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Pathology > Thrombosis, embolism, ischaemia and infarction > Flashcards

Thrombosis, embolism, ischaemia and infarction Flashcards

1
Q

What are arteries lined by?

A

Endothelial cells - a teflon coating on the inside of blood vessels

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2
Q

What is laminar flow?

A

A nice organised stream of flow with cells in the middle and plasma at the edges
Cells travel in the centre of arterial vessels and dont touch the sides

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3
Q

Why are clots quite rare?

A

Due to laminar flow and endothelial cells which are not ‘sticky’ when healthy

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4
Q

What happens if we damage the endothelium?

A

Lose teflon coating from wall of artery which contains lots of collagen which is naturally sticky to cells.
Endothelial cells lift up into stream of the blood in the vessel causing turbulent flow rather than laminar flow

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5
Q

What happens in turbulent flow?

A

Platelets heavily attracted to collagen so come in and bind to the collagen

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6
Q

Tell me about platelets

A

Positive feedback - platelet aggregation

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7
Q

What are the role of platelets in thrombosis

A
  • No nucleus, derived from megakaryocytes
  • Contain alpha granules and dense granules
  • Alpha granules are involved in platelet adhesion, e.g. fibrinogen
  • Dense granules cause platelets to aggregate, e.g. ADP
  • Platelets are activated, releasing their granules when they come into contact with collagen
  • If this happens within an intact vessel, a thrombus is formed
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8
Q

Thrombus formation

A

Red blood cells caught up in platelet aggregation, get entrapped causes thrombus formation
Clotting factors like fibrin - inactive form fibrinogen - polymerises into fibrin by chemicals released by platelets
More platelet aggregate more platelet aggregating factor released
More fibrin causes more fibrinogen to polymerise into fibrin
Could cause thrombus that blocks of a vessel

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9
Q

Thrombosis formation

A
  1. First stage is platelet aggregation, which starts the clotting cascade
  2. These both have positive feedback loops > hard to stop
  3. Thrombosis is caused by 3 major factors > Virchow’s triad
    Typically thrombi are formed by 2 of these factors
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10
Q

Thrombosis definition

A

The formation of a solid mass of blood constituents formed within intact vascular system during life

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11
Q

How does an arterial thrombosis form?

A

An atheromatous plaque will result in a change in the vessel wall
1. Atheromatous plaque may have a fatty streak
2. Over time, the plaque grows and protrudes into the lumen causing a degree of turbulence in blood flow
3. This turbulence results in the loss of intimal cells
4. Fibrin deposition and platelet clumping occurs
5. Once this has started, the process is self-perpetuating, leading to the formation of the platelet layer (first layer of thrombus)
6. This layer allows for the precipitation of a fibrin meshwork in which RBCs get trapped
7. The structure protrudes further into the lumen causing more turbulence and more platelet deposition
8. Thrombi grow in the direction of blood flow  propagation

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12
Q

What happens in venous thrombosis

A
  • There is lower blood pressure in veins and atheroma do not occur
  • lack of smooth muscle cells, no smooth muscle proliferation
  • Thrombi begin at valves
  • Valves produce a degree of turbulence, and can be damaged, e.g. trauma, stasis
  • When blood pressure falls, flow through the veins slows, allowing for a thrombus to form
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13
Q

What are the clinical features of an arterial thrombosis?

A

-Loss of pulse distal to thrombus
-Area becomes cold, pale and painful
-Possible gangrene

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14
Q

The clinical features of venous thrombi

A

Tender
Area becomes reddened and swollen

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15
Q

Clinical examples of thrombosis

A

Myocardial infarction in LAD

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16
Q

Thrombosis: Virchow’s triangle

A

Change in vessel wall (endothelial damage)
Change in blood flow
Change in blood constituents

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17
Q

What is the fate of thrombi?

A
  1. Resolve
    Best case scenario
    Body dissolves and clears it
  2. Organised
    Becomes a scar
    Results in slight narrowing of the vessel lumen
  3. Recanalisation
    Intimal cells may proliferate
    Capillaries may grow into the thrombus and fuse to form larger vessels
  4. Embolus
    Fragments of the thrombus break off into the circulation
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18
Q

What is an embolism

A

Mass of material in the vascular system able to become lodged within vessel and block it.
Is the process of a solid mass in the blood being carried through the circulation to a place where it gets stuck and blocks the vessel.

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19
Q

What is an arterial embolism

A
  • A Systemic embolism
  • Arterial emboli can travel anywhere downstream of its entry point
  • Mural thrombi in the left ventricle can go anywhere
  • Cholesterol crystals from an atheromatous plaque in the descending aorta can go to any lower limb or renal artery
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20
Q

What is a venous pulmonary embolism?

A

In the venous system, emboli travel to the vena cava and lodge in the pulmonary arteries
This results in a PE

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21
Q

What happens in small venous emboli?

A

May occur unnoticed
Can cause idiopathic pulmonary hypertension

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22
Q

What can happen in a large venous emboli?

A

Can result in acute respiratory or cardiac problems
Resolve slowly
Result in chest pain and shortness of breath

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23
Q

What can happen in a massive emboli?

A

Result in sudden death
Long thrombi derived from the leg veins
Often impacted across the bifurcation of one of the pulmonary arteries

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24
Q

What is the most common cause of an embolus

A

Thrombus
e.g a deep venous thrombosis of the leg veins
which breaks off and embolises through the large veins and
right side of the heart to the lungs

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25
What are the less common causes of an embolus?
Air, cholesterol crystals, tumours, amniotic fluid, fat
26
What happens if an embolus enters the venous system?
1. Will travel to the vena cava through right side of heart and lodge somewhere in pulmonary arteries 2. Cannot go through arterial circulation because blood vessels in lungs split down to capillary size so lungs act as a filter for any venous emboli
27
What is ischaemia?
Reduction in blood flow to a tissue without any other implications
28
What is an infarction?
Reduction in blood flow with subsequent death of cells
29
What is an infarction usually caused by?
Usually a macroscopic event caused by thrombosis of an artery e.g thrombus in the left anterior descending coronary artery causing infarction of the anterior wall of the left ventricle
30
What is a reperfusion injury?
Damage to tissue during re-oxygenation
31
Why are many organs very susceptible to an infarction?
Most organs in the human body have only a single artery supplying them (end arterial supply) so they are very susceptible to infarction of this supply is interrupted.
32
Which organs have dual arterial supply?
A few organs have a dual arterial supply so are much less susceptible to infarction: liver - with portal venous and hepatic artery supplies, lung - with pulmonary venous and bronchial artery supplies, brain around the circle of Willis with multiple arterial supplies.
33
What plays the most important role in thrombosis? (Especially arterial)
Platelets
34
Arterial circulation
High pressure platelet rich
35
Venous circulation
Low pressure Fibrin rich
36
Driving force in venous circulation?
Fibrin
37
Presentations of arterial thrombosis:
Myocardial infarction CVA Peripheral vascular disease, Others Angina Cerebral – TIA, strokes
38
Coronary arterial thrombosis treatment
Aspirin and other antiplatelets LMWH or Fondraparinux – safer than heparin Thrombolytic therapy: streptokinase, tissue plasminogen activator Reperfusion – Catheter directed treatments and stents Aspirin inhibits platelet function TPA generates plasmin, degrades fibrin
39
What type of heparin is used usually - fractionated or unfractionated?
Unfractionated
40
Why not use anticoagulants here?
Increase risk of bleeding
41
Cerebral arterial thrombosis treatment
Aspirin, other anti-platelets Thrombolysis - catheter directed treatments Reperfusion
42
Why is heparin not used in cerebral artery thrombosis treatment?
No heparin or systemic heparin - risk of bleeding and haemorrhage
43
Difference between venous and arterial circulation
Venous side lower flow smaller pressure system Thrombosis here driven by fibrin
44
Where does venous thrombosis often happen?
Peripheral –Ileofemoral, femoro-popliteal Other sites – Cerebral, Visceral
45
Venous thrombosis - diagnosis
Signs and symptoms-very non specific Blood tests –D-dimer –sensitive but not specific Imaging-usually required
46
What is venous thrombosis caused by?
Smoking Trauma
47
What reduces venous flow?
immobility – venous flow relies on you moving
48
Virchow's triad
blood flow/endothelium/blood constituents
49
What causes Virchow's triad that could lead to thrombosis?
Surgery Immobilisation Oestrogens: OC, HRT Malignancy - play role in immobility and endothelial damage Long haul flights
50
Blood constituent problems - genetic
Factor V Leiden (5%) PT20210A (3%) Antithrombin deficiency Protein C deficiency Protein S deficiency
51
Anti-phospholipid syndrome
unique coagulation defect which predisposes arterial thrombosis
52
Venous thrombosis treatment
Heparin or LMWH Warfarin DOAC Endo-vascular Surgical
53
When would treatment of DVT be more aggressive?
When its big enough to cause a PE
54
Prevention of venous thrombosis:
Mechanical or chemical thromboprophylaxsis Also early mobilisation and good hydration What can we do to encourage blood flow – get them moving also use compression stocking – helps with venous return – encourages blood flow
55
Heparin
Glycoaminoglycan Binds to antithrombin and increases its activity Indirect thrombin inhibitor most important anticoagulant short half life 4 hours Monitor with APTT, aim ratio 1.8-2.8 Given by continuous infusion
56
Low molecular weight heparin (LMWH)
Smaller molecule, less variation in dose and renally excreted Once daily, weight-adjusted dose given subcutaneously Used for treatment and prophylaxsis Don’t need to monitor them as half life is predictable – have to take renal function into account – otherwise accumulation of LMWH
57
What is HIT?
heparin induced thrombocytopenia if you give heparin if they’ve had in the past high doses of heparin then at higher risk of Developing HIT – affects platelets – platelet count really drops – drops drastically
58
Warfarin
Orally active Prevents synthesis of active factors II, VII, IX and X (1972) Antagonist of vitamin K Long half life (36 hours) Prolongs the prothrombin time Difficult to use Need to monitor Reverse by giving vitamin K
59
New Oral Anticoagulant Drugs (NOAC/DOAC)
Orally active – like aspirin and warfarin Directly acting on factor II or X No blood tests or monitoring Shorter half lives Used for extended thromboprophylasis and treatment of AF and DVT/PE ( equivalent to INR 2-3, not higher, so not heart valves) Not used in pregnancy
60
Where are NOAC/DOAC's not used?
Metal heart valves - risk of thrombosis is really high Pregnancy
61
Aspirin
Inhibits cyclo-oxygenase irreversibly Act for lifetime of platelet, 7-10 days Inhibits thromboxane formation and hence platelet aggregation Used in arterial thrombosis, 75-300 mg od
62
Other antiplatelets
Clopidogrel -inhibits ADP induced platelet aggregation by irreversibly binding to the p2y12 receptors Ticagrelor – p2y12 receptor antagonist Prasugrel – p2y12 receptor antagonist
63
DVT/ PE
Deep vein of the legs Normal blood flow in vein Blood clot (thrombus) occurs - deep vein thrombosis
64
DVT incidence
25,000 people a year die of DVT and PE a year in UK 50% preventable, premature mortality More than RTA, AIDS and breast cancer combined
65
Risk factors for DVT
Surgery, immobility, leg fracture POP OC pill, HRT, Pregnancy Long haul flights/ travel (rare) inherited thrombophilia- genetic predisposition; 5% population, familial
66
Signs and symptoms of DVT
Symptoms: leg pain, swelling Signs: tenderness, swelling, warmth, discolouration
67
Complications of DVT
Phlegmasia alba dolens and phlegmasia cerulae dolens, PE
68
Why does a DVT lead to ischaemia?
rare complication – does happen – can cause limb loss – you get all the veins thrombosed – all small tibial veins thrombose – leads in increased compartment pressures – causes pressure of small arterioles leading to ischaemia/ infarction – massive rise in compartment pressure
69
Investigations for DVT?
D-dimer: normal excludes diagnosis positive does not confirm diagnosis Ultrasound compression – gold standard CT or MR venogram catheter venogram
70
DVT treatment
LMW Heparin s/c od for min 5 days Oral warfarin, INR 2-3, (2.5) for 3-6 months DOAC/NOAC Compression stockings Treat/ seek underlying cause: malignancy, thrombophilia, compression
71
Re-cannalisation
Endovenous: Chemical Mechanical Mechanico-chemical Stents – used all the time – in venous side stents evolving and developing
72
Prevention of DVT
Mechanical- hydration and early mobilisation, Compression stockings, Foot pumps Chemical- LMW Heparin
73
Who are at high risk for thromboprophylaxis?
hip and knee, pelvis, malignancy, risk factors, prolonged immobility All immobile medical, many surgical/ O+G Daltrparin s/c od. No monitoring
74
What is pulmnary embolism
A consequence of DVT – clot breaks up and goes up to the lungs – when these patients present with suspicion of PE – most likely DVT underlying
75
Symptoms of PE?
breathlessness pleuritic chest pain may have signs/ symptoms of DVT may have risk factors no other diagnosis more likely
76
Signs of PE?
tachycardia tachypnoea pleural rub those of precipitating cause none of alternative diagnosis
77
Differential diagnosis of PE?
chest pain and sob Consider also musculoskeletal, infection, malignancy, pneumothorax, cardiac, gastro causes
78
PE initial investigations
CXR usually normal ECG sinus tachy, (QI,SI,TIII) Blood gases: type 1 resp failure, decreased O2 and CO2 Mainly done to exclude alternative causes
79
Further investigations of PE?
D-dimer: normal excludes diagnosis CTPA spiral CT with contrast, visualise major segmental thrombi Ventilation/ Perfusion scan: mismatch defects
80
Treatment of PE
Supportive treatment LMW Heparin s/c od weight adjusted 5/7 Oral warfarin INR 2-3 (2.5) for 6 months DOAC Treat underlying cause
81
Prevention of PE
Early mobilisation and hydration Mechanical Chemical IVC filters Anticoagulation

Pathology (7 decks)

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