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*Medicine: Cellular Pathology > Cardiovascular pathology (1) > Flashcards

Cardiovascular pathology (1) Flashcards

1
Q

What are the 3 basic pathological processes which account for the majority of diseases in adult patients?

A
  • inflammation
  • neoplasia
  • thrombosis/embolism
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2
Q

What is haemostasis?

A
  • physiological process
  • initiated when there is damage to a blood vessel
  • involves rapid formation of a solid plug at site of injury
  • stopping haemorrhage
  • formed from platelets, fibrin + RBCs
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3
Q

Haemostasis depends on close interactions between the vessel wall, platelets and the coagulation cascade.

How is the loose platelet plug formed?

A
  • endothelial injury -> adhesion + aggregation of platelets
  • platelets adhere to exposed collagen by von willebrand factor
  • RBCs become enmeshed with the platelets
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4
Q

As the loose platelet plug is formed, what else is happening to initiate coagulation cascade? What does this do to the loose clot?

A
  • exposure of tissue factor initiates coagulation cascade
  • formation of insuluble fibrin
  • fibrin stabilises the loose platelet plug
  • forming a stable haemostatic plug
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5
Q

Why is haemostasis a good thing?

A

Protective process preventing blood loss from circulation

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6
Q

What is fibrinolysis and why is it important?

A
  • fibrinolytic system ensures haemostatic plug doesn’t become too big
  • fibrinolysis activated by same injury that initiates haemostasis
  • plasmin is formed + breaks down insoluble fibrin to soluble products

this fibrinolytic system helps ensure that haemostasis is very tightly regulated and limited to the site of injury

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7
Q

What is thrombosis?

A
  • inappropriate activation of hameostasis
  • overwhelms capacity of fibrinolytic system
  • resulting in formation of solid plug called thrombus
  • it’s a bad thing - thrombosis is pathological
  • (whereas, haemostasis is physiological)
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8
Q

What is a thrombus made up of?

A

Same components as a haemostatic plug, ie. platelets, fibrin and RBCs

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9
Q

What is the difference between a thrombus and a clot?

A
  • thrombus contains platelets whereas a clot doesn’t
  • thrombus forms within the CVS, clots form outside CVS eg. in a test tube or skin surface
  • thrombus forms in flowing blood (ie only in life), clot forms in stationary blood (ie. during or after life)

nb. clinicians often use the terms thrombus and clot interchangeably

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10
Q

Virchow’s triad describes the 3 major predisposing factors to thrombus formation, being?

A
  • endothelial injury
  • abnormal blood flow
  • hypercoagulability
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11
Q

What are examples of endothelial injury?

A
  • atherosclerosis
  • vasculitis
  • direct trauma eg. heat/chemical injury
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12
Q

What are examples of abnormal blood flow?

A
  • Turbulence:
    • atherosclerosis
    • artifical valves, stents, implanted devices
  • Stasis:
    • post-operative, trauma
    • congestive cardiac failure
    • immobility
    • pelvic obstruction eg. mass
    • aneurysms
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13
Q

What are examples of hypercoagulability?

A
  • Too many blood cells
    • erythrocytosis
    • thrombocytosis
  • Coagulation factor defects
    • hereditary eg. factor V Leiden, protein C/S deficiency
    • acquired eg. OCP, malignancy, pregnancy, lupus anticoagulant, DIC
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14
Q

What is the most important risk factor for thrombosis in an artery?

A

atherosclerosis

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15
Q

What are the most important risk factors for thrombosis in a vein?

A
  • stasis
  • hypercoagulability
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16
Q

What are the 3 main ways a thrombi can cause disease?

A
  • partial occlusion of vessel at site of thrombosis
  • complete occlusion of the vessel at site of thrombosis
  • embolism to a distant site
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17
Q

What may a partial or complete occlusion result in?

A
  • can cause ischaemia of tissue supplied by that vessel
  • if occlusion isn’t reversed, ischaemia -> infarction

the clinical effects depend on which vessel is occluded and the type of tissue supplied by that vessel

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18
Q

What is ischaemia?

A
  • tissue dysfunction
  • due to interference with blood flow to a tissue
  • reversible
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19
Q

What is infarction?

A
  • tissue death (necrosis)
  • due to interference w/ blood flow to tissue
  • irreversible
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20
Q

What is necrosis?

A
  • cell death
  • due to a pathological process
  • infarction is one cause
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21
Q

What are the categories of causes of ‘interference with blood flow’?

A
  • occlusion to arterial supply
  • occlusion to venous drainage
  • non-occlusion (globally reduced perfusion) eg. shock
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22
Q

What does embolism refer to?

A
  • the occlusion of a vessel -> ischaemia or infarction
  • by undissolved material that is transported in blood stream
  • clinical effects depend on the vessel occluded + tissue supplied
  • in clinical practice most emboli are thrombi (‘thromboemboli’)
  • other type of emboli refer to fat/bone marrow, air, amniotic fluid entering maternal circulation, tumour, septic emboli, atheromatous debris
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23
Q

What artery will emboli originating in the venous system occlude?

A
  • pulmonary artery
    • -> swollen calf
    • -> deep vein thrombosis
    • -> pulmonary embolism -> pulmonary infarct
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24
Q

Emboli originating in the arterial system will occlude which artery?

A
  • systemic arteries (of which there are many)
    • mesenteric artery occlusion -> bowel infarction
    • cerebral artery occlusion -> infarct-type stroke
    • renal artery occlusion -> renal infarct
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25
Q

What is atherosclerosis?

A
  • chronic inflammatory process
  • affecting intima of arteries (endothelium)
  • characterised by formation of lipid-rich plaques in vessel wall
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26
Q

What are the 4 important modifiable risk factors for developing atherosclerosis?

A
  • smoking
  • hypertension
  • diabetes mellitus
  • dyslipidaemia
  • others: obesity, diet, exercise

important non-modifiable risk factors include FHx + male gender

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27
Q

The risk factors mentioned previously can damage the endothelium. How does the damaged endothelium become dysfunctional?

A
  • there is increased permeability
  • they produce adhesion molecules and cytokines which attract inflammatory cells and prothrombotic molecules
  • eg. VCAM-1 (vascular cell adhesion molecule 1) binds to monocytes and T-cells
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28
Q

Following damage of the endothelium, there is consequently recruitment of inflammatory cells to the site of the injury.

Monocytes and T cells adhere to the endothelium and migrate into the intima. The monocytes differentiate into macrophages. What do the macrophages do here?

A
  • they produce free radicals that drive LDL oxidation to form oxidised LDL (native LDL is not atherogenic but oxidised LDL is highly atherogenic)
  • they engulf oxidised LDL + cholesterol crystals, becoming foam cells (foam cell = macrophage containing abundant cytoplasmic lipid)
  • foam cells produce growth factors that stimulate migration of smooth muscle cells from the media to the intima

The migration and activation of smooth muscle cells is also driven by factors released by activated platelets and endothelial cells

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29
Q

What is meant by the ‘fatty streak’?

A
  • oxidised LDL accumulates within macrophages + sm muscle cells just underneath endothelial cells
  • collections of lipid-laden macrophages sitting in intimal layer visible as yellow elevations called fatty streaks
  • fatty streak has no clinical significance but is important bc it may progress to an atherosclerotic plaque
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30
Q

What is an atherosclerotic plaque?

A
  • core of lipid debris forms as foamy macrophages die and the lipid in their cytoplasm is released
  • sm muscle cells proliferate + change their behaviour
    • secrete collagen + other ECM proteins
    • resulting in formation of fibrous cap over core
    • core is composed of oxidised lipid and inflammatory cells
  • the cap represents the body’s attempt to repair by scarring
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31
Q

Atherosclerosis exhibits the 3 hallmarks of a chronic inflammatory process, being?

A
  • persistent injury (endothelial damage due to prev described risk factors)
  • on-going inflammation (macrophages + lymphocytes)
  • repair w/ scarring (fibrous cap of plaque)
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32
Q

Atheroscleoritc plaques are dynamic structures which undergo continuous remodelling.

What is meant by plaque stability?

A

Plaque stability is determined by the balance between the # of sm muscle cells and the number of inflammatory cells in fibrous cap:

  • inflammatory cells destabilise plaques by producing MMPs -> they digest the fibrous cap. Infl cells cause sm muscle cells within the intima to undergo apoptosis
  • sm muscle cells are protective bc they produce the fibrous cap that stabilises the plaque. Also, tissue inhibitors of MMPs (TIMPs) are produced by sm muscle cells
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33
Q

What is the structure of stable plaques?

A
  • contain few inflammatory cells
  • large numbers of sm muscle cells
  • have a thick fibrous cap resistant to rupture
  • grow slowly in size over decades resulting in gradual stenosis
  • plaque rupture is less likely bc the thick fibrous cap protects from rupture
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34
Q

What is the structure of unstable ‘vulnerable’ plaques?

A
  • contain more inflammatory cells (foam cells etc)
  • have a thinner fibrous cap
  • more prone to acute rupture
  • resulting thrombosis and/or embolism
  • presenting as acute clinical events
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35
Q

What are the 3 main mechanisms by which atherosclerosis can cause disease?

A
  1. gradual** enlargement of a **stable plaque leading to luminal stenosis and reduced blood flow through the artery
  2. sudden rupture of a vulnerable plaque
  3. aneurysm formation
36
Q

How does gradual enlargement of a stable plaque cause stenosis?

A
  • plaque increases in size slowly over # of years
  • leading to gradual occlusion of lumen
  • gradual reduction in blood flow through artery
  • flow is proportional to 4th power of radius (Poiseuille’s law)
  • thus, reducing radius of a vessel by half leads to a 16x reduction in blood flow
  • eg. stable angina
37
Q

How does sudden rupture of a vulnerable plaque cause problems?

A
  • results in exposure of tissue factor + other pro-thrombotic substances
  • thrombus forms over site of ruptured plaque
  • thrombus may cause partial or complete occlusion of artery at site of plaque rupture eg. myocardial infarction
  • or may embolise to a distant site eg. ischaemic stroke
38
Q

Why is aneurysm formation a possible complication of atherosclerosis?

A
  • aneurysms form due to atherosclerotic plaque enroaching on and weakening the media
  • complications of aneurysms include rupture and formation of thrombus within the aneurysm
  • the thrombus can then embolise
  • eg. abdominal aortic aneurysm
39
Q

What is ischaemic heart disease?

A

term used to describe the spectrum of heart disease which results from coronary artery atherosclerosis

  • ac causes gradual or complete occlusion of 1+ coronary arteries -> gradual or sudden reduction of BF to myocardium
  • mismatch between demand + supply of O2/nutrients
  • myocardial ischaemia results
  • when BF reduction is sudden + total occlusion -> infarction
  • IHD represents a clinical spectrum, includes stable angina, ACS and sudden cardiac death
  • IHD an important cause of heart failure
40
Q

Angina is a clinical syndrome and not a disease. What is stable angina?

A
  • occurs when there is imbalance between supply + demand of O2/nutrients to the myocardium (eg. during exercise)
  • results in myocardial ischaemia which presents with predictable cardiac-type pain
  • precipitated by exertion, lasts for 1-2mins, relieved by GTN
41
Q

What is the most common cause of stable angina?

A
  • atherosclerosis - stable but gradually enlarging plaque in a coronary artery -> gradually progressive stenosis
  • stenosis results in a gradual reduction in BF through artery

Other diseases may also cause imbalance between O2/nutrient supply + demand resulting in angina syndrome, eg. aortic stenosis - results in significant left ventricular hypertrophy, which may cause a significant imbalance between supply and demand and manifest as angina.

42
Q

What will a microscopic section through a coronary artery show in stable angina?

A
43
Q

What is acute coronary syndrome?

A
  • ACS represent a spectrum of clinical conditions which occur when there is a sudden severe reduction in myocardial perfusion leading to ischaemia and/or infarction
  • ACS are due to an acute sudden change in a coronary artery atherosclerotic plaque
    • typically there is a sudden rupture of a vulnerable atherosclerotic plaque with superimposed thrombosis in the lumen at the site of rupture
44
Q

What are the clinical features of ACS?

A
  • typically there is chest pain similar to stable angina, but it is unpredictable and often it is much more severe
  • in MI, the pain often lasts >30 mins and is associated w/ nausea and sweating
45
Q

What changes occur on an ECG in ACS?

A

presence or absence of ST elevation

46
Q

What is the use of measuring cardiac troponin levels in ACS?

A
  • troponin is a contractile protein mainly bound as part of the actin/myosin complex
  • exists in 3 forms, T and I are used clinically (George’s uses Troponin I)
  • troponins are highly sensitive + specific for myocardial necrosis
  • the level of troponin rise correlates w/ amount of myocyte damage
  • levels rise following myocardial injury, peak at ~24hr + remain elevated for up to 14days
  • some hospitals measure Troponin I at time of admission and then at specific time intervals
47
Q

Is a troponin rise specific for MI?

A

a troponin rise is not in itself specific for MI since myocardial damage of any aetiology will cause a troponin release + rise. Other causes include coronary artery spasm due to cocaine, hypotension, chronic heart failure, myocarditis, some drugs etc.

48
Q

What are the three pathologies of acute coronary syndromes?

A
  • unstable angina
  • non-STEMI
  • STEMI
49
Q

When do unstable angina and NSTEMIs occur?

A
  • when coronary artery is partially occluded
  • ischaemic chest pain w/ ST depression and/or T wave inversion
  • they differ mainly in severity of myocardial ischemia
  • NSTEMI - ischaemia severe enough to result in release of cardiac troponins into blood
  • rise in troponin delayed so distinction between unstable angina and NSTEMI is made retrospectively
50
Q

What happens in a STEMI?

A
  • when there is total occlusion of a coronary artery which results in transmural myocardial infarction
  • there is ST elevation and raised troponin (greater than in NSTEMI)
51
Q

Summary of classification of acute coronary syndromes

A
52
Q

The management of acute coronary syndromes is different with respect to coronary reperfusion therapy.

What is the treatment for STEMI?

A

Pts assessed for eligibility for immediate coronary reperfusion therapy:

  • the preferred treatment is coronary angiography w/ follow-on primary percutaneous coronary intervention (PCI), if indicated
  • this is offered if pt presents within 12hrs of onset of symptoms AND primary PCI can be delivered within 120 mins (the quicker the better)
  • fibrinolytic treatment (thrombolysis) using agents such as alteplase or reteplase is offered to pts presenting within 12hrs of onset symptoms + when primary PCI cannot be delivered within 120 mins
53
Q

What is the treatment for NSTEMI and unstable angina?

A
  • pts who have an intermediate to higher risk of adverse CVS events* are offered coronary angiography w/ follow-on PCI (if indicated) within 96 hours of first admission
  • patients who are clinically unstable are offered angiography as soon as possible

*risk assessed using established risk scoring system that predicts 6 month mortality eg. GRACE

54
Q

What is the body’s response to myocardial infarction?

A
  • the dead myocardium incites a host acute inflammatory response
  • remember, inflammation is the body’s response to cell injury. The death of cells (as in MI) is the most severe form of cell injury and so incites an inflammatory response
  • myocardium is unable to regenerate and so the infarcted myocardium undergoes a process of repair, resulting in the formation of a scar (fibrous tissue)
55
Q

The site of infarction depends on which coronary artery is involved.

What does the right coronary artery supply and what ECG leads are affected?

A
  • RA, RV, pacemaker, inferior LV
    • -> Inferior MI
    • ECG leads II, III, aVF
56
Q

What does the left circumflex artery supply and what ECG leads are affected?

A
  • Lateral LV
    • -> lateral MI
    • ECG leads I, aVL, V5-6
57
Q

What does the left anterior descending artery supply and what ECG leads are affected?

A
  • Anterior LV
    • -> anterior MI
    • ECG leads V1-4
58
Q

List the short term complications of myocardial infarction

A
  • ventricular fibrilation
  • other arrhythmias
  • acute cardiac failure or cardiogenic shock
  • myocardium rupture
  • pericarditis
  • mural thrombus
59
Q

Why does ventricular fibrilation result from MI?

A
  • can cause sudden death
  • probably related to K+ released from necrotic myocytes which induce arrhythmias in the hyper-excitable tissue around the infarct
  • other arrhythmias are common in inferior infarcts eg. bradycardia, ventricular tachycardia, supraventricular tachycardia
60
Q

How does acute cardiac failure or cardiogenic shock result from MI? What is the difference between the two?

A
  • the infarcted myocardium no longer contracts
  • this may cause heart failure or cardiogenic shock (if significant proportion of myocardium affected)
  • key difference between acute cardiac failure and cardiogenic shock is the blood pressure
  • when acute cardiac failure is so severe that BP falls + adequate tissue perfusion can’t be maintained, the condition is called cardiogenic shock (has a high mortality)
  • this complication is directly related to infarct size
  • infarcts that involve >40-50% of total left ventricular mass usually lead to cardiac failure or shock
61
Q

Another complication of MI mentioned is myocardium rupture. What happens as different parts of the myocardium rupture?

A
  • the infarcted myocardium may rupture
  • the effects depend on which part of the myocardium ruptures
  • rupture of the free wall of ventricles -> haemopericardium and cardiac tamponade
  • rupture of papillary muscle of mitral valve -> acute mitral regurg
    • when there is a sudden onset of mitral regurg, heart cannot compensate so blood flows back into LA causing pressure in LA to rise
    • high pressure in LA is transmitted back into pulmonary circulation - causes transudation of fluid from circulation into lung interstitium + alveoli (pulmonary oedema) -> acute LVF
  • rupture of interventricular septum -> acute ventricular septal defect + presents as acute heart failure
62
Q

How does pericarditis result from MI?

A
  • a transmural infarct extends to involve the pericardium
  • inciting an inflammatory response
  • this manifests as acute pericarditis
63
Q

Why might a mural thrombus result from MI?

A
  • a thrombus may form in a heart chamber, usually the left ventricle
  • thrombus may form bc of a # of factors (Virchow’s triad)
    • endothelial injury (a transmural infarct extends to involve endothelium causing damage to endothelium)
    • stasis (infarcted myocardium doesn’t contract + so there is an akinetic zone)
  • thrombus may embolise + cause problems somewhere in systemic circulation
64
Q

What are the long-term complications of MI?

A
  • recurrent MI - due to coronary artery atherosclerosis
  • chronic congestive cardiac failure - due to loss of contractile myocardium
  • Dressler’s syndrome (=post myocardial infarction syndrome) - usually a self-limiting autoimmune pericarditis 2-10 months after full-thickness MI. In the era of PCI it is uncommon
  • Ventricular aneurysm formation, which predisposes to:
    • congestive cardiac failure
    • arrhythmia
    • thrombus formation within aneurysm (due to stasis) + hence embolisation

n.b. ventricular aneurysms only rupture very rarely bc they are composed of tough fibrous tissue

65
Q

The aim of PCI and thrombolysis is reperfusion of the myocardium. If reperfusion occurs before onset of irreversible injury to myocytes, then all myocytes survive. In contract, if reperfusion occurs after irreversible injury, then myocytes that are already necrotic are lost but mycoytes that are reversibly injured may be salvaged, thus reducing size of the infarct.

What is meant by ‘reperfusion injury’?

A
  • the process of reperfusion may damage some myocytes that were not already dead when reflow occurred
  • termed ‘reperfusion injury’
  • mediated by toxic oxygen species that are over-produced on restoration of the blood supply
  • if large, reperfusion infarcts may result in fatal arrhythmia or rupture
66
Q

What is meant by a ‘stunned myocardium’? Why is this?

A
  • most often myocardium that is viable at time of reflow, recovers
  • but critical abnormalities in biochemistry and function may persist
  • for several days as prolonged post-ischaemic ventricular dysfunction
  • due to reduced intercellular calcium or decreased sensitivity of contractile process
67
Q

How does the gradual enlargement of stable atherosclerotic plaques in coronary arteries result in the onset of progressive chronic heart failure?

A
68
Q

What is the most common type of stroke?

A
  • ischaemic stroke
  • account for about 80% of strokes
69
Q

How does ischaemic stroke lead to infarction?

A
  • caused by sudden occlusion of a cerebral artery
  • leading to sudden reduction in blood flow to part of brain
  • -> infarction of brain tissue
70
Q

What are ischaemic strokes due to (ie. which artery is involved and what then happens)?

A
  • most commonly rupture of an atherosclerotic plaque
  • in an internal carotid artery
  • thrombus forms on surface of ruptured plaque
  • part of thrombus embolises
  • and occludes one of the cerebral arteries -> stroke
  • clinical effects depend on which part of brain infarcted + which cerebral artery occluded

nb. only a small proportion of cerebral infarctions are due to rupture of an atheromatous plaque in a cerebral artery with thrombotic occlusion at site of plaque rupture, this is bc cerebral arteries are much less severely affected by atherosclerosis than the internal carotid arteries

71
Q

Thromboemboli causing an ischaemic stroke may also come from the left side of the heart - who is this common in?

A
  • pts w/ atrial fibrilation - risk of developing thrombus in LA, relevant Virchow triad risk factor is stasis within atrium caused by fibrilation. Part of thrombus may embolise + travel via circulation to occlude a cerebral artery. One of main reasons pts w/ AF are anticoagulated is to reduce risk of stroke
  • pts w/ infective endocarditis + vegetations on mitral or aortic valve
72
Q

What is an aneurysm?

A

localised, permanent, abnormal dilatation of a blood vessel by greater than at least 50% of its normal diameter

73
Q

What are the two classifications (according to appearance) of aneurysms?

A
  • saccular - spherical shape, bulges out of side of vessel
  • fusiform - spindle shape, involving all the circumference of the vessel
74
Q

What is a false aneurysm?

A
  • expanding pulsatile haematoma in continuity with a vessel lumen; it is not lined by endothelium
75
Q

What is the definition of an aortic aneurysm?

A
  • defined as aortic diameter of >3cm (norm = 2cm)
  • 95% arise in the abdominal aorta (AAAs)
  • 5% arise in the thoracic aorta
76
Q

What is the pathogenesis of AAA development?

A
  • not fully understood
  • atherosclerosis important role (remember risk factors for this)
  • the media (sm muscle) layer of aorta gives it its strength
  • an enlarging atherosclerotic plaque causes pressure atrophy or ischaemic atrophy of media + loss of elastic tissue
  • -> aortic wall is weakened and it dilates, forming aneurysm
  • over time it may get bigger
  • less commonly, connective tissue disorders (eg Marfans and Ehler Danlos syndrome) cause AAAs
77
Q

Why would an AAA rupture?

A
  • remember LaPlace’s law
  • tension in wall is porportional to radius
  • as radius increases, so does tension in wall
  • therefore risk of rupture of the wall
  • risk of rupture increases exponentially w/ diameter
78
Q

Why might thrombus/embolism form from AAA?

A
  • thrombus may form within an aneurysm
  • relevant Virchow triad risk factors for thrombosis are stasis of blood within aneurysm and endothelial injury due to atherosclerosis
  • thrombus may then embolise
  • clinical manifestations depend on which vessel thrombus occludes:
    • eg. occlusion of mesenteric artery will cause bowel infarction
79
Q

What is the NHS AAA screening programme?

A
80
Q

Pulmonary embolism refers to transportation of undissolved material in the bloodstream and its impaction in the pulmonary arteries.

What is this due to?

A
  • in ~70-80% cases due to thrombus originating in a vein in the leg (DVT)
  • in ~10-15% cases thrombus originates from vein in the pelvis
  • remember that within venous system, most important Virchow’s risk factors for developing thrombosis are stasis and hypercoagulability
81
Q

What will a medium-sized pulmonary embolus result in? What are the clinical effects?

A
  • causes occlusion of a segmental pulmonary artery
  • results in segment of lung being ventilated but not perfused
  • -> ventilation/perfusion defect
  • causes resp compromise
  • manifests as pulmonary infarction +/- pleuritis and an effusion
  • clinically there is typically pleuritic chest pain + SoB
  • may be haemoptysis due to infarction of non-perfused lung tissue
  • may also be pleural rub, crackles, effuison
82
Q

Venous thromboembolism (VTE) is a major cause of hospital deaths. What is venous thromboembolism prevention?

A
  • all pts admitted to hosp should have documented VTE risk assessment
  • pts should be reassessed within 24hr of admission + whenever clinical situation changes
  • appropriate prophylaxis should be administered, weighing up the VTE risk vs bleeding risk for each patient
  • options incl:
    • subcutaneous low molecular weight heparin (dalterparin at George’s)
    • mechanical interventions such as anti-embolism stockings
  • pts should be encouraged to mobilise ASAP
  • pts should be given info about VTE risk on admission + discharge
83
Q

What is Wells criteria?

A
  • the Wells criteria assess the clinical likelihood of pulmonary embolus
84
Q

What is the role of D-dimer in the diagnosis of PE?

A
  • D-dimers are cross linked fibrin degradation products formed by action of plasmin
  • D-dimers are raised in PE but also in other conditions eg. post-op, MI, stroke, trauma, pregnancy
  • thus, raised D-dimer not useful for making positive diagnosis of PE as not v specific
  • A normal (negative) D-dimer is useful since it has a >90% NPV (negative predictive value) for PE ie. >90% of patients with a negative D-dimer do not have a PE
  • When to use D-dimers:
    • when a PE is suspected clinically and the two-level PE Wells score is less than 4
    • not appropriate if the two-level PE Wells score is 4+; these pts need a CTPA
85
Q

What is the investigation of choice for imaging of PE?

A
  • CT pulmonary angiogram
  • NICE recommended
  • if CTPA is not appropriate then a ventilation:perfusion scan to be considered
  • for CTPA, radiocontrast injected into circulation + CT done
  • blood vessels filled w/ blood mixed w/ contrast so appear white
  • thrombus will appear as a dark area (a ‘filling defect’) bc it formed before contrast was administered
  • thus the thrombus does not contain contrast + appears dark

*Medicine: Cellular Pathology (16 decks)

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