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RW Cardiovascular > Vascular & Ischaemic Heart Disease > Flashcards

Vascular & Ischaemic Heart Disease Flashcards

1
Q

What is the difference between a thrombus and embolus?

A

A thrombus is a solid mass of blood components that forms locally in a vessel, while an embolus is a particle that moves about in our blood vessels, either in the veins or arteries.

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2
Q

What are fatty streaks and what causes them?

A

Lipids within macrophages causes by endothelial damage

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3
Q

What are the stages of atherosclerosis?

A

1) Endothelial damage stimulates the accumulation and oxidation of LDL-C in the vessel wall. 2) Monocytes migrate from the blood into the subendothelial intima and transform into macrophages, which accumulate lipids to form foam cells which appear as fatty streaks. 3) Production of inflammatory mediators stimulate deposition of elastin and collagen, leading to formation of the fibrous cap - fibrofatty plaque. 4) This causes the vessels to lose elasticity and leads to a cycle of more endothelial damage > streaks > fibrosis 4) Eventually the fibrous cap may weaken and rupture, exposing the underlying thrombogenic tissues. 5) This can induce further thrombus formation resulting in continued luminal narrowing or even arterial occlusion

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4
Q

Atheroma

A

An atheroma is an accumulation of degenerative material in the tunica intima of artery walls

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5
Q

Where do atheroma tend to form first and worst?

A

At areas of turbulent flow such as where vessels branch

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6
Q

What are the complications of atheroma?

A

1) Arterial stenosis (narrowing of the lumen) 2) Ischaemia 3) Thrombosis with infarct 4) Aneurysm (due to weakening of wall) 5) Arterial dissection 6) Embolism

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7
Q

Which arteries does arterial stenosis from atherosclerosis commonly occur?

A

Coronary, carotid, renal and peripheral arteries (eg. claudication)

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8
Q

Thrombosis

A

Formation of a solid or semi-solid mass from the constituents of blood, within the vascular system, during life.

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9
Q

How does an embolism form from atherosclerosis?

A

Piece of the plaque or thrombus breaks off and moves along the circulation until it reaches a smaller vessel and lodges

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10
Q

Ischaemia

A

Result of impaired vascular perfusion depriving the affected tissue of nutrients (inc. O2).

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11
Q

Infarction

A

Ischaemic necrosis of a tissue or organ secondary to occlusion/reduction of the arterial supply or venous drainage.

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12
Q

What is Virchow’s Triad of factors which contributes to thrombosis?

A
  1. Changes in vessel walls (endothelial injury) 2. Changes in blood constituents (hypercoagulability) 3. Changes in blood flow (stasis)
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13
Q

What is the role of platelets?

A

Close small breaches in vessel walls by temporary patching with collagen when in contact with sub-endothelial layers. If activated in a vessel = thrombus

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14
Q

What is the role of the endothelial cell?

A
  • Maintains a permeability barrier - Manages anticoagulant, antithrombotic, fibrinolytic regulators (Keeps the blood in a fluid state) - Manages prothrombotic molecules (When damaged, allows the blood to clot) - Produces EC Matrix - Modulates blood flow and vascular reactivity via vasoconstrictors - ACE and vasodilators – NO - Regulates inflammation and immunity - Regulates cell growth - Role in LDL oxidation
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15
Q

What 2 groups can conditions causing hyper coagulability be split into?

A

Acquired e.g. MI, prosthetic valves, AF and genetic e.g. factor V mutations

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16
Q

What are the main underlying causes of thrombosis in arteries and veins?

A

In arteries: atheroma In veins: stasis

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17
Q

Embolism

A

Any detached intravascular solid, liquid or gaseous mass which is carried by the bloodstream to a site distant from the point of origin.

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18
Q

What types of embolism re there?

A
  • Thromboembolism - Fat embolism - Marrow embolism - Air embolism - Septic embolism - Amniotic fluid embolism - Tumour embolism
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19
Q

Pulmonary thromboembolism

A

Emboli where 95% of which derive from large leg veins (popliteal, femoral, iliac) and travel via IVC to pulmonary circulation

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20
Q

True or False: Venous emboli cause infarcts in peripheral arterial circulation

A

False, DVTs etc only cause infants in the venous circulation or pulmonary circulation. Except if if there is an atrial/ventricular septal defect

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21
Q

What usually predisposes pts to fat emboli?

A

Generally follows soft tissue trauma or major bone fractures

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22
Q

What usually predisposes pts to gas/air emboli?

A

Barotrauma eg. in divers or others such as delivery/abortion

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23
Q

What occurs in amniotic fluid embolism?

A

Amniotic fluid and debris enters torn veins and embolises to lungs

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24
Q

What 3 disease patterns does arteriosclerosis cover?

A

1) Atherosclerosis 2) Arteriolosclerosis 3) Monckeberg Medial Calcific Sclerosis

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25
Q

Angina

A

Visceral pain from myocardial hypoxia

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26
Q

What are the characteristic patterns of angina?

A

• Provocation – exercise, cold day • Relief – within a few seconds – minute after stopping/resting or GTN spray • Timing – generally lasts less than a few hours

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27
Q

What investigations can be done for angina?

A
  • Exercise testing - Perfusion imaging - CT angiography
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28
Q

Which drugs can be used in the management of aspirin?

A
  • Aspirin: Antiplatelet - ß blockers: Slow heart rate, reduce O2 demand - Statin: Reduces cholesterol - ACE inhibitor: Reduces blood pressure
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29
Q

What are the general indications for PCI vs revascularisation (CABG)?

A

PCI - acute coronary syndrome Revascularisaton - chronic stable angina

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30
Q

Peripheral vascular disease

A

Circulation disorders affecting the vasculature outside the heart and brain, most often caused by atherosclerosis. Can affect either the arteries of veins

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31
Q

Peripheral arterial disease

A

Vascular disease specifically occurring in the arteries

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32
Q

Chronic lower limb ischaemia

A

Form of peripheral arterial disease. The gradual loss of blood supply to the lower limbs,

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33
Q

Intermittent claudication

A

Symptom of peripheral vascular disease - ‘angina of the legs’. - Mostly occurs due to atherosclerosis thus limiting the blood supply particularly when demand increases

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34
Q

Which system is used to classify the severity of PAD symptoms?

A

Fontaine classification

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35
Q

What is the main investigation for peripheral arterial disease?

A

-Ankle Brachial Pressure Index (ABPI) -Doppler US if highly calcified

36
Q

What is a normal ankle branchial pressure index?

A

0.9-1.2

37
Q

What does a ABPI

A

Claudication or Severe arterial disease

38
Q

What does a ABPI >1.2 indicate?

A

Abnormal vessel hardening

39
Q

What is the management for intermittent claudication in PAD?

A

-Guardian therapy - slow progression by modifying risk - Exercise : 30 mins 3x a week for 6 mo beyond pain - Main drug: Cilostozol (Phosphodiesterase inhibitor) - Endovascular: Angioplasty and stenting - Surgical: resection and bypass grafting

40
Q

Critical limb ischaemia

A

aka Acute limb ischaemia, occurs when there is a sudden lack of blood flow to a limb. Often occurs as acute-on-chronic limb ischameia when a thromboembolism breaks off of the atherosclerosis in the limb. Can also occur due to other embolism or trauma etc.

41
Q

Why are the nerve endings particularly affected at night by critical limb ischaemia?

A

Because you rely on gravity to get blood to the nerves at the bottom, so when you stop and lie down at night your nerves become ischaemic

42
Q

What 2 factors determine the level of amputation?

A

Healing: has to be at a point where there’s enough blood supply to be able to heal Function: the longer the stump, the more mobile you are going to be

43
Q

What are the clinical features of critical/acute limb ischaemia?

A

6 P’s: Pain, pallor, pulseless, perishingly cold, parasthesia, paralysis

44
Q

What is the management for critical/acute limb ischaemia?

A
  • Anti-Coagulate to stop the infarct propagating down the artery - Thrombolysis e.g. streptokinase delivered intra-arterial catheter - Embolectomy with fasciotomy (to avoid compartment syndrome) - Bypass surgery
45
Q

What are the main diabetic foot problems?

A

• Diabetic neuropathy – may stand on something and not feel it • Peripheral vascular disease – not enough blood supply to deal with infections etc • Prone to infections

46
Q

What occurs in diabetic foot sepsis?

A

Often starts with a puncture would of them standing on something and not feeling it. Then pus can’t escape to get compartment syndrome, exacerbated by lack of blood supply

47
Q

Aneurysm

A

Dilating of the vessels 50% greater than normal diameter

48
Q

What is the underlying cause of aneurysm?

A

Related to an imbalance of proteins in the aortic vessel waslls (specifically Metalo-protinase 9)

49
Q

Are aneurysms more common in males or females?

A

Males

50
Q

What is the cut-off diameter of an aortic aneurysm for intervention?

A

>5.5cm

51
Q

What investigations are used for monitoring AAA?

A
  • US (only confirms presence) - Duplex US (confirms size and iliac a. involvement( - CT scan (only method which can detect if ruptured)
52
Q

What are the 2 methods for elective surgical repair of AAA?

A

Endovascular Aneurysm Repair (EVAR) and Open repair

53
Q

What do you need to get blood out of the legs?

A

1) Vessel (2 parallel systems - deep e.g. tibias, popliteal and femoral and superficial eg. saphenous and perforators) 2 ) Some valves 3) A pump

54
Q

Varicose veins

A

Swollen and enlarged veins as a result of small valves in veins not working properly so blood starts to pool

55
Q

Which veins are most commonly affected by peripheral vascular disease?

A

Long and short saphenous veins

56
Q

True or False: Varicose veins can occur as a result of DVT

A

True, this is a secondary cause as there is an obstruction in the deep system, and still have pumping effect then the blood has to get pumped out to more superficial veins, and gets backed up

57
Q

What are the complications of varicose veins?

A
  • Bleeding - Thrombophlebitis (inflammation of a vein caused by a clot) - Chronic venous insufficiency (irreversible skin damage as result of sustained ambulatory venous hypertension)
58
Q

What are the 3 stages of chronic venous insufficiency?

A

1) Haemosiderin deposits 2) Lipodetmatosclerosis 3) Chronic venous ulceration

59
Q

What is the management for varicose veins?

A
  • Graduated compression e.g. stockings - Endovenous: foam sclerotherapy (causes inflammation by damage then put on stockings) and endovenous ablation - Surgical: high tie, stripping etc
60
Q

Deep Vein Thrombosis (DVT)

A

Formation of thrombi within the lumen of the vessels that make up the deep venous system

61
Q

Distal DVT

A

DVT of the calves

62
Q

Proximal DVT

A

DVT of the popliteal or femoral vein

63
Q

What is the differenced between provoked and unprovoked DVT?

A

Unprovoked DVTs have no identifiable cause. While provoked DVTs have causes, either: continuing/irreversible factors e.g. cancer or transient/reversible factors e.g. surgery or hospitalisation

64
Q

Post-thrombotic syndrome (PTS)

A

Consequence of DVT. Vessels are damaged so the series of valves aren’t functioning so the blood pools at the bottom of the legs, results in iron staining and deposition and eventually the breakdown of the leg

65
Q

Chronic thromboembolic pulmonary hypertension (CTEPH)

A

If a clot forms in the pulmonary arteries due to VTE, then it results in chronic high pressure in the lungs between the heart

66
Q

What is the main investigations for DVT?

A

D- dimer, probability score and then doppler US for final diagnosis

67
Q

What scoring system is used to determine the probability of DVT?

A

Well’s score (used alongside D-dimer)

68
Q

What scoring system is used to determine the probability of PE?

A

Modified Well’s score and Geneva score

69
Q

D - dimer

A

D-dimer is breakdown product of cross linked fibrin so high levels indicate a blood clot

70
Q

What investigations are used for PE?

A

D - dimer, probability scoring, CT pulmonary angiography (gold standard) or V/Q scan

71
Q

What are the treatment options for PE and DVT?

A

Pharmacological: anticoagulation - NOACs (main), thrombolysis and analgesias (used to be Vit K antagonists) Mechanical: graduated compression stockings (especially for post thrombotic syndrome), IVC filters (essentially a bird cage put in to catch clots)

72
Q

What are NOACs and give examples?

A

Novel Oral Anticoagulants - Replacing Vitamine K antagonists as anticoagulant treatment for DVT/PE as doesnt need to be monitored as large therapeutic window. Examples: Apixaban and rivaroxaban

73
Q

Stroke

A

Acute onset of focal neurological symptoms and signs due to disruption of blood supply

74
Q

What causes haemorrhagic stroke?

A

Weakened blood vessel wall due to: • structural abnormalities like aneurysm, arteriovenous malformation(AVM) • inflammation of vessel wall(vasculitis) • Hardening of vessels with age

75
Q

What causes ischaemic stroke?

A

Cutting off the blood supply due to: thrombus, embolus or hypopoerfusion

76
Q

What is the biggest risk following stroke?

A

Recurrence

77
Q

When can thrombolysis be used for stroke?

A

Only for ischaemic stroke and only for 4.5 hours following stroke symptoms

78
Q

What do you use to treat stroke when thrombolysis isn’t possible?

A

Medical: Antiplatelets, antigoagulation (if due to AF) and anti-hypertensives Surgical: haematoma evacuation, relief of raised ICP and carotid endarterectomy

79
Q

What are the 2 main classes of causes of PVD?

A

1) Functional (The body responds to certain external stimuli by restricting blood flow to the peripheral vessels eg. stress, smoking or cold) 2) Organic (Physical changes can affect the structure of blood vessels eg. atherosclerosis)

80
Q

What is the probable underlying cause for the link between diabetes and PVD?

A

Elevated levels of CRP are strongly associated with the development of PAD, and CRP levels are raised in diabetes. CRP has been found to bind to endothelial cell receptors promoting apoptosis and coexist with oxidized LDL in atherosclerotic plaques.Also stimulates pro-coagulants, inhibits fibrinolysis and raising vascular tone.

81
Q

What are the clinical features of PVD?

A

• Hair loss • Shiny appearance of leg and foot • Muscle wasting of calves • Thickening of toenails

82
Q

What BP prevents DVLA from allowing you a licence?

A

A resting BP consistently 180 mm Hg systolic or more and/or 100 mm Hg diastolic or more disqualifies a person from driving

83
Q

What are the DVLA guidelines regarding angina?

A

DVLA recommends that a licence should be refused or revoked with continuing symptoms (treated and/or untreated). Re-licensing may be permitted thereafter provided: • free from angina for at least 6/52 • the exercise or other functional test requirements can be met • there is no other disqualifying condition

84
Q

How does hypertension relate to the pathogenesis of atheroma?

A

increases the sheer stress on the vessel walls due to increased flow

85
Q

How does diabetes relate to the pathogenesis of atheroma?

A

High blood sugar, associated with diabetes has two effects on cells lining blood vessels as part of atheroslerosis. • First, it increases the production of free radicals, highly reactive molecules that cause premature cell death (apoptosis). • This process also reduces the availability of nitric oxide (NO), which would otherwise enable blood vessels to relax and blood flow to increase – instead the walls become stickier and cause increased hardening

86
Q

How does smoking relate to the pathogenesis of atheroma?

A

• Impairs the endothelium’s ability to vasodilate, by reducing NO availability •Toxins in cigarette smoke also result in an increase in leukocyte adhesion • Smoking also has an effect on the lipid profile as the toxins lower the level of HDL, while raising the LDL levels, specifically increases the rate of oxidation of LDLs

87
Q

How does hypercholesterolaemia relate to the pathogenesis of atheroma?

A

High levels of LDL mean there is a higher rate of transfer of LDLs into the endothelium to be oxidised. There are also less HDLs available to help mop up the other lipids

RW Cardiovascular (14 decks)

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