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Cardiovascular Block > Week 3 > Flashcards

Week 3 Flashcards

1
Q

What is a stroke?

A
  • A blocked or ruptured blood vessel in the brain causing a failure of neuronal function leading (usually) to some deficit in brain function.
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2
Q

what % of stroke are caused by infarction?

A

80-95%

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3
Q

what % of stroke are caused by haemorrhage?

A

10-15%

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4
Q

how can atrial fibrillation cause a cardioembolic stroke?

A
  • Atria beating in an irregular, uncontrolled manner,
  • This causes the blood to swirl and stay within the atria.
  • This can cause a blood clot to form in the left atrial appendage.
  • This embolism can travel to arteries supplying brain with blood, causing a blockage and subsequent stroke.
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5
Q

What’s a rarer cause of stroke?

A

carotid dissection : idiopathic or trauma

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6
Q

what are the risk factors for stroke?

A
  • Hypertension.
  • Diabetes.
  • Heart and blood vessel diseases such as coronary heart disease, atrial fibrillation, heart valve disease and carotid artery disease.
  • High LDL cholesterol levels.
  • Smoking.
  • Age.
  • Family history.
  • Bleeding disorders.
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7
Q

what are some of the causes of haemorrhagic stroke?

A
  • Hypertension (60-70%).
  • Amyloid (15-20%).
  • Excess alcohol.
  • Hypercholesterolaemia.
  • Haemorrhagic transformation.
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8
Q

what’s the pathophysiology of ischaemic stroke?

A
  • Hypoxia stresses the metabolic machinery of brain cells which malfunction but are still alive.
  • If prolonged, the hypoxia becomes anoxia (no oxygen).
  • Anoxia results in infarction (complete cell death, leading to necrosis). This is a completed stroke.
  • Further damage can result from oedema (swelling), depending on the size and location of the stroke, or secondary haemorrhage into the stroke.
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9
Q

What are the signs and symptoms of stroke?

A
  • Motor (clumsy or weak limb).
  • Sensory (loss of feeling).
  • Speck: dysarthria/dysphasia.
  • Neglect/visuospatial problems.
  • Vision: loss in one eye, or hemianopia.
  • Gaze palsy.
  • Ataxia/vertigo/incoordination/nystagmus.
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10
Q

What are the stroke subtypes?

A
  • TACS: total anterior circulation stroke.
  • PACS: partial anterior circulation stroke.
  • LACS: lacunar stroke, most associated with hypertension.
  • POCS: posterior circulation stroke.
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11
Q

Describe the acute treatments for stroke.

A
  • Thrombolysis: alteplase, benefit is highly time dependent.
  • Antiplatelets.
  • Statins
  • Blood pressure management.
  • Anticoagulation (apixaban, rivaroxaban).
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12
Q

what are some primary prevention strategies?

A

o Controlling blood pressure.
o Managing cholesterol levels.
o Smoking cessation.
o Diabetes management.
o Healthy diet.

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13
Q

what are some secondary prevention strategies of stroke?

A

o Antiplatelet therapy such as aspirin.
o Anticoagulant therapy such as warfarin.
o Blood pressure management.
o Cholesterol management with e.g., statins
o Lifestyle changes.
o Carotid artery surgery.
o Cardiac procedures e.g., atrial fibrillation ablation, pacemaker insertion and valve repair/replacement.

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14
Q

What are the investigations of stroke?

A
  • Medial history and physical examination.
  • CT scan.
  • MRI scan.
  • Blood tests to check for factors that can increase risk of stroke such as high blood pressure, high cholesterol and diabetes.
  • ECG can identify irregular rhythms that can cause stroke.
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15
Q

the thoracic aorta is partitioned into which three segments?

A

the ascending aorta, aortic arch and descending aorta.

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16
Q

what are the branches of the ascending aorta?

A

left and right coronary branches.

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17
Q

what are the branches of the aortic arch?

A

o Brachiocephalic trunk which divides into the right subclavian and the right common carotid arteries.
o Left common carotid artery.
o Left subclavian artery.

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18
Q

what are the descending aorta branches?

A

o Visceral branches: pericardial, bronchial, oesophageal, and mediastinal arteries.
o Parietal branches: intercostal, subcostal arteries and superior phrenic arteries.

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19
Q

what is the basic histology of the aorta?

A

tunica intima
tunica media
tunica adventitia

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20
Q

what does the tunica intima contain?

A

o Tunica intima: layer of endothelial cells, a subendothelial layer composed of collagen and elastic fibres, separated from tunica media by an internal elastic membrane.

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21
Q

what does the tunica media contain?

A

o Tunica media: smooth muscle cells, that secrete elastin in the form of sheets, or lamellae.

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22
Q

what does the tunica adventitia contain?

A

o Tunica adventitia: thin connective tissue layer, collagen fibres and elastic fibres, the collagen prevents elastic arteries from stretching beyond their physiological limits during systole.

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23
Q

what is am aneurysm?

A
  • An aneurysm is a localised enlargement of an artery caused by a weakening of the vessel wall.
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24
Q

what % enlargement is considered an aneurysm?

A

50%

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25
Q

features of a true aneurysm

A
  • True aneurysms can be saccular (on one side of the vessel wall) or fusiform (on both sides of the vessel wall). It involves all three layers.
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26
Q

what are true aneurysms associated with?

A

o Hypertension.
o Atherosclerosis.
o Smoking.
o Bicuspid aortic valve.
o Collagen abnormalities (Marfans).
o Infection (mycotic/syphilis).
o Trauma.

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27
Q

what causes a false aneurysm?

A
  • False aneurysms can be caused by rupture of the wall of the aorta with the resulting hematoma either contained by the thin adventitial layer or by the surrounding soft tissue.
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28
Q

false aneurysms are associated with?

A

o Trauma.
o Iatrogenic.
o Inflammation (e.g., endocarditis with septic emboli).

29
Q

what is an aortic dissection?

A
  • An aortic dissection is a tear in the inner wall of the aorta. Blood then forces the walls apart. Can be acute > medical/surgical emergency, or chronic.
30
Q

what are the risk factors for aortic dissection?

A

o Hypertension.
o Atherosclerosis.
o Marfan’s syndrome.
o Bicuspid aortic valve.
o Trauma.

31
Q

What is classified as a stanford type A dissection?

A

all dissections involving the ascending aorta, regardless of the site of origin.

32
Q

what is classified as a type B dissection?

A

all dissections not involving the ascending aorta

33
Q

describe the clinical presentation of acute thoracic aneurysm

A
  • Can be asymptomatic.
  • Based on the location of the aneurysm:
    o Shortness of breath (associated with aortic regurgitation).
    o Dysphagia and hoarseness.
    o Back pain.
    o Symptoms of dissection – sharp chest pain radiating to the back (between shoulder blades), hypotension.
    o Pulsatile mass.
34
Q

describe the symptoms of acute aortic dissection

A

o Chest pain- severe, sharp, radiating to back (interscapular).
o Collapse (tamponade, acute aortic regurgitation, external rupture).
o Stroke (involvement of carotid arteries).

35
Q

describe the clinical examination finding in acute aortic dissection

A

o Reduced or absent peripheral pulses.
o Hypertension or hypotension.
o BP mismatch between sides.
o Soft early diastolic murmur (aortic regurgitation).
o Pulmonary oedema.
o Signs of CVA.

36
Q

what is coarctation of the aorta?

A
  • Coarctation is aortic narrowing close to where the ductus arteriosus inserts (ligamentum arteriosum).
37
Q

what is the most common form of aortic coarctatiobn in adults, give features.

A
  • Post-ductal coarctation is the most common form in adults. It causes hypertension in the upper extremities and weak pulses in the lower limbs. It is also associated with rib-notching.
38
Q

What is marfans syndrome?

A
  • Marfan’s syndrome an autosomal dominant genetic disease caused by a defect in the Fibrillin 1 gene causing connective tissue weakness.
39
Q

what are possible aortic manifestations of marfans syndrome?

A
  • This can cause aortic/mitral valve prolapse – regurgitation, as well as aortic aneurysm and dissection.
40
Q

what is arterial occlusive disease?

A
  • Arterial occlusive disease is a condition in which there is a partial or complete blockage of the arteries that supply blood into the limbs, typically the legs.
41
Q

what is the clinical presentation of arterial occlusive disease? In stages

A
  • Stage 1: asymptomatic, incomplete blood vessel obstruction.
  • Stage 2: mild claudication pain in the limb on exertion.
  • Stage 3: rest pain, mostly in feet.
  • Stage 4: necrosis and/or gangrene of the limb.
42
Q

what is aneurysmal disease?

A
  • Aneurysmal disease is a condition in which there is a bulging or ballooning out of a weakened area in the wall of an artery.
43
Q

what are the clinical presentations of aneurysmal disease?

A

o No symptoms: may be discovered incidentally on imaging studies performed for other reasons.
o Abdominal pain or discomfort: AAA patients may describe the pain as aching or pulsating, and it may be severe in some cases.
o Thoracic pain or discomfort: TAA patients may describe the pain as sharp or stabbing, and it may be worse with deep breaths or coughing.
o Limb ischaemia: aneurysms in the peripheral arteries can cause a decreased blood flow to the limbs, resulting in pain, weakness, or numbness in the affected limb.
o Neurological symptoms: aneurysms in the brain can cause neurological symptoms such as headaches, visual changes, weakness, or numbness in the face, arms or legs.
o Rupture: aneurysms that rupture can cause sudden, severe pain, or discomfort and can be life-threatening. Patients may also experience symptoms such as dizziness fainting or shock.

44
Q

what is carotid endarterectomy (CEA)?

A
  • CEA is a surgical procedure used to treat carotid artery stenosis, which is a narrowing of the carotid artery that can lead to stroke. The procedure involves removing plaque build-up from the inner lining of the carotid artery to restore blood flow to the brain.
45
Q

strengths of CEA?

A

o Effective in preventing stroke.
o Long-lasting benefits: reduces the risk of stroke for up to 10 years after the procedure.
o Lower risk of restenosis.

46
Q

weaknesses of CEA?

A

o Risk of complications: although CEA is effective in preventing stroke, there is a risk of complications such as nerve damage, hematoma, or carotid artery dissection during the procedure.

47
Q

clinical presentation of venous disorders

A

o Swelling.
o Pain.
o Skin changes: discolouration, thickening, and the development of ulcers.
o Varicose veins: bulging and twisting of the veins, may be accompanied by pain or discomfort, as well as a feeling of heaviness or tiredness in affected limb.
o Deep vein thrombosis.

48
Q

describe the progression of venous disorders

A
  • The progression of venous disorders can vary depending on the underlying condition and the individual patient factors. Some venous disorders may be relatively benign and may not progress over time, while others can lead to serious complications if left untreated. For example, DVT can lead to pulmonary embolism. Varicose veins can develop, while not typically life-threatening, can cause significant discomfort and can lead to skin changes and ulcers if left untreated.
49
Q

identify the possible surgical interventions for the treatment of arterial occlusive disease.

A
  • Open surgery:
    o Bypass and/or
    o Endarterectomy.
  • Endovascular intervention:
    o Balloon angioplasty.
    o Stent replacement.
    o Atherectomy.
50
Q

what is the main role of the venous system in the lower limbs?

A
  • The main role is to return deoxygenated blood back to the heart from the lower body. The veins in the lower limbs have one-way valves that prevent the backflow of blood and aid in the upwards flow of blood against gravity towards the heart.
51
Q

what is the function of the venous system in the lower limbs?

A

o Drain deoxygenated blood.
o Maintain blood pressure by providing a low resistance pathway for blood to return to the heart.
o Aid in circulation by acting as a blood reservoir. Blood can be released when there is a sudden demand such as during exercise.
o Regulate body temperature by transporting heat away from the body’s surface.
o Prevent fluid build-up.

52
Q

what is superficial venous incompetence? and what are the complications?

A
  • Superficial vein incompetence occurs when the valves in the superficial veins, which are close to the skins surface, do not function properly. As a result, blood can pool in these, causing them to bulge and become varicose veins. This condition can cause symptoms such as pain, swelling, and skin changes.
53
Q

what is deep venous incompetence? and what are the complications?

A
  • Deep vein incompetence, on the other hand, occurs when the valves in the deep veins, which are located deeper in the leg muscles, do not work correctly. This can cause blood to flow backwards and pool in the deep veins, leading to a condition called deep vein thrombosis (DVT). DVT can cause pain, swelling, and redness in the affected leg, and in severe cases, it can lead to a life threatening pulmonary embolism (PE).
54
Q

changes of chronic venous insufficieny

A

o Varicose veins.
o Oedema.
o Skin changes.
o Venous ulcers.
o Pain.
o Skin infections such as cellulitis.
o Restless leg syndrome.

55
Q

what investigations are required to confirm the diagnosis of venous insufficiency?

A
  • Duplex ultrasound.
  • MRI venogram.
  • CT venogram.
  • Venogram.
56
Q

what is the role of the lymphatic system?

A
  • The lymphatic system collects excess fluid, proteins and toxins from your cells and tissues and returns them to your bloodstream.
57
Q

what happens when the lymphatic system doesn’t work?

A
  • When the lymphatic system doesn’t work, the body accumulated fluid and may begin to swell > lymphedema.
  • Lymphedema also increases the risk of developing an infection at the site of swelling.
58
Q

Chronic venous insufficiency may be caused by a DVT.
TRUE OR FALSE?

A

TRUE

59
Q

Regarding stroke: MCA occlusion can lead to loss of vision in one eye.
TRUE OR FALSE?

A

FALSE- it can lead to a homonymous hemianopia. This means the same field of vision is lost in both eyes.

60
Q

Strokes are often caused by emboli from deep vein thrombosis.
TRUE OR FALSE?

A

FALSE- Deep vein thrombosis will embolise through the venous system, ending up in the right side of the heart. Emboli then travel through the pulmonary artery, becoming lodged in the pulmonary vascular bed – causing a pulmonary embolis.

61
Q

Ultrasound scans have different phases which show up different tissues in the body
TRUE OR FALSE?

A

FALSE- CT scans do. Arterial, venous, nephrogenic and delayed phases occur at different time intervals from dye injection: within 15seconds for arterial, and 6-10 mins for delayed phase of CT scan

62
Q

Risk factors for varicose veins do not include DVTs.
TRUE OR FALSE?

A

FALSE- A DVT disrupts the valve system in veins causing back pressure in the superficial system which results in varicose veins.

63
Q

What is the investigation of choice to assess varicose veins?

A

Doppler US scanning

64
Q

Carotid Endarterectomy should be considered if there is more than 70% stenosis of the internal carotid artery which is symptomatic.
TRUE OR FALSE?

A

TRUE

65
Q

What is the preferred treatment for varicose veins?

A

Endovenous treatment and ultrasound guided foam sclerotherapy are 1st and 2nd line options. Open surgery is now 3rd line option for treatment of varicose veins.

66
Q

what is the diameter of the abdominal aorta?

A

2cm

67
Q

an AAA is defined as being how many cm or more?

A

2cm or more

68
Q

where is the classic site of a venous ulcer?

A

just above the malleoli

69
Q

what are the benefits on rate-limiting CCBs? give an example

A

rate-limiting CCBs such as verapamil reduce heart rate and produce some vasodilation.

Cardiovascular Block (5 decks)

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