Vascular medicine and surgery

Question 1

What are the associated risks with increasing systemic blood pressure?

Answer 1

Major risk factors for:

• Stroke
• MI
• Heart failure
• Chronic kidney disease
• Cognitive decline

Each 2mmHg rise in systolic BP is associated with a 7% increase in risk of mortality from IHD and 10% increase in risk of mortality from stroke

Question 2

How is hypertension classified? (by the british hypertension society)

Answer 2

• Stage 1 Hypertension:
  
  • Clinic BP > 140/90 and ABPM >135/85
• Stage 2 Hypertension:
  
  • Clinic BP >160/100 and ABPM >150/95
• Severe Hypertension:
  
  • Clinic BP SBP>180 or DBP>110

ABPM: two measurements per hour taken, average reading used. Using the average of at least 14 values will enable a diagnosis.

(At least three measurements are required to confirm hypertension)

Question 3

Compare primary hypertension to secondary hypertension

(not an objective)

Answer 3

Primary (essential) hypertension:

• 95% of cases
• Cause is not known but is likely to be multifactorial

Secondary hypertension:

• Caused by a range of pathology
• (next question is the causes)

Question 4

What are the causes of secondary hypertension?

Answer 4

• Adrenal cortical diseases:
  
  • Primary hyperaldosteronism (e.g. Conn’s): most common secondary cause
  • Cushing’s
  • Acromegaly
• Renal artery stenosis
  
  • Second most common cause
• Chronic kidney disease
• Pheochromocytoma (rare cause)
  
  • a neuroendocrine tumor of the medulla of the adrenal glands
• Coartation of the aorta
  
  • Congential narrowing of the aorta leading to increased peripheral vascular resistance
• Neurogenic causes
  
  • Raised ICP
• Pregnancy

Question 5

What is accelerated/malignant hypertension?

Describe the clinical signs and pathological features of it

How is it diagnosed?

Answer 5

• Rapid sustained increase in blood pressure
• This leads to intimal proliferation, reducing the luminal size and leading to cessation of blood flow through the small vessels
• This causes foci of tissue necrosis e.g. in the glomeruli
• Carries an untreated 1 year mortality of 20%
• Diagnosed if there is SBP>200 or DBP>120 and bilateral retinal haemorrhages/exudates
• Papillodema may be present

Question 6

What are the pathological consequences of hypertension?

(cardiovascular, cerebrovascular, renal systems and vision)

Answer 6

Heart:

• Left ventricular hypertrophy with dilation and eventual failure

Aorta:

• Predisposes to AAAs & aortic dissection

Brain:

• Intracerebral haemorrhage due to vessel rupture

Kidney:

• CKD due to progressive nephron ischaemia & glomerular destruction

Eyes:

• Hypertensive retinopathy

Question 7

How would you explain to a patient they have hypertension?

Answer 7

Your blood pressure is above “normal ranges”. A higher than normal blood pressure, which we call hypertension, is associated with increased risk of cardiovascular disease, which is disease of blood vessels and the heart – the major two diseases being stroke and heart attack. In order to reduce the risk of these diseases we need to get your blood pressure down to a lower level. We can do this using lifestyle measures and using some tablets and medicines.

Question 8

What are signs of left ventricular hypertrophy on an ECG?

Answer 8

• Tall R waves on V5 and 6
• deep S waves on V1 and 2
• inverted T waves in leads I, AvL, V5 and 6.

Question 9

What Korotkoff sounds should you hear when measuring blood pressure?

Answer 9

1. Sound 1: clear tapping sound (systolic BP)
2. Sound 2: Soft swishing murmur
3. Sound 3: Loud slapping sound
4. Sound 4: Muffling of sound
5. Sound 5: Disappearance of sound (diastolic BP – depends what book you read).

Question 10

Outline the epidiological link between cholesterol and vascular risk

Answer 10

Most men with LDL receptor defects will die before the age of 60, a majority due to coronary artery disease.

HDL protects against cardiovascular disease.

Serum cholesterol has been graphed to deaths per 1000 men; 4mM – 2, 5mM – 4.5, 6mM – 8, 7mM – 14.

Targets: Total cholesterol < 5mM, LDL < 3mM.

Question 11

How would you tell a patient they have diagnosis of hyperlipidaemia in lay terms?

Answer 11

The test results show that you have a level of lipids, which are fats, in your blood. One of these lipids that has become a bit of a household name is cholesterol. Unfortunately, having high levels of these substances in your blood increases the risk of certain adverse events to do with the circulation system, such as heart and stroke. Hopefully we can work together to reduce the amounts in the blood, and reduce the “modifiable” risk of blood vessel disease as far as possible, through lifestyle and medication measures.

Question 12

Define atherosclerosis

Answer 12

• Non-specific thickening and hardening of the walls of arteries causing a loss of contractility and elasicity, and decreased blood flow
• Often due to prolonged hypertension in smaller arteries

Question 13

What are the risk factors for atherosclerosis development?

Answer 13

• Age: older
• Male
• Family history
• Smoking
• Diet: high fat, low fruit and veg
• Obesity
• Hypertension
• Hyperlipidaemia - high serum cholesterol, low HDLs, high LDLs
• Diabetes

Question 14

Distinguish between macro- and micro-vascular diseases

Answer 14

Macrovascular disease may result in MI, stroke, or peripheral vascular disease, and would present as such. Initially, ischaemia of the leg may provoke intermittent claudication.

Microvascular diseases are unique to diabetes and are nephropathy, neuropathy and retinopathy, presenting as decline in “organ” function.

Question 15

List specific sites where atheroma may develop and describe the clinical consequences and complications

Answer 15

Common sites of atheroma:

• aortic bifurcation
• branch points
• around ostia (funnel-shaped openings, especially in abdominal aorta near kidneys)
• other sites of haemodynamic stress (where endothelial damage is most commonly present).

Clinical complications:

• stenosis
• resulting hypoperfusion of distal tissues
• thrombus on the plaque causing total occlusion
• bleeding into the plaque
• aneurysm formation
• cholesterol embolism to distal sites.

Question 16

What can you do to modify the atherosclerotic process?

Answer 16

General lifestyle: (most important)

• Stop smoking
• Exercise more
• Eat a balanced diet
• Lose weight if obese
• (opposite to risk factors)

Hypertension, hyperlipidaemia and diabetes are risk factors for progression of the disease state, and their reduction (via lifestyle, diet and pharmacology) will decrease risk of complications.

Pro-thrombotic state is a risk factor for complications of atherosclerosis, so antiplatelet agents reduce risk of complications

Question 17

What is an aneurysm?

How can it present?

Answer 17

Aneurysm = a focal dilation of an artery >150% of its normal diameter.

They can present in different ways:

• Mass effects: pressuring adjacent structures
• Embolic events: due to development of mural thrombi
• Haemorrhage: due to rupture

Question 18

Describe the common sites of atherosclerotic aneurysms

Answer 18

The more common sites are in descending, strong-flow vessels (and in descending order of incidence)

• the abdominal aorta
• iliac
• popliteal
• femoral arteries
• thoracic aorta.

Question 19

What is the relative incidence of abdominal aortic aneurysms?

Answer 19

AAA is the most common atherosclerotic arterial aneurysm

• Present in 5% of males over 60
• They are 5x more common in males and are mainly asymptomatic

Question 20

Describe the pathophysiology of arterial dissection.

What are possible outcomes of arterial dissection?

Answer 20

• A tear in the intima leads to blood tracking into the arterial media
• The arterial media spilts, forming a false channel
• This most commonly occurs in the aorta
• There are two patterns:
  
  • Type A (70%): involves the ascending aorta
  • Type B (30%): do not involve the ascending aorta
• Possible outcomes:
  
  • External rupture: massive fatal haemorrhage
  • Internal rupture: Rare, blood tracks back into the lumen to produce a double-channelled aorta
  • Cardiac tamponade: retrograde spread into the pericardial cavity

Question 21

What are causes of arterial dissection?

Answer 21

Hypertension

Atheroma

Congential disease (Marfan’s/Ehlers-Danlos)

Question 22

What are complications of arterial dissection as the dissection spreads?

Answer 22

• Retrograde spread can lead to cardiac tamponade
• If the dissection spreads distally then the origins of the main arterial branches become blocked; leading to symptms on the arteries involved:
  
  • Coronary arteries - MI
  • Brachiocephalic trunk - unequal arm pulses and central neurological symptoms
  • Renal arteries - haematuria, anuria, AKI
  • Iliac arteries - acute lower limb ischaemia

Question 23

What is the presentation of a patient with a thoracic aortic dissection?

Answer 23

• Severe, very sudden onset central chest pain, describing as ‘tearing’
• It may radiate down the arm/to the back (mimicking MI)
• The patient is shocked
• There may be signs of blockage of distal arterial trunks

Question 24

What are the signs and symptoms of a ruptured abdominal aortic aneurysm?

Answer 24

Until rupture most AAAs are asymptomatic

Rupture presentation:

• Severe epigastic pain radiating to the the back
• Pulsatile, expansile abdominal mass
• Signs of shock:
  
  • Hypotension
  • Tachycardia
  • Rapid breathing ect.

Question 25

What are differential diagnosis for signs of an abdominal aortic aneurysm?

Answer 25

• renal colic
• diverticulitis
• pancreatitis
• gastric/duodenal ulcer perforation
• MI

Question 26

What is the management for an unruptured AAA?

Answer 26

Depends on size

• AAAs that measure <5.5cm
  
  • Monitor by regular USS/CT
  • Modification of risk factors: e.g. control of hypertension
  • 75% of monitored aneurysms will eventually require surgery
• Indications for surgery:
  
  • AAAs >6cm - risk of rupture increases from 1% to 25% at 6cm
  • AAAs expanding at >1cm per year
  • Symptomatic aneurysms

Question 27

How is chronic peripheral lower limb peripheral arterial disease classified?

Answer 27

The Fontaine classification outlines the progression of chronic lower limb peripheral arterial disease:

1. Asymptomatic
2. Intermittent claudication (a condition in which cramping pain in the leg is induced by exercise, due to narrowing of arteries)
3. Ischaemic rest pain
4. Ulceration/gangrene

Question 28

List the clinical manifestations of chronic peripheral arterial occulsive disease

(signs and symtoms)

Answer 28

Symptoms:

• The classic symptom is leg pain when walking which resolves with rest, known as intermittent claudication
• Ischaemic ‘cramping’ muscle pain on walking, relieved by rest
• Pain is reproducible at a similar level, the ‘claudication distance’
• Most commonly in the calf, suggesting femoral disease
• Pain in the thigh/buttock suggests ileal disease, which will often be bilateral
  
  • Associated absent penile function = Leriche syndrone

Signs:

• Absent pulses
• Cold, pale legs
• Atrophic, hairless & shiny skin
• Beurger’s angle <20 degrees
• Arterial ulcers

Question 29

How can you differentiate between symptoms of ischaemic rest pain and neuropathy as a cause of chronic foot pain?

Answer 29

Peripheral neuropathy has 3 main effects whch ischaemic rest pain doesn’t:

• Sensory neuropathy
  
  • Reduces protective reactions to minor injury, and reduces awareness of symptoms of infection/ischaemia
• Autonomic neuropathy
  
  • A lack of sweating leads to development of dry, fissured skin, allowing entry of bacteria
• Motor neuropathy
  
  • Wasting of the small muscles of the foot lead to loss of the arches and development of abnormal pressure areas in the feet

Neuropathy is associated with tingling and numbness, and is not relieved by swinging a leg out of bed.

Neuropathy general conforms to a glove and stocking distribution.

Ischaemic pain will get worse on raising the leg; unlike neuropathic pain unless it is caused by nerve entrapment (Buerger’s test can differentiate for vascular causes as the leg will go pale).

Question 30

Describe the pathophysiology of intermittent claudication

(how and why does it occur)

Answer 30

• The calf is most often affected, as it the femoral artery that most comonly becomes atheromatous
• At rest, the oxygen requirement of muscles is met by the collateral system of the profunda femoris (therefore no pain)
• Exercise produces a demand that cannot be met, and the calf muscles become ischaemic
• By resting, the collateral system can once again supply enough blood for the pain to be relieved

Question 31

What are differential diagnosis for intermittent claudication? (other leg pain causes)

Answer 31

Spinal stenosis

• Most commonly due to spinal osteophyte formation
• Symptoms are due to lumbar nerve root/cauda equina compression
• Features similar to intermittent claudication, but pain is relieved by sitting down or flexing the spine rather than standing still
• Variable symptoms from day to day

Venous claudication

• Obstruction of the venous outflow of the leg (iliofemoral occulsion)
• Pain comes on gradually from the moment walking starts
• Pain affects the whole leg, and is ‘bursting’ in nature
• Leg elevation can relieve the pain
• There are signs of venous disease and often history of DVT

Other causes of leg pain are musculoskeletal (osteoarthritis/rheumatoid arthritis), pepherial neuorpathy, Buergers disease (young men, heavy smokers) or popliteal artery entrapment

Question 32

What is the conservative management of arterial occlusive disease?

Answer 32

• Lifestyle changes:
  
  • Stop smoking
  • Exercise to the point of claudication to improve collaterals
  • Weight loss
• Raising the heel of shoes (decrease calf work)
• Foot care to prevent minor trauma leading to ulceration ect.
• Optimisation of blood pressure (avoid B-blockers) and diabetes
• Started on antiplatelet (clopidogrel) and a statin (atorvastatin)

Question 33

How can you investigate arterial disease?

Answer 33

• Doppler ultrasound scan
• Duplex ultrasound scan
• angiography
• Ankle/Brachial pressure index
  
  • Management depends on ABPI result & level of symptoms

Intermittent claudication is associated with an ABPI of 0.4-0.9, values of <0.4 are associated with critical limb ischaemia. ABPI may appear higher than its actual value in calcified/hardened arteries

Question 34

What are the common causes of acute arterial occlusion?

Answer 34

• Embolus (40%)
• Thrombus (40%)
• Trauma (including during angioplasty)

Predisposing factors include dehydration, hypotension, unusual posture, malignancy, hyperviscosity, AF and thrombophilia

Question 35

How can you differentiate between embolic and thrombotic occulsion?

Answer 35

Onset:

• Embolus:
  
  • sudden onset
  • very severe symptoms due to lack of collaterals
• Thrombosis:
  
  • Inidious onset
  • Less severe symptoms as advanced collaterals

Source:

• Embolus
  
  • Normally identifiable e.g. AF/AAA/post MI/endocarditis (heart valve)
• Thrombosis
  
  • No obvious source

Pulses:

• Embolus
  
  • Previously normal
  • normal contralateral pulses
• Thrombosis
  
  • Long-standing decreased pulse bilaterally

History:

• Embolus
  
  • No history of arterial disease
• Thrombosis
  
  • Previous history of intermittent claudication, stroke, MI ect.)

Question 36

What is thombosis prediposed by?

What is embolic occulsion prediposed from?

Answer 36

• Thrombosis is prediposed to by Virchow’s triad:
  
  • Endothelial dysfunction: trauma, inflammation or atheroma
  • Changes in blood flow: statis or slow flow
  • Changes in blood coagulability: inflammatory response/congential causes
• Embolic occulsion is occulsion of a vessel by a mass of material transported in the bloodstream, most commonly fragments of thrombus (thromboemboli).
• Thromboemboli may arise from the left atrium in AF, the left ventricle post MI, heart valve in endocarditis or mural thrombi from an AAA

Question 37

List the clinical symptoms of acute arterial occulsion

Answer 37

The six P’s:

• Pulseless
• Painful
• Pallor
• Perishingly cold
• Paralysis*
• Paraesthesia* (abnormal sensation such as tingling, tickling, pricking, numbness or burning)

*Paralysis and paraesthesia indicate a threatened limb, as well as pain on passive movement or squeezing the calf

Question 38

How can you differentiate the symptoms and signs of acute arterial from acute venous occlusion?

Answer 38

• Acute arterial occlusion will cause the 6 P’s
  
  • Pulseless
  • Painful
  • Pallor
  • Perishingly cold
  • Paralysis
  • Paraesthesia
• Venous occlusion will cause:
  
  • swelling
  • redness
  • warmth
  • pain.
  • Engorgement of superficial vessels, ankle oedema and Homan’s sign (pain on dorsiflexion of foot) may be present

Question 39

Describe the natural history of untreated acute arterial occulsion

Answer 39

Untreated, the patient will lose the limb, and the degeneration process will cause life-threatening illness

Question 40

Describe the natural history of treated arterial occulsion

Answer 40

• Treatment hopes to save the limb, but it is mandatory to observe the risk of reperfusion injury.
• Reperfusion injury may cause more damage than the ischaemia itself.
• The increased blood supply brings nutrients and immune mediators that increase inflammation.
• Cell leakage leads to acidosis and hyperkalaemia.
• Compartment syndrome may occur in tight fascial planes.
• Acute limb ischaemia may lead to peripheral nerve damage and chronic pain syndromes.

Question 41

List the underlying diseases/disorders associated with vasopastic changes in the extremities

Answer 41

Reynaud’s phenomenon

• General term describing episodic digital vasopasm in the absence of an identifiable associated disorder

Reynaud’s syndrome

• Reynaud’s phenomenon occuring secondary to another condition
• Secondary causes:
  
  • Connective tissue disorders
    
    • Systemic sclerosis, mixed connective tissue disease, SLE, Sjogren’s syndrome, polyarteritis nodosa
  • Macrovascular disease
    
    • Atherosclerosis, thoracic outlet obstruction, Buerger’s disease
  • Occupational trauma
    
    • Vibration white finger, repeated extreme cold or chemical exposure
  • Drugs
    
    • B-blockers, cytotoxic drugs
  • Others
    
    • Malignancy, Arteriovenous Fistula

Question 42

What are the clinical characteristics of Rayaund’s phenomenon?

What hapens as fingers return to normal?

Duration of onset?

Answer 42

Raynaud’s phenomenon can be brought on by cold exposure, or emotional stress and there are three phases:

1. Pallor: due to digital artery spasm
2. Cyanosis: due to accumulation of deoxygenated blood
3. Rubor (blush): erythema due to reactive hyperaemia (an excess of blood in the vessels)

As the fingers return to normal, there may be numbness, a burning sensation and severe pain. Attacks are usually <45 min in duration but can last for hours, with very sever cases involving tissue infarction and loss of digits

Question 43

What are varicose veins?

Answer 43

• Abnormally dilated and lengthened superficial veins
• Commonly in the lower limbs

Question 44

How are varicose veins classified?

How do they differ? - what are they due to?

Answer 44

They can be primary (idiopathic) or secondary

Primary (idiopathic)

• Most common cause
• Twice as common in women
• Likely to be due to primary superficial valve defect, with familial elements
• There is no deep venous incompetence

Secondary

• Superifical varicosities occur secondary to deep venous incompetence
  
  • Previous DVT: although occluded veins recanalise, their valves remain incompetent
  • Raised systemic venous pressure: due to compression (pelvic tumour, pregnancy), arterio-venous fistula or severe tricuspid incompetence

Question 45

What are the complications that may occur from varicose veins?

Answer 45

Symptoms:

• Most patients are most affected by the unsightly appearance
• Can cause tiredness, aching or throbbing of the legs
• Oedema of the ankles, particularly on standing for long periods
• Ithing and noctural cramps are reported
• Signs of deep venous insufficiency -painful:
  
  • Haemosiderosis (iron overload disorder resulting in the accumulation of hemosiderin), eczema, lipodermatosclerosis (t is an inflammation of the subcutaneous fat)

Question 46

Outline the normal venous physiology

Describe the roles of supericial and deep veins of the lower limb

Answer 46

• There are two venous systems taking blood from the lower limb back to the trunk, the superficial venous system and the deep venous system
• The deep venous system comprises a nuber of veins the accompany the major arteries of the lower limb and drain the muscular compartment
• The superficial venous system comprises the medial long (great) saphenous vein which drains to the saphenofemoral junction and the laterally placed short saphenous vein which drains into the popliteal vein
• The superfical system drains the skin and superficial tissues
• The two systems are joined at the saphenofemoral and saphenopopliteal junctions
• Perforating veins are additional communications between the two systems

Question 47

What is the role of the valves in the veins of the lower limb?

How does the blood return to the heart from the lower limb?

Answer 47

• All the leg veins have valves to prevent backflow
• Venous return to the heart is driven by pressure from the muscular pumps below and inspiration decreasing intrathoracic pressure
• As the calf muscles contracts the deeps veins are squeezed and emptied to force blood upwards
• As the muscle relaxes, blood from the superficial system will flow into the deep veins via the perforators which will again be squeezed upwards as the calf muscles contract once more

Question 48

How do hand held doppler and duplex-scanning tests work in diagnosing venous disease?

Answer 48

• Handheld Doppler ultrasound identifies backward reflux of blood.
• Colour duplex scans (using B mode and Doppler ultrasounds) produce a colour picture of blood flow – blue forward, red back – and thus the presence of valvular incompetence.

Question 49

Define lymphedema

Answer 49

Swelling which results from an increased quantity of fluid in the intertitial space of soft tissues, due to failure of lymphatic drainage

It causes chronic non-pitting oedema, commonly affecting the leg and progressing with age

Question 50

What are common causes of lymphoedema?

Answer 50

Primary lymphoedema:

• A result of an inherited deficiency of lymphatic vessels
• E.g. Milroy’s disease

Secondary lymphoedema:

• Due to obstruction of lymphatic vessels
• E.g. Filaria infection, repeated cellulitis, malignancy, post operative