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Medicine 2 - 05 Heart Failure > 5 Thrombosis and Embolism > Flashcards

5 Thrombosis and Embolism Flashcards

1
Q

Define thrombosis

A

Thrombosis:

- is the process leading to the formation of thrombus

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2
Q

Define thrombus

A

Thrombus:
- is a solid mass composed of blood constituents that have been aggregated together in blood flowing in the lumen of a blood vessel

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3
Q

State the main constituents of a thrombus

A
  • Platelets

- Fibrin

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4
Q

Describe what occurs during the physiological formation of a thrombus

A
  • Primary haemostasis

- Secondary Haemostasis

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5
Q

Describe primary haemostasis (as the first stage of physiological formation of a thrombus)

A

Primary haemostasis

  • Vessel wall is breached
  • Circulating platelets aggregate to plug the gap
  • Platelets release factors that trigger the coagulation cascade
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6
Q

Describe secondary haemostasis (as the second stage of physiological formation of a thrombus)

A

Secondary Haemostasis

  • Coagulation cascade converts fibrinogen to large molecules of insoluble fibrin
  • Long fibrin molecules bind together platelets and entrapped white and red blood cells
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7
Q

Describe the course of the coagulation pathway, and how different pathways are activated, as well as how they all end in the same end result (common pathway)

A

The coagulation cascade is composed of the intrinsic and extrinsic pathways, which both lead to the common pathway (X -> Xa);
- where Thrombin converts fibrinogen to fibrin (clot)

Intrinsic - contact activation with collagen (Factor XII - XIIa to XI to IX to X)

Extrinsic - damage to blood vessel or release of Tissue factor (Factor VII to VIIa, X to Xa)

Common - Xa converts Prothrombin (II) to thrombin (which then converts fibrinogen to fibrin)

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8
Q

Define the process of Fibrinolysis

A

Fibrin holds thrombin together

Fibrinolysis - Fibrin is broken down, where the thrombus ‘dissolves’

  • Plasmin is the active enzyme that fragments Fibrin
  • The fragmented fibrin is called ‘Fibrin degradation products’ - FDP
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9
Q

Describe the process of Fibrinolysis

A

Plasma contains the inactive proenzyme plasminogen
- Plasminogen is converted to plasmin by plasminogen activators
> particularly tissue plasminogen activator (t-PA), which is secreted by endothelial cells and urokinase

When fibrin is formed, plasminogen and t-PA bind to it

  • The t-PA converts nearby plasminogen to plasmin
  • Which then begins to degrade the fibrin

THIS controls the size of the Thrombus

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10
Q

Describe the role of the feedback mechanism loops that govern the breakdown of clots, including the role of Plasmin, t-PA and other species

A

Plasmin makes more plasmin by t-PA

  • BUT both plasmin activators (t-PA and urokinase) are inhibited by plasminogen activator inhibitor 1 + 2
  • Plasmin itself is inhibited by antiplasmin
  • Products of plasmin breakdown (FDP’s) also compete with thrombin to convert less fibrinogen to fibrin

Breakdown of clots occur like this

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11
Q

Define and describe a pathological thrombus

A

A pathological thrombus occurs when the thrombus enlarges beyond vessel healing requirements and continues to grow

Beyond a certain thrombus size and rate of development, the intrinsic fibrinolytic system is incapable of controlling the size to which the thrombus grows

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12
Q

Describe the D-dimer test

A

D-dimers are Fibrin Degradation Products (FDP)

  • they are detected by mAb tests to D fragment
  • D-dimer levels are seen to be elevated in the blood during thrombosis

This is a ‘rule-out test’
- so negative tests means coagulation isn’t activated

BUT, a positive test May mean coagulation cascade is activated, or other factors we know

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13
Q

Describe what a positive D-dimer test may indicate

A

A positive test in presence of active thrombosis:

  • Pulmonary embolus
  • Deep vein thrombosis (DVT)
  • Aortic Dissection

BUT, this test is best used as a test of EXCLUSION

A false-positive test can be found in:

  • Inflammation
  • Malignancy
  • Trauma
  • Pregnancy
  • Recent surgery
  • Liver disease
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14
Q

Describe what factors may predispose someone to thrombus formation

A

Virchow’s triad:

  • Damage to vessel wall - especially endothelium
  • Stasis - slow or turbulent blood flow
  • Hypercoagulability - change in the character of blood (especially increased platelets, increased RBC’s, increased viscosity)
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15
Q

Describe where a pathological thrombus occurs

A
  • Arteries - main predisposing factors are vessel wall damage
  • Veins - stasis most important (low pressure + flow systems)
  • Heart
    > Ventricles - chamber wall damage most important
    > Atrium - stasis most important (AF)
    > Heart Valves - valve surface damage most important (Endocarditis, congenital)
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16
Q

Describe a thrombus in an artery,

and what effect it may have on a patient

A

A thrombus can form an atheroma in a coronary artery

  • There will be an atheromatous plaque
  • There will be the thrombus (which may fill the lumen)

Effect on patient:
- Myocardium distal to this occlusion point will infarct, so the px will have a MI, and the myocardium will undergo necrosis

17
Q

Describe a thrombosis in a vein,

and what effect it may have on a patient

A

A thrombosis can occur in a vein with no visible wall damage

Effect on the patient:

  • Not the same infarction as seen in artery:
  • Prevents venous drainage of a territory or organ
  • Causing congestion + increased venous pressure within the organ
  • This leads to infarction
  • Haemorrhagic infarction
  • Embolisation
18
Q

Describe a thrombus on the wall of a heart,

and what effect it may have on a patient

A

The thrombus can form over a damaged endocardium:

  • This is usually consequential on a myocardial infarction that causes thinning and disruption of the endothelium, as it heals over to form a scar
  • And that then forms a nidus bethrombus

Effect on the patient:
- If thrombus stays in the ventricular cavity (nothing much) - could lead to Myocardial infarction
> severity means a reduction in the ejection of blood

  • BUT the thrombus MAY break off and embolise into the systemic arterial circulation
  • MOST common - L ventricular embolism is to go to the cerebral artery - stroke
19
Q

Describe a thrombus on a heart valve,

and what effect it may have on a patient

A

A thrombus may form on the damaged endocardium of the mitral valve:

  • AV valve on the left side of the heart, there may be a vegetational disruption on endothelium on the valve,
  • due to infective processes
  • So. there is thrombus formation on vegetation

Effect on the patient:

  • LV thrombus - embolisation of the L AV valve,
  • break off into systemic circulation - [Stroke]
  • Coronary artery (through aortic valve) - myocardial infarction

SO, when the thrombus embolises into any organ in the systemic circulation, it can lead to damaging that organ

20
Q

Describe some common outcomes for a pathological thrombus

A
  • It may be lysed by intrinsic fibrinolysis - RARE
  • It may completely block the lumen (occlusion)
  • It may undergo organisation + recanalisation
  • It may extend locally (propagation)
  • It may fragment or detach completely + travel elsewhere in the circulation (THROMBO-EMBOLISM)
21
Q

Describe what happens when a thrombus occludes a vessel?

A
  • In an artery, thrombotic occlusion stops the flow of blood and cuts off oxygen supply - INFARCTION
  • In a vein occlusion prevents drainage of tissue, blood then pools, cannot escape - CONGESTION + infarction (that is often haemorrhagic)
22
Q

Describe the process of organisation of thrombi + recanalisation

A
  • New vessels grow into the thrombus
  • Vascular granulation tissue develops
  • Fibroblasts invade + deposit collagen
  • Fibrovascular granulation tissue develops

This is an organised thrombus.
- Sometimes, the vessels link up + some degree of recanalisation occurs

23
Q

Define + describe embolism

A

Embolism is the transference of abnormal material by the bloodstream with eventual impaction of the material in a vessel distal to its site of origin

The most important materials to embolise are:

  • Thrombus
  • Cancer cells (metastasis)
24
Q

Define and describe thromboembolism:

A

Thromboembolism
- A thrombus can break off and pass in the blood stream to a distal site, where they can impact and occlude a distal vessel

It can have a different effect, depending on whether the thrombus originates in the L or R side of the heart
- or in a systemic artery OR vein

25
Q

Describe what a thrombus in an artery of the L side of the heart can embolise to

(and what distal branches may it block)

A

A thrombus in an artery or the L side of the heart embolises into the systemic arterial system

The thromboembolism may block distal branches:

  • of Brain arteries - Stroke
  • of Lower limb arteries - Gangrene of leg
  • of Mesenteric arteries - Bowel infarct
  • of Renal arteries - Kidney infarct
  • of Splenic arteries - Splenic infarct
26
Q

Describe what a thrombus in a systemic vein can embolise to

and what the impact on the patient might be

A

A thrombus in a systemic vein eventually embolises to a pulmonary artery (pulmonary embolism)

The impact on the patient depends on the size of the embolus:

  • Small embolus - small peripheral lung infarct
  • Large embolus - sudden death
27
Q

Describe what a VTE risk assessment is, and its use in the clinical setting

A

Venous thromboembolism assessment
- given to px on entry to the hospital, as VTE is common in hospital

VTE risk assessments:

  • Assess the level of mobility (as it is going to be reduced)
  • Look for patient-related risk factors for thrombosis
  • Look for patient-related risk factors for bleeding

So, judgements must be made to balance the risk of thrombosis vs bleeding
- in order to treat with prophylactic therapy to prevent DVT
> e.g. as much mobilisation as possible
> stockings (venous return increases)
> flowtron (inflatable cuffs on the leg that goes up and down to mimic contraction of calf muscles - to promote return of venous blood from leg - [in ICU]

28
Q

Describe factors that are going to make people most likely at risk of Venous Thromboembolism

A
  • Active cancer/cancer treatment
  • Age > 60 years
  • Dehydration
  • Known thrombophilias
  • Obesity (BMI > 30kg/m^2)
  • One or more significant medical co-morbidities
    > Heart disease, metabolic, endocrine or respiratory pathologies, acute infectious diseases, inflammatory conditions
29
Q

Describe some other risk factors for Venous TE

A
  • Personal history or 1st degree relative with a history of VTE
  • Hormone replacement therapy (HRT)
  • Use of oestrogen-containing contraceptive therapy
  • Varicose veins with phlebitis
  • Pregnancy or < 6 weeks post-partum
30
Q

Name some other non-thrombotic materials to embolise

A

Thrombus and malignant tumour are the most important materials to embolise

Others include:

  • Fat and marrow
  • Air
  • Nitrogen
  • Amniotic fluid
31
Q

Describe fat embolism

A

Long bone fracture (femur, pelvis)

  • Marrow and fat can enter circulation
  • can travel to the lungs
  • Or systemically travel to the brain (resulting in reduced consciousness)
32
Q

Describe nitrogen embolism

A

Rising too quickly once diving deep

  • Causes gas + nitrogen to dissolve into tissues at high pressure
  • Once pressure rapidly reduces, bubbles precipitate in different tissues (Boyle’s law)

To prevent this:
- decompression needs to happen slowly

33
Q

Describe clinical presentations of nitrogen embolism

A
  • Severe joint pains (in the shoulder)
  • Neurological (headache, visual disturbance)
  • Itchy skin, oedema skin
  • Issues with the spinal cord, or paraplegia
34
Q

Describe treatments for nitrogen embolism

A
  • Hyperbaric pressure
    (high pressure in a chamber - to force bubbles into solution and stop precipitating, and gradually decrease the pressure)
35
Q

Describe air embolism

A

Air can get into circulation (introduced in cannulation in venous to outside)

  • Lungs - barotrauma - too high air pressure - can enter through air spaces into blood
  • Brain - dark black speck (black is air) - air in circulation in the brain

Risk
- Tubes + equipment into the coronary artery (femoral artery) - air can enter into proximal aorta + enter into the brain

36
Q

Describe amniotic embolism

A

Rare - 1 in 20,000

Foetal cells can embolise into the maternal circulation
- this can be very bad - can lead to systemic circulatory failure - can be very serious with widespread clotting and bleeding

Medicine 2 - 05 Heart Failure (8 decks)

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