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2. Year 4 Surgery > Vascular Clinical > Flashcards

Vascular Clinical Flashcards

1
Q

Name the layers of a blood vessel.

A
  • tunica intima (endothelium)
  • internal elastic lamina
  • tunica media (smooth muscle cells, collagen)
  • external elastic lamina
  • tunica adventitia (connective tissue)
  • vasa vasorum (blood vessels that supply blood to larger arteries)
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2
Q

Describe the three different types of capillary.

A
  • continuous, fenestrated, and sinusoidal; these have variably sized gaps, acting as a ‘sieve’ controlling which molecules/structures can leave the capillary
  • e.g., continuous capillaries are found in skeletal muscle and allow only water and select ions to move
  • e.g., sinusoidal capillaries are found in the liver and allow larger structures, such as cells and proteins, to move
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3
Q

Describe the pathophysiology of atherosclerosis.

A
  • low density lipoproteins (LDL) deposit in weakened endothelium, undergoing oxidation by ROS to form OXLDL
  • newly activated endothelium causes adhesion of monocytes (which become macrophages) and T cells
  • monocytes migrate to the intima and ingest OXLDL to form foam cells
  • foam cells promote proliferation and migration of smooth muscle cells from the media to the intima, causing increased collagen production and subsequent hardening of the plaque
  • foam cell death releases OXLDL, causing additional hardening
  • the plaque is then known as an atheroma. rupture of an atheroma may activate the haemostatic system and create a thrombus
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4
Q

Name the risk factors for atherosclerosis.

A
  • non-modifiable: family history (atherosclerosis, cardiac disease), ethnicity (black African, Caribbean, South Asian), age (>65)
  • other medical conditions: hypercholesterolaemia, diabetes, hypertension
  • lifestyle: overweight/obesity, excess alcohol consumption, poor diet, lack of exercise, smoking/tobacco
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5
Q

Describe the renin-angiotensin-aldosterone system (RAAS).

A
  • renin is released from the kidney in response to low blood pressure, which converts the hepatic pro-enzyme angiotensinogen into angiotensin I
  • angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE) in the lungs
  • angiotensin II acts upon the adrenal glands to release aldosterone
  • aldosterone acts upon the collecting ducts of the renal nephron to promote water retention, subsequently increasing blood pressure
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6
Q

Describe the staging of hypertension.

A
  • stage 1: 140/90 clinic + 135/85 ABPM
  • stage 2: 160/100 clinic + 150/95 ABPM
  • stage 3: 180/110+ (either systolic/diastolic)
  • malignant: diastolic >130
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7
Q

Describe the investigations that should be undertaken after a diagnosis of hypertension.

A
  • cardiovascular risk assessment: ASSESS (Scotland), QRISK (UK)
  • urinalysis (albumin, creatinine kinase - is there renal injury?)
  • blood tests
  • fundoscopy (is there a retinopathy?)
  • 12-lead ECG (is LVH present?)
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8
Q

Describe the lifestyle and pharmacological management of hypertension.

A
  • lifestyle: diet, exercise, reduced alcohol and salt intake, smoking cessation, weight management
  • <55, non-fertile female, or diabetes of any age: ACEi/ARB
  • <55, fertile female: beta-blocker
  • > 55, black of any age: CCB/thiazide diuretic
  • escalation: add the other drug (ACEi/ARB or CCB), then a thiazide, then spironolactone
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9
Q

Name and describe the MoA and side effects of the five main classes of cholesterol-lowering drugs.

A
  • statins: blocks HMG-CoA-reductase; S/E rhabdomyolysis, hepatotoxicity
  • fibrates: upregulates LPL by PPAR alpha; S/E: cholesterol gallstones, hepatotoxicity
  • cholestyramine: bile acid sequestrant, using up cholesterol to create more bile acid; S/E: cholesterol gallstones, decreased absorption of fat-soluble vitamins, foul taste/GI upset
  • ezetimibe: decreases dietary absorption of cholesterol by blocking small intestine brush border enzyme NPC1LP; S/E: diarrhoea (increased fat excretion), increased LFT values
  • niacin: hormone sensitive lipase inhibitor, decreasing lipolysis in peripheral adipose tissue; S/E: flushing (reduced by aspirin), hyperglycaemia, hyperuricaemia
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10
Q

Describe the presentation of peripheral arterial disease (PAD).

A
  • three main patterns of presentation:
    – intermittent claudication: ‘leg angina’ - leg pain on exertion, but relieved by rest
    – (chronic) critical limb ischaemia - leg pain on rest
    – acute limb-threatening ischaemia - 6 P’s (pain, pallor, paraesthesia, polar, paralysis, and pulses absent) +/- ulcers/gangrene
  • haemosiderin deposits and lipodermatosclerosis may also be observed
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11
Q

Acute limb-threatening ischaemia generally occurs secondary to a thrombus (rupture of an atherosclerotic plaque) or an embolus (part of a plaque that travels through the blood). Which features help distinguish the pathology?

A
  • thrombus: pre-existing claudication w/ sudden deterioration, no obvious source for emboli, reduced/absent pulses in contralateral limb, evidence of widespread vascular disease (e.g., MI, stroke, TIA, previous vascular surgery)
  • embolus: sudden onset (<24hr) of painful leg with no history of claudication, clinically obvious source of emboli (e.g., atrial fibrillation, recent MI), no evidence of peripheral vascular disease (normal pulse in contralateral limb), evidence of proximal aneurysm (e.g., abdominal or popliteal)
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12
Q

Which simple investigation helps distinguish the type of peripheral arterial disease a patient has?

A
  • ankle-brachial pressure index (ABPI)
  • this is ankle systolic BP/brachial systolic BP
    – >0.9: normal
    – 0.4-0.9: intermittent claudication
    – <0.4: critical/acute limb-threatening ischaemia
  • NB MRI/CT/catheter angiography should be used in cases where there is false elevation of ABPI, such as in renal or diabetic disease
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13
Q

What is the main differential diagnosis of peripheral arterial disease (PAD) and how can it be distinguished from PAD?

A
  • spinal stenosis
  • also presents with unilateral/bilateral leg pain improving on rest or crouching
  • however, spinal stenosis presents with muscle weakness in the legs and/or a lack of smoking or cardiovascular history
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14
Q

Describe the initial and pharmacological management of peripheral arterial disease (PAD).

A
  • first-line management for early stage PAD is an exercise management program
  • all patients with PAD should be treated with atorvastatin 80mg and clopidogrel 75mg for secondary prevention of cardiovascular/stroke disease
    – NB doses are different for primary prevention
    – NB aspirin used to be recommended first line but clopidogrel is now first-line as it has fewer contraindications
  • additional drugs include
    – PDE3 inhibitors (e.g., cilostazol)
    – Naftidrofuryl (5HT2/serotonin receptor antagonist, which vasodilates)
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15
Q

Describe the surgical options for peripheral arterial disease (PAD).

A
  • endovascular revascularisation (angioplasty +/- stent): for short stenosis (<10cm), aortic/iliac disease, and high-risk patients
  • open surgical revascularisation: for long lesions (>10cm), multifocal lesions, lesions of the common femoral, purely infrapopliteal disease
    – surgical bypass
    – endarterectomy
  • amputation: for irreversible ischaemia or for patients who are not suitable for other interventions
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16
Q

Name the risk factors for DVT/PE (deep vein thrombosis/pulmonary embolism).

A
  • immobility
  • recent surgery
  • long-haul travel
  • pregnancy
  • hormone therapy (combined OCP, HRT)
  • malignancy
  • polycythaemia (high RBC count)
  • thrombophilia (particularly anti-phospholipid syndrome, but also various rarer haem conditions)
  • systemic lupus erythematosus
17
Q

Describe the presentation and Wells score for DVT/PE.

A
  • DVT: unilateral painful/swollen calf, oedema, redness, superficial engorged veins, Homan’s sign (pain on dorsiflexion of the foot)
  • PE: signs of DVT + dyspnoea, palpitation, pleuritic chest pain, haemoptysis etc.
  • Wells score:
    – 3 points: clinical signs of DVT, PE is the most likely diagnosis
    – 1.5 points: tachycardia, recent surgery or immobility, history of DVT/PE
    – 1 point: haemoptysis, malignancy
    – score >4 indicates probable PE
18
Q

Describe the use of D-dimer tests in DVT/PE.

A
  • D-dimers are sensitive but not specific, meaning 95% of patients with a DVT/PE will have a raised D-dimer, but not all patients with a raised D-dimer have a DVT/PE
    – other conditions that increase D-dimer include pneumonia, malignancy, heart failure, surgery, pregnancy etc.
  • this means D-dimer is useful only in excluding DVT/PE in patients with low clinical suspicion of DVT/PE
19
Q

Describe the investigations used in DVT and PE.

A
  • D-dimer as a test of exclusion in patients with low clincial suspicion
  • DVT: Doppler ultrasound, repeated after 6-8 days if negative and high suspicion (D-dimer positive, Wells score positive)
  • PE: ECG (S1Q3T3 sign classical), ABG, CTPA (first line), V/Q scan (if renal disease or contrast allergy)
20
Q

Describe the use of anticoagulants in DVT/PE.

A
  • DOACs (apixaban, rivaroxaban, edoxaban, dabigatran) first line, as these require no monitoring and are suitable for most patients, including those with malignancy
  • warfarin (vitamin K antagonist) used first-line for those with anti-phospholipid syndrome. INR target range is 2-3
  • LMWH: first-line in pregnancy
  • 3mo if there is a clear, reversible cause
  • > 3mo if there is no clear cause, VTE is recurrent, or there is an irreversible cause (e.g., thrombophilia)
  • 3-6 months: active malignancy
21
Q

Describe the pathology, classification, and risk factors for aortic dissection.

A
  • splitting of the tunica media; a tear in the tunica intima allows a false lumen to form and fill with blood
  • classification:
    – Stanford A: dissection of the ascending aorta; more common (2/3) and more fatal than B
    – Stanford B: dissection of the descending aorta (1/3)
  • RF:
    – hypertension (most important)
    – trauma
    – bicuspid aortic valve
    – collagen disorders (Marfan’s, Ehlers-Danlos)
    – Turner’s and Noonan’s syndrome
    – pregnancy (also causes hypertension)
    – syphilis
22
Q

Describe the clinical features and investigations for aortic dissection.

A
  • sharp chest pain, maximal on presentation, often described as ripping
  • chest pain is more common in Stanford A and abdominal pain in Stanford B, although pain very much overlaps
  • differing systolic BP in the arms (>20mmHg) due to differences in subclavian artery blood flow
  • weak downstream pulses
  • rupture and subsequent internal haemorrhage may lead to shock and hypotension
  • Ix:
    – CT angiography C/A/P first-line, suitable for stable patients and for planning surgery
    – transoesophageal echocardiogram (TOE) for less stable patients
    – CXR shows a widened mediastinum
    – presence of a false lumen is key to diagnosis
23
Q

Describe the management of aortic dissection.

A
  • management depends on the type of aortic dissection
  • Stanford A: emergency, requires surgical reconstruction with synthetic graft aortic arch replacement, often held open by a stunt
  • Stanford B: managed conservatively, with beta-blockers and nitroprusside
  • > 50% are hypertensive and require blood pressure control with IV labetalol prior to intervention (target systolic BP 100-120mmHg)
24
Q

Describe the pathology and risk factors for aortic aneurysms.

A
  • abnormal and persistent dilatation of the artery due to wall weakness; true aneurysms involve all layers of the vessel
  • RF:
    – male sex
    – age
    – smoking
    – hypertension
    – Marfan’s syndrome
    – family history, existing cardiovascular history
25
Q

Describe the screening and classification of aortic aneurysms.

A
  • men are offered screening between ages 65-74; women and men outside this age are generally at lower risk
  • normal (<3cm): 98%, no further action
  • small (3 - 4.4cm): >1%, rescan in 12mo and refer to vascular surgery clinic within 12wk
  • medium (4.5 - 5.4cm): <0.5%, rescan in 3mo and refer to vascular surgery clinic within 12wk
  • large (>5.5cm): <0.5cm, 2 week wait referral to vascular surgery for elective repair
26
Q

Describe the presentation and investigation of aortic aneurysms.

A
  • 75% are asymptomatic
  • 25% have symptoms, including
    – a pulsatile, expansile mass
    – left flank or abdominal pain, which may radiate to the lower back and/or groin
    – tachycardia, hypotension
    – DDx: renal colic, peptic ulcer, pancreatitis, appendicitis, diverticulitis, mesenteric ischaemia
  • USS is usually used as an initial test whereas CT angiogram gives more detail and helps guide elective surgery
27
Q

Describe the management of aortic aneurysms.

A
  • smoking cessation and management of co-morbidities (hypertension, diabetes, hyperlipidaemia)
  • elective surgery is indicated if:
    – aneursym is symptomatic
    – aneurysm is growing >1cm/yr
    – aneurysm is large (>5.5cm)
  • two main surgical options
    – endovascular aneurysm repair (EVAR) via femoral artery
    – laparotomy repair
28
Q

Describe the presentation and risk factors of carotid artery stenosis.

A
  • mostly asymptomatic; most are diagnosed after a stroke or TIA
  • additional signs/symptoms: carotid bruit, amaurosis fugax
  • RF:
    – hypertension, diabetes, hyperlipidaemia
    – smoking, sedentary lifestyle, obesity
    – age, male sex
29
Q

Describe the investigations and grading of carotid artery stenosis.

A
  • bloods (FBC, WCC, CRP, cholesterol, lipids, HbA1c)
  • intitial imaging: carotid arterial duplex ultrasound; all patients with TIA/stroke undergo ultrasound
  • CT angiography: gives more information and helps plan surgery
  • grading:
    – mild: <50% stenosis
    – moderate: 50-69% stenosis
    – high grade: 70-99% stenosis
    – complete occlusion: 100% stenosis

2. Year 4 Surgery (6 decks)

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