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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
Q

What are the less common causes of an embolus?

A

Air, cholesterol crystals, tumours, amniotic fluid, fat

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26
Q

What happens if an embolus enters the venous system?

A
  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
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27
Q

What is ischaemia?

A

Reduction in blood flow to a tissue without any other implications

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28
Q

What is an infarction?

A

Reduction in blood flow with subsequent death of cells

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29
Q

What is an infarction usually caused by?

A

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

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30
Q

What is a reperfusion injury?

A

Damage to tissue during re-oxygenation

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31
Q

Why are many organs very susceptible to an infarction?

A

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.

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32
Q

Which organs have dual arterial supply?

A

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.

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33
Q

What plays the most important role in thrombosis? (Especially arterial)

A

Platelets

34
Q

Arterial circulation

A

High pressure platelet rich

35
Q

Venous circulation

A

Low pressure Fibrin rich

36
Q

Driving force in venous circulation?

A

Fibrin

37
Q

Presentations of arterial thrombosis:

A

Myocardial infarction
CVA
Peripheral vascular disease,
Others
Angina
Cerebral – TIA, strokes

38
Q

Coronary arterial thrombosis treatment

A

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
Q

What type of heparin is used usually - fractionated or unfractionated?

A

Unfractionated

40
Q

Why not use anticoagulants here?

A

Increase risk of bleeding

41
Q

Cerebral arterial thrombosis treatment

A

Aspirin, other anti-platelets
Thrombolysis
- catheter directed treatments
Reperfusion

42
Q

Why is heparin not used in cerebral artery thrombosis treatment?

A

No heparin or systemic heparin - risk of bleeding and haemorrhage

43
Q

Difference between venous and arterial circulation

A

Venous side lower flow smaller pressure system
Thrombosis here driven by fibrin

44
Q

Where does venous thrombosis often happen?

A

Peripheral –Ileofemoral, femoro-popliteal

Other sites – Cerebral, Visceral

45
Q

Venous thrombosis - diagnosis

A

Signs and symptoms-very non specific
Blood tests –D-dimer –sensitive but not specific
Imaging-usually required

46
Q

What is venous thrombosis caused by?

A

Smoking
Trauma

47
Q

What reduces venous flow?

A

immobility – venous flow relies on you moving

48
Q

Virchow’s triad

A

blood flow/endothelium/blood constituents

49
Q

What causes Virchow’s triad that could lead to thrombosis?

A

Surgery
Immobilisation
Oestrogens: OC, HRT
Malignancy - play role in immobility and endothelial damage
Long haul flights

50
Q

Blood constituent problems - genetic

A

Factor V Leiden (5%)
PT20210A (3%)
Antithrombin deficiency
Protein C deficiency
Protein S deficiency

51
Q

Anti-phospholipid syndrome

A

unique coagulation defect which predisposes arterial thrombosis

52
Q

Venous thrombosis treatment

A

Heparin or LMWH
Warfarin
DOAC

Endo-vascular

Surgical

53
Q

When would treatment of DVT be more aggressive?

A

When its big enough to cause a PE

54
Q

Prevention of venous thrombosis:

A

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
Q

Heparin

A

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
Q

Low molecular weight heparin (LMWH)

A

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
Q

What is HIT?

A

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
Q

Warfarin

A

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
Q

New Oral Anticoagulant Drugs (NOAC/DOAC)

A

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
Q

Where are NOAC/DOAC’s not used?

A

Metal heart valves - risk of thrombosis is really high
Pregnancy

61
Q

Aspirin

A

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
Q

Other antiplatelets

A

Clopidogrel -inhibits ADP induced platelet aggregation by irreversibly binding to the p2y12 receptors
Ticagrelor – p2y12 receptor antagonist
Prasugrel – p2y12 receptor antagonist

63
Q

DVT/ PE

A

Deep vein of the legs
Normal blood flow in vein
Blood clot (thrombus) occurs - deep vein thrombosis

64
Q

DVT incidence

A

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
Q

Risk factors for DVT

A

Surgery,
immobility,
leg fracture
POPOC pill,
HRT,
Pregnancy
Long haul flights/ travel (rare)
inherited thrombophilia- genetic predisposition; 5% population, familial

66
Q

Signs and symptoms of DVT

A

Symptoms: leg pain, swelling
Signs: tenderness, swelling, warmth, discolouration

67
Q

Complications of DVT

A

Phlegmasia alba dolens and phlegmasia cerulae dolens, PE

68
Q

Why does a DVT lead to ischaemia?

A

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
Q

Investigations for DVT?

A

D-dimer: normal excludes diagnosis
positive does not confirm diagnosis
Ultrasound compression – gold standard
CT or MR venogram
catheter venogram

70
Q

DVT treatment

A

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
Q

Re-cannalisation

A

Endovenous:
Chemical
Mechanical
Mechanico-chemical
Stents – used all the time – in venous side stents evolving and developing

72
Q

Prevention of DVT

A

Mechanical- hydration and early mobilisation, Compression stockings, Foot pumps
Chemical- LMW Heparin

73
Q

Who are at high risk for thromboprophylaxis?

A

hip and knee, pelvis, malignancy, risk factors, prolonged immobility
All immobile medical, many surgical/ O+G Daltrparin s/c od. No monitoring

74
Q

What is pulmnary embolism

A

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
Q

Symptoms of PE?

A

breathlessness
pleuritic chest pain
may have signs/ symptoms of DVT
may have risk factors
no other diagnosis more likely

76
Q

Signs of PE?

A

tachycardia
tachypnoea
pleural rub
those of precipitating cause
none of alternative diagnosis

77
Q

Differential diagnosis of PE?

A

chest pain and sob
Consider also musculoskeletal, infection, malignancy, pneumothorax, cardiac, gastro causes

78
Q

PE initial investigations

A

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
Q

Further investigations of PE?

A

D-dimer: normal excludes diagnosis
CTPA spiral CT with contrast, visualise major segmental thrombi
Ventilation/ Perfusion scan: mismatch defects

80
Q

Treatment of PE

A

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
Q

Prevention of PE

A

Early mobilisation and hydration
Mechanical
Chemical
IVC filters
Anticoagulation

Pathology (7 decks)

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