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Year 3 - Surgery > Vascular > Flashcards

Vascular Flashcards

1
Q

List the definitions for the following:
- Ischaemia
- Necrosis
- Gangrene

A

Ischaemia - inadequate oxygen supply to the tissues, as a result of reduced blood supply

Necrosis - death of tissue

Gangrene - death of tissue, specifically as a result of reduced blood supply

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2
Q

Outline the pathophysiology of peripheral arterial disease and how it leads to symptoms

A

Narrowing of the arteries supplying the (lower) limbs, which reduces blood supply to these areas and leads to claudiation

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3
Q

List features of end stage peripheral arterial disease

A
  • Pain at rest
  • Non-healing ulcers and gangrene
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4
Q

Acute limb ischaemia - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Rapid onset of ischaemia in a limb
- Typically occurs due to obstruction by a thrombus within the arterial supply in the distal aspect of a limb (can also occur due to compartment syndrome)

Presentation:
Sudden onset of the 6 P’s
1. Pain
2. Pallor
3. Paralysis
4. Pulseless
5. Paraesthesia
6. Perishingly cold

Investigations:
- Routine bloods including serum lactate, ECG and group and save
- Doppler ultrasound
- CT angiogram

Management:
Surgical emergency -salvageability within 6 hrs
- Endovascular thrombectomy
- Endovascular thrombolysis
- Bypass surgery
- Angioplasty
- Amputation
Also
- Bolus of heparin
- Analgesia

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5
Q

Outline 3 vascular changes that occur as a result of atherosclerosis

A
  1. Stiffness…resulting in hypertension
  2. Stenosis…resulting in reduced blood flow
  3. Plaque rupture (thrombus formation)
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6
Q

List modifiable and non-modifiable risk factors for atherosclerosis

A

Modifiable:
- Hypertension
- Alcohol intake
- Diet
- Exercise / sedentary lifestyle
- Smoking
- Stress
- Poorly controlled co-morbidities e.g. diabetes
- Poor sleep

Non-modifiable:
- Age
- Genger (male)
- Family history

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7
Q

List co-morbidities that increase the risk of atherosclerosis

A
  • Diabetes
  • Hypertension
  • CKD
  • Inflammatory conditions
  • Atypical anti-psychotics
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8
Q

List the end results/consequences of atherosclerosis (what it predisposes you to)

A
  • Angina / MI
  • TIA / stroke
  • Peripheral arterial disease
  • Chronic mesenteric ischaemia
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9
Q

Outline the presentation of someone with intermittent claudication

A
  • ‘Crampy’ pain
  • Commonly in calves, but also buttocks and thighs
  • Onset after walking a certain distance
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10
Q

List the 6 P’s of critical limb ischaemia

A
  1. Pain
  2. Pallor
  3. Paralysis
  4. Pulseless
  5. Paraesthesia
  6. Perishingly cold
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11
Q

Signs of peripheral arterial disease

A
  • Ulcers
  • Poor wound healing / gangrene
  • Pallor
  • Cyanosis
  • Rubor if limb is below rest of the body
  • Hair loss
  • Muscle wasting
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12
Q

Explain the Buerger’s test

A

Used to assess peripheral arterial disease - 2 parts

Part 1:
- Patient lies down
- Elevate leg at 45 degrees and hold for 1-2 minutes
- If pallor, indicates peripheral arterial disease
(if no disease legs will remain pink)

Part 2:
- Patient hangs legs over the bed
- If blue initially then dark red, indicates peripheral arterial disease
(if no disease legs will remain pink)

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13
Q

List investigations for peripheral arterial disease

A
  • Ankle-brachial pressure index
  • Duplex ultrasound
  • Angiography
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14
Q

Outline the management for peripheral arterial disease

A

Conservative:
- Risk factor modification
- Smoking cessation
- Weight management
- Supervised exercise programme

Medical:
- Analgesia (vasodilators work well e.g. Naftidrofuryl oxalate)
- Medications to reduce risk factors e.g. optimum diabetes control

Surgical:
- Endovascular revascularisation (minor stenosis)
- Surgical revascularisation (significant stenosis)
- May need an amputation

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15
Q

When might an amputation be required in perihperal arterial disease

A

Amputation if there is:
- Critical limb ischaemia unsuitable for other interventions
- Intractable pain (pain that can’t be helped with analgesia)
- Unresolving ulcer
- Severe loss of function

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16
Q

Ankle brachial index - describe the test, how it’s calculated and outline values and their meaning

A

Ankle brachial index:
- Ratio of the systolic blood pressure in the arm compared to the ankle
- Calculated by:
Ankle systolic reading / Brachial systolic reading = RATIO

Values:
>1.3 = artery calcification
0.9-1.3 = normal
0.6-0.9 = mild PAD
0.3-0.6 = moderate PAD
<0.3 = severe PAD

17
Q

List some common thrombophilias

A
  • Anti-phospholipid syndrome
  • Factor 5 Leiden
  • Protein C or S deficiency
18
Q

Deep vein thrombosis (DVT) - state the following:
- Pathophysiology
- Risk factors
- Methods of prophylaxis
- Presentation
- Wells Score
- Diagnosis
- Management
- Long term anticoagulation (options and duration)

A

Pathophysiology:
- Development of a blood clot in the venous circulation (most commonly in lower limbs)
- The clot is then at risk at embolising to a distant site e.g. lungs causing a PE
- Commonly a result of a hypercoaguable state or blood stasis

Risk factors:
- Previous DVT
- Immobility
- Pregnancy
- Long haul travel
- Cancer
- Thrombophilia / polycythaemia
- Oestrogen based hormone therapy
- Smoking

Methods of prophylaxis:
- Limit risk factors if possible
- LMWH e.g. Enoxaparin
- Compression stockings

Presentation:
- Erythema
- Swelling
- Tenderness
- Oedema
- Dilated superficial veins

Wells Score:
- Takes into account risk factors and clinical presentation
- Score > 2 means likely to be DVT

Diagnosis:
- D-dimer (sensitive but not specific, more helpful for excluding DVT)
- Doppler ultrasound
- If pulmonary embolism suspected, CTPA

Management:
- Immediate anti-coagulation -> recommenced Apixaban or Rivaroxaban
- Catheter-directed thrombolysis if symptomatic DVT

Long term anticoagulation:
- DOAC
- Warfarin
- LMWH
- 3 months if reversible cause found
- 3-6 months if active cancer
- > 3 months if unclear cause
If unable to use anticoagulation - inferior vena cava filter

19
Q

Varicose Veins - state the following:
- Pathophysiology
- Risk factors
- Presentation
- Diagnosis
- Special tests
- Management
- Complications

A

Pathophysiology:
- Incompetent valves, resulting in to bidirectional flow
- Reduced venous return leads to dilation and engorgement of veins and venous pooling
- Incompetence due to weakening of walls, particularly impactful if perforating veins

Risk factors:
- Age
- Female sex
- Family history
- Pregnancy
- Obesity
- Occupations with long periods of standing
- DVT (damage to vessels)

Presentation:
- Engorged or dilated veins
- Aching sensation
- Itching / burning
- Oedema
- Restless legs
- Muscle cramps

Diagnosis:
- Duplex ultrasound
- Carry out special tests
Special tests:
1. Tap test
2. Cough test
3. Trendelenburg test
4. Perthes test

Management:
Conservative treatment
- Weight loss
- Activity
- Elevate legs when resting
- Compression stockings
Surgical
- Endothermal ablation
- Sclerotherapy
- Venous stripping

Complications:
- Prolonged and heavy bleeding after trauma
- Superficial thrombophlebitis
- DVT
- Chronic venous insufficiency

20
Q

Chronic venous insufficiency - state the following:
- Pathophysiology
- Risk factors
- Key presentation features seen
- Complications
- Management

A

Pathophysiology:
- Occurs when there is not complete drainage of blood from the legs back to the heart
- Results in venous hypertension which then leads to skin changes over time
- Often due to damage to the veins

Risk factors:
- Age
- Immobility
- Obesity
- Occupations with long periods of standing
- DVT

Key presentation features seen:
- Most commonly affects Gaiter area of legs
- Haemosiderin staining (haemoglobin leaks into skin)
- Venous eczema (chronic inflammatory response)
- Lipodermatosclerosis (chronic inflammation of subcut tissue)
- Atrophie blanche

Complications:
- Cellulitis
- Poor healing post-injury
- Ulcers
- Pain

Management:
- Keep skin healthy e.g. emollient use
- Improve venous drainage e.g. weight loss, elevate legs on resting
- Managing any complications e.g. wound care or antibiotics if infections

21
Q

State the different types of ulcers

A

Arterial ulcers:
- Due to insufficient blood supply

Venous ulcers:
- Due to blood pooling and waste products

Diabetic ulcers:
- Damage to blood vessels from diabetes leads to reduced blood supply and wound healing

Pressure ulcers:
- Occurs due to reduced mobility
- Leads to skin breakdown by: reduced blood supply, reduced lymph drainage and localised ischaemia

22
Q

Compare the following for arterial and venous ulcers:
Common location:
Associated with which disease:
Small or large:
Deep or shallow:
Border:
Likely to bleed:
Painful:
Made worse by:
Made better by:

A

Common location:
- Arterial: distal (dorsum of foot or toes)
- Venous: Gaiter area

Associated with which disease:
- Arterial: peripheral arterial disease
- Venous: chronic venous insufficiency

Small or large:
- Arterial: small
- Venous: large

Deep or shallow:
- Arterial: deep
- Venous: shallow

Border:
- Arterial: well defined
- Venous: poorly defined

Likely to bleed:
- Arterial: less likely
- Venous: more likely

Painful:
- Arterial: more painful
- Venous: less painful

Made worse by:
- Arterial: elevating leg
- Venous: lowering leg

Made better by:
- Arterial: lowering leg
- Venous: elevating leg

23
Q

Skin ulcers - state the following:
- Pathophysiology
- Types of ulcers
- Investigations to investigate cause
- Management for arterial and venous ulcers

A

Pathophysiology:
- Wounds or breaks in the skin that heal slowly due to underlying pathology
- May become bigger with time or become more difficult to heal

Types of ulcers:
- Arterial
- Venous
- Diabetic
- Pressure

Investigations to investigate cause:
- Ankle-brachial pressure index (assess for arterial disease)
- Blood tests (infection or co-morbidities)
- Skin swabs (infection)
- Skin biopsy (?skin cancer)

Management for arterial and venous ulcers:
General:
- Analgesia or pain management clinic
- Tissue viability referral
- Good wound care
- Antibiotics if infected
Arterial:
- Manage underlying condition
- Vascular surgery
Venous:
- Compression therapy

24
Q

Lymphoedema - state the following:
- Pathophysiology
- Assessment
- Management

A

Pathophysiology:
- Chronic condition caused by impaired lymphatic drainage of an area
- Primary lymphoedema = rare, genetic condition
- Secondary lymphoedema = acquired e.g. after breast cancer surgery
- Individuals have a higher risk of infection in the area of impaired drainage (reduced lymph node function)

Assessment:
- Stemmer’s sign
- Limb volume measurement
- Bioelectric impedance spectrometry
- Lymphoscinitgraphy

Management:
Non-surgical techniques
- Massage therapy or exercises
- Weight loss
- Compression bandages
- CBT / antidepressants
- Antibiotics if infections
Surgical techniques
- Lymphaticovenular anastomosis surgery

25
Q

Abdominal aortic aneurysm (not ruptured) - state the following:
- Pathophysiology
- Risk factors
- Screening
- Presentation
- Diagnosis
- Classification
- Management

A

Pathophysiology:
- Dilation of the abdominal aorta > 3cm (most commonly intra-renal)
- High mortality rate if ruptures (80%)

Risk factors:
- Male
- Age
- Smoking
- Hypertension
- Family history
- Existing cardiovascular disease

Screening:
- Offered to all MEN > 65 yrs
- Ultrasound scan to detect asymptomatic AAA early
- Only offered to women > 70 yrs, with risk factors

Presentation:
- Most patients are asymptomatic
- Pulsatile and expansile mass in abdomen
- Non-specific abdominal pain
- May be an incidental finding on screening / during other investigations

Diagnosis:
- Ultrasound
- CT angiogram for a more detailed picture (e.g. prior to surgery)

Classification:
Based on aorta diameter
- Normal < 3cm
- Small (3-4.5cm)
- Medium (4.5-5.5cm)
- Large (> 5.5cm)

Management:
- Reduce any modifiable risk factors e.g. stop smoking
- Depends on size
- Monitor if small (once yearly) or medium (3 monthly)
- Surgery if symptomatic, growing > 1cm per year or > 5.5cm
- Surgery either open (elective) or EVAR (emergency)

26
Q

Ruptured abdominal aortic aneurysm - state the following:
- Presentation
- Explain the concept of permissive hypotension
- State the investigation to diagnose/exclude ruptured AAA in haemodynamically stable patients

A

Presentation:
- Severe abdominal pain that may radiate to back/groin
- Haemodynamic instability
- Pulsatile and expansile mass
- Collapse
- Unconscious

Permissive hypotension:
- When you accept a lower blood pressure when doing fluid resuscitation, to reduce blood loss

State the investigation to diagnose/exclude ruptured AAA in haemodynamically stable patients:
- CT angiogram

27
Q

Aortic dissection - state the following:
- Pathophysiology
- Risk factors
- Presentation
- Diagnosis
- Classification
- Management (for both types)
- Complications

A

Pathophysiology:
- A break or tear in the wall of the tunica intima layer of the aorta (most commonly ascending aorta or aortic arch)
- This creates a false lumen between the tunica intima and tunica media

Risk factors:
- Hypertension
- Male
- Age
- Smoking
- Coarctation (aortic narrowing)
- Bicuspid aortic valve
- Marfan’s syndrome
- Ehlers-Danlos

Presentation:
- Severe ‘ripping’ chest pain (may migrate forward or backward)
- Difference in BP between arms
- Radial pulse deficit
- Diastolic murmur
- Hypotension or collapse

Diagnosis:
- CT angiogram or MRI angiogram (more detail but longer)
- May want to do a transoesophageal echo
- Chest x-ray and ECG to rule out other causes

Classification:
Stanford classification
Type A - first part of the aorta (ascending)
Type B - second part of the aorta (descending)

Management:
- Analgesia
Surgery
- Type A = Midline sternotomy, repair affected area with synthetic graft
- Uncomplicated type B = Medical management, control/lower BP and heart rate e.g. b-blockers, may need EVAR if complications occur

Complications:
- Cardiac tamponade
- Stroke
- MI
- Aortic valve regurgitation

28
Q

Carotid artery stenosis - state the following:
- Pathophysiology
- Risk factors
- Presentation and one potential positive finding on examination
- Investigations
- Outline severity classification
- Management

A

Pathophysiology:
- Narrowing of the carotid arteries leading to stenosis, usually secondary to atherosclerosis
- Part of plaque may break away, leading to embolic stroke

Risk factors:
- Male
- Age
- Smoking
- Hypertension
- Hypercholesterolaemia
- Obesity
- Diabetes mellitus
- Family history of cardiovascular disease

Presentation:
- Usually asymptomatic, commonly diagnosed after a stroke/TIA
- May hear a carotid bruit on auscultation (whooshing sound during systole)

Investigations:
- Carotid ultrasound
- CT or MRI angiogram

Severity classification:
- Mild = <50% diameter reduction
- Moderate = 50-70% diameter reduction
- Severe = >70% diameter reduction

Management:
Conservative
- Reduce modifiable risk factors
- Manage co-morbidities
Surgery
- Carotid endarterectomy (narrowing >50%)
- Angioplasty / stenting

29
Q

Buerger Disease - state the following:
- Pathophysiology
- Presentation
- Outline key feature seen on angiogram
- Management

A

Pathophysiology:
- Inflammatory condition that causes thrombus formation in small and medium sized distal arteries
- Also known as thromboangitis obliterans
- VERY strong association with smoking

Presentation:
- Typically young male with smoking history (25-35 yrs)
- Painful, blue discolouration of fingers/toes
- Pain is worse at night
- May have associated ulcers, gangrene or amputation

Key feature seen on angiogram:
- Corkscrew collateral vessels on angiogram (bypasses affected vessels)

Management:
- Stop smoking!! Usually results in significant improvement

30
Q

Outline cranial nerves that can be damaged during a carotid endarterectomy and how they would present

A

Nerve damage can be temporary or permanent

  1. CN7 (Facial nerve) - unilateral face droop
  2. CN9 (Glossopharyngeal nerve) - difficulty swallowing
  3. CN10 (Recurrent laryngeal nerve) - hoarse voice
  4. CN12 (Hypoglossal nerve) - unilateral tongue weakness/paralysis
31
Q

Explain the significance of triphasic, biphasic and monophasic pulses with respect to arterial disease

A

Helps to localize any occlusion or stenosis

Normally, waveform should be triphasic, corresponding to the three phases of a heart beat (systole, diastole, elastic recoil)

Biphasic pulse = mild to moderate disease

Monophasic pulse = significant disease

32
Q

Outline the values for ABPI and what symptoms you get within each range

A

> 1 = Symptom free
0.95 - 0.5 = Intermittent claudication
0.5 - 0.3 = Rest pain
< 0.2 = Gangrene and ulceration

33
Q

Outline the difference between an aneurysm and a pseudoaneurysm

A

Aneurysm
- Dilation of an artery that involves all three layers of the arterial wall (intima, media and adventitia)
- More common in: males, increasing age, smokers and family history

Pseudoaneurysm
- Collection of blood between the media and adventitia layers only
- Typically caused by direct trauma to the vessel

34
Q

Acute mesenteric ischaemia - state the following:
- Pathophysiology
- Types of occlusion
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Sudden decrease in the blood supply to the bowel
- Results in bowel ischaemia, can be fatal

Types of occlusion:
- Thrombus
- Embolism e.g. AF or aortic dissection
- Non-occlusive cause e.g. hypotension
- Venous occlusion and congestion e.g. coagulopathy, malignancy

Presentation:
- Acute onset of constant, generalised abdominal pain and tenderness, out of proportion to clinical findings
- Associated N&V

Investigations:
- Gold standard: CT scan with IV contrast
- ABG (for lactate and acidosis)
- Routine bloods

Management:
- Early senior involvement and ITU input
- Fluid resuscitation (IV fluids) and fluid balance chart
- Broad-spectrum antibiotic prophylaxis (in case of perforation)
- Eventually surgery to either re-vascularise bowel with thrombectomy or resect bowel if ischaemic

35
Q

Chronic mesenteric ischaemia - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Gradual decrease in the blood supply to the bowel, which reduces over time
- Occurs secondary to atherosclerosis (in coeliac trunk, SMA or IMA)
- Patients are generally asymptomatic due to collateral vessels, however any addition strain can cause symptoms e.g. after eating
- Generalised abdominal tenderness

Presentation:
- Abdominal pain 10mins - 4hrs after eating
- Weight loss
- Concurrent vascular comorbidities e.g. stroke
- Loose stool
- N&V

Investigations:
- Gold standard: CT angiography

Management:
- Early senior involvement and ITU input
- Fluid resuscitation (IV fluids) and fluid balance chart
- Broad-spectrum antibiotic prophylaxis (in case of perforation)
- Eventually surgery to either re-vascularise bowel with thrombectomy or resect bowel if ischaemic

36
Q

Outline how the presentation varies between vascular claudication and neurogenic claudication
- Distance
- Relieved by (sitting/standing)
- Resolves in (secs/mins)

A

Vascular:
- Fixed distance
- Relieved on standing
- Resolves in seconds

Neurogenic:
- Variable distance
- Relieved on sitting
- Resolves in mins

37
Q

Outline the scars for the following endovascular procedures:
- Femero-popliteal bypass
- Femoral-femoral bypass
- Axillo-femoral bypass
- Ileo-femoral bypass

A

Femero-popliteal bypass:
- Vertical groin scar
- Distal lower limb scar

Femoral-femoral bypass:
- 2 vertical groin scars

Axillo-femoral bypass:
- Scar over the left pectoral region (left chest)
- Scar over left groin

Ileo-femoral bypass:
- Oblique left iliac fossa scar (access the iliac arteries)
- Vertical groin scar (access the femoral arteries)

Year 3 - Surgery (10 decks)

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