Vascular 2

Question 1

PAD definition

Answer 1

Narrowing/occlusion of peripheral arteries, reducing blood supply to lower limbs

Question 2

Chronic limb ischaemia types

Answer 2

Intermittent claudication
Critical limb ischaemia
Chronic limb-threatening ischaemia

Question 3

Acute limb ischaemia definition

Answer 3

Sudden decrease in limb perfusion due to thrombotic/embolic cause

Question 4

Atheroma formation

Answer 4

Endothelial dysfunction (LDL/HTN) allows LDL deposits.
LDL enters intima and gets oxidised, activates endothelial cells to recruit leukocytes
Monocytes/Th enter intima.
Monocytes - > macrophages. Take up LDL -> Foam cells (Fatty streak)
foam cells promote myocyte migration from tunica media (collagen synthesis)
Foam cell dies, lipid content released.
Have atheroma plaque formation.
Plaque ruptures and thrombus forms.
High risk plaques have thin cap with large lipid core.

Question 5

Common atheroma sites

Answer 5

Circle of willis
Carotid arteries
Popliteal arteries
Coronary arteries
Abdominal aorta

Question 6

Athersclerosis sequelae

Answer 6

Weakened vessel wall (arterial aneurysm, dissection)
Demand/supply mismatch (CHD, PAD, vascular dementia)
Thrombosis (ACS, stroke, acute limb ischaemia)
Renovascular hypertension

Question 7

Atheroma RF

Answer 7

Hypercholesterolaemia, DM, old age, inactivity, HTN, smoking, obesity

Question 8

Atherosclerosis S+S

Answer 8

Generally asymptomatic, but can have xanthalasma, carotid/ abdo bruit, AAA and loss of peripheral pulse

Question 9

Intermittent Claudication

Answer 9

Pain on walking (ischaemia), relieved by rest
Gripping calf/thigh/buttock pain. Predominates in one leg, reproducible by walking same distance. If bilateral then internal iliacs often affected and may have ED

Question 10

Comparison between intermittent claudication and cauda equina

Answer 10

Fixed distance in ID, variable in CE
Pain worse on uphill, better downhill in IC. Worse downhill in CE
Pain disappears in 1-2 mins in IC, takes 15-30 mins in CE
Absent peripheral pulse and reduced ABPI in IC. LMN findings in CE

Question 11

Chronic peripheral arterial disease epidemiology and RF

Answer 11

Age over 50, but more so over 70
Associated with CHD, cerebrovascular disease and diabetes.
RF: Obesity, HTN, inactivity, smoking, hypercholesterolaemia, DM and older age. Men also higher risk. Smoking is biggest link and correlates to pack years and risk of limb amputation
DM is strong RF (esp poor control) due to accererated atherosclerosis and poor healing

Caused by atherosclerosis (commonly) but can be vasculitis (inflammatory) or fibromuscular dysplasia (non-inflammatory)

Question 12

Signs of PAD

Answer 12

Pale, cold, hairless leg with reduced Cap refill, weak/absent pulse, arterial bruit and arterial ulceration (deep, punched out, painful, small. Esp over toe joints/heel and lateral aspect (malleolus)

Question 13

Critical limb ischaemia

Answer 13

Defined as circulation impaired to imminent risk of limb loss. 2 symptoms are rest pain and tissue loss (becomes gangrene if infected and can get osteomyelitis)

Question 14

Investigations for PAD

Answer 14

Bedside (obs/ECG)
Bloods (FBC, ESR, thrombophilia screen, lipid profile, BM)
Scans (ABPI, duplex USS (non-invasive, determine site/severity)
Can also use MRI/CT

Question 15

APBI

Answer 15

> 1.2 is abnormally hard/calcified vessel
1.0-1.2 is normal
0.8-0.9 is mild arterial disease/claudication (mod RF)
0.5-0.79 is mod arterial disease/severe claudication (specialist referral)
<0.5 is severe arterial disease and critical ischaemia. Urgent referral

Question 16

Conservative PAD management

Answer 16

Smoking cessation (atherosclerosis RF but also post stent insertion occlusion)
Diet/exercise mods
Lipid mod/statins
Manage T2D/HTN
Antiplatelet therapy (aspirin/clopidogrel)
Peripheral vasodilators

Question 17

Chronic limb threatening ischaemia

Answer 17

End stage PAD where there is threatened limb viability

Question 18

Acute limb ischaemia pathology

Answer 18

Normally thrombotic (blood clot around atherosclerotic plaque) but can also be embolic (15% of cases)
Prognosis is linked to severity of arterial disease, acute onset and how rapidly reperfusion achieved

Question 19

Comparison of thrombotic acute limb ischaemia vs embolic

Answer 19

Embolus is acute onset, severe ischaemia and associated with AF, endocarditis, mitral stenosis, aneurysms, athersclerotic disease and graft presence. Leg pale, other leg unaffected.
Thrombotic tends to be slower onset, less severe pain. Associated with PVD, IHD, CVD, graft presence and blood disorders. Often both legs affected to some degree due to atherosclerosis

Question 20

Acute limb ischaemia classical features

Answer 20

Pain, pallor, paraestheia, pulseless, perishingly cold, paralysis

Pain often not relieved with pain killers. Paralysis is due to nerve damage. Skin may be cyanosed and mottled. Fixed mottling, skin blitering and hard woody muscles is irreversible

Question 21

Differentials for acute limb ischaemia

Answer 21

Chronic peripheral neuropathy (e.g. diabetic neuropathy, but would have normal temp/pulses)
Compartment syndrome (hard muscles)
DVT (red, hot swollen calf. Pulses normally present)

Question 22

Management of Acute Limb ischaemia

Answer 22

Surgical emergency (6 hours to save limb) but start with heparinisation to prevent thrombus propagation. 
Embolus is generally embolectomy.
Thombus gets angioplasty, bypass surgery or intra arterial thrombolysis

Question 23

Acute limb ischaemia complications

Answer 23

Reperfusion of ischaemic muscles leads to oedema (compartment syndrome risk)
Also, products of cell death (KPO4, myoglobin) can cause rhabdymyolysis and AKI.
Necrosis after 6h and amputation needed. If not appropriate then palliative care.

Question 24

Vasospastic disorder pathology

Answer 24

Mismatch between vasodilation (prostacyclin and NO) and vasoconstriction mediated by atherosclerosis.
Examples include Raynaud’s syndrome, acrocyanosis, livedo reticularis

Question 25

Raynaud’s disease

Answer 25

Paroxysmal vasospastic and vasodilatory events affecting peripheral arterioles (toes and fingers, thumb spared with clear demarcation of affected skin)
More common in women, precipitated by cold and smotion (but also trauma, smoking and overuse)
Colour changes pale (ischaemia), blue (cyanosis) and red (reactive hyperaemia)

Question 26

primary raynaud’s

Answer 26

Young female with genetic (no vascular disease)

Question 27

Secondary Raynaud’s

Answer 27

Phenomenon
Tend to be older with severe symptoms (digital scar, ulceration, gangrene, nail changes). Associated with autoimmunes, environmental exposure (smoking, trauma, chronic vibration, chemicals) endocrine (diabetes, hypothyroidism),
Arterial disease (e.g. Buerger’s), blood disease (lymphoma, polycythaemia),
drugs (beta blocker, coc, cytotoxic)

Question 28

Management of Raynaud’s

Answer 28

CCB/peripheral dilators

Question 29

PE S+S

Answer 29

Dyspnoea, tachypnoea. Plueritic chest pain. DVT

Additional symptoms: cough, substernal chest pain, fever, haemoptysis, syncope, unilateral leg pain

Question 30

WELLS PE

Answer 30

Looks at clinical signs+ symptoms of DVT, tachycardia, haemoptysis
Immobilisation for 3+ days or surgery within 4 weeks, previous DVT/PE, malignancy
Add 3 points is no more likely diagnosis

Score of more than 4- PE likely. 4 or less is unlikely

Question 31

PE pathway

Answer 31

If Wells score >4, then hospital admission (CTPA or V/Q). If tests not immediately available then give anticoagulation
If less then D dimer within 4h or send to hospital. If D dimer positive then CTPA. If negative then probs not PE

Question 32

PE diagnostic

Answer 32

CTPA is definitive diagnosis. CI in patients with poor renal function (use scintigraphy instead)

ECG changes non specific and may be normal. Often sinus tachycardia.

Question 33

PE ECG

Answer 33

Sinus tachycardia
Dominant R wave in V1
T wave inversion in leads V1-V4 or RBBB
Slurred S in Lead 1, Q and T inversion in III (rare, but indicates cor pulmonale)

Question 34

PE classification: Massive

Answer 34

Massive (large/extensive bilateral.) Shows PE signs, and haemodynamic compromise (syncope, LoC)
Acute with sustained hypotension (<90 sys or drop of 40 from baseline, or 15mins of <40bpm bradycardia)

Question 35

Submassive PE

Answer 35

Larger thrombus than low risk. Right heart strain (ECG changes/echo changes, elevated troponin)

Question 36

Low risk PE

Answer 36

Acute PE without clinical markers of massive or submassive PE
Sinus tachycardia might be only abnormality.
Can be asymptomatic, or pleuritic chest pain, SOB, DVT