction causes inflammation, release of cytokines and inflammatory mediators, reduced productio of vasoactive mediators, damage to venous wall and valves.
3. Other changes
   - Oedema (metaloprteinases break down ECM and cause increased permeability)
   - Ulcers due to proteolytic enzymes
   - Hemosiderin deposition (breakdown of migrating RBC to area causes oxidative stress, ulcer formation, delayed wound healign)
   - Stasis dermatitis: Inflammation secondary to stasis
   - Lipodermatosclerosis: Fibrosing panniculitis of subcut tissue tethers skin down to subcut tissue