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Pathological Processes > PP 5 Thrombosis + Embolism > Flashcards

PP 5 Thrombosis + Embolism Flashcards

1
Q

Thrombosis defintion

A

Formation of solid mass of blood within the circulatory system

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2
Q

Thrombus definition

A

Solid mass of blood within circulatory system

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3
Q

Clot defintion

A

Mass of blood outside vessel wall

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4
Q

Thrombus vs clot

A

Thrombus is within circulatory system
Clot is outside circulatory system

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5
Q

What is Virchow’s triad?

A

Thrombus form when there’s abnormalities in:
- vascular wall
- blood flow
- blood components

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6
Q

What can cause damage to vascular system?

A

Atheroma
Inflammation - vasculitis
Direct injury
Damage to heart

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7
Q

Atheroma definition

A

Degeneration of arteries due to fatty deposition

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8
Q

What causes change to blood flow?

A

Stasis
Turbulent blood flow

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9
Q

Stasis in blood meaning

A

Slowing of blood

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10
Q

Causes of blood stasis

A

Narrowing of vessels
Low BP
Immobility

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11
Q

Causes of turbulent blood flow

A

Defects in walls + heart valves
Atrial fibrillation

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12
Q

Hypercoagulable state of blood meaning

A

Sticky blood

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13
Q

Who is at risk of hypercoagulable blood?

A

Smokers
Pregnancy + post-partum
Trauma + burns
Post-operative patients
Genetic diseases e.g anti thrombin III deficiency

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14
Q

Appearance of an atrial thrombus

A

Pale
Granular
Lower cell content
Lines of Zahn

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15
Q

Appearance of a venous thrombus

A

Deep red
Soft
Gelatinous
Higher cell content

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16
Q

Why are lines of Zahn present in arterial thrombi but not venous?

A

There is a degree of shielding by valves in veins

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17
Q

Describe the formation of thrombus

A

1- platelets are activated
2- platelets aggregate + bind together by fibrin
3- RBCs get trapped
4- thrombus formed

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18
Q

Role of plasmin

A

Degrades fibrin
Dissolves thrombus

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19
Q

What is a breakdown product of fibrin?

A

D-dimers

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20
Q

What can D-diners be detected in the blood for?

A

Indicate clotting occurring

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21
Q

What converts plasminogen to plasmin/

A

tPA tissue plasminogen activator

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22
Q

What breaksdown fibrin?

A

Plasmin

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23
Q

List possible outcomes of thrombosis

A

Lysis
Propagation
Organisation
Recanalisation
Embolism

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24
Q

What process restores complete blood flow after thrombosis?

A

Lysis

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25
Q

What is lysis of thrombosis?

A

Breakdown of thrombus

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26
Q

What type thrombi does lysis occur to?

A

Small ones

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27
Q

What is propagation of thrombus?

A

Spread of thrombosis

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28
Q

What is organisation of thrombus?

A

In growth of fibroblasts + capillaries
Lumen remains obstructed

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29
Q

What is recanalisation of thrombus?

A

Channel formation through an organised thrombus

30
Q

What process restores partial blood flow after a thrombus?

A

Recanalisation

31
Q

What is embolism of a thrombus?

A

Part of thrombus breaks off
Travels in bloodstream
Lodges at distant site

32
Q

Effects of venous thrombosis

A

Congestion
Oedema
Ischaemia
Infarction

33
Q

Common locations of venous thrombosis

A

Cavernous sinus
Subclavian vein
Inferior vena cava
Uteroplacental
Deep vein thrombosis

34
Q

Effects of arterial thrombosis

A

Ischaemia
Infarction
Dependent on site + collateral blood supply

35
Q

Common locations of arterial thrombosis

A

Cerebral artery
Carotid artery
Coronary artery
Mesenteric + renal artery
Femoral, iliac + popliteal artery

36
Q

What can thrombosis in cerebral artery cause?

A

Ischaemic stroke

37
Q

What can thrombosis in coronary artery cause?

A

Myocardial infarction

38
Q

Embolism definition

A

Blockage of blood vessel by solid, liquid or gas at distant site room organ

39
Q

Examples of embolisms

A

Thrombus
Air
Amniotic fluid
Nitrogen
Medical equipment
Fat
Tumour cells

40
Q

List come predisposing factors to DVT

A

Immobility/bed rest
Post-operative
Pregnancy + post-partum
Oral contraceptives
Severe burns
Cardiac failure
Disseminated cancer
Superficial thrombophlebitis
Obesity
Old age
Previous/family history of DVT

41
Q

What is Superficial thrombophlebitis?

A

Inflammation in superficial vein of leg

42
Q

What can you do to prevent thromboembolism caused by bed rest?

A

Identify patients at high risk
Mobilise early + decrease bed rest
+/- aspirin
Low molecular weight heparin subcutaneously
Leg compression during surgery e.g. TED stockings + ‘flowtron boots’

43
Q

Different types of pulmonary thromboembolisms + their effects

A
  • massive coiled embolus in main PA - death
  • small embolus lodges in peripheral PA - pulmonary infarct
  • multiple repeated small emboli - pulmonary hypertension
44
Q

What can be used to identify DVT in leg?

A

Ultrasound

45
Q

What can be used to identify an embolism?

A

CT pulmonary angiogram

46
Q

Why are NOAC/DOACs better than oral warfarin

A

Easier to manage - no tests needed
Warfarin requires many tests
Easy to accidentally overdose on warfarin

47
Q

What does NOAC/DOAC stand for?

A

Noval/Direct Oral AntiCoagulant

48
Q

Examples of NOAC/DOACs

A

Rivaroxaban
Apixaban
Dabigatron

49
Q

Treatments of thrombosis

A

Clot busters/thrombolysis
Low molecular weight heparin
Oral warfarin
NOAC/DOAC
Embolectomy
Filters in IVc
Aspirin

50
Q

Examples of clot busters

A

Streptokinase
Ateplase

51
Q

How has warfarin work?

A

Inhibits synthesis of vitamin K dependent clotting factors

52
Q

What drug increases PT and is monitored by regular INR measurements?

A

Warfarin

53
Q

Conditions for which warfarin is used

A

DVT
Pulmonary embolism
Cardiac arrhythmias
After cardiac valve replacement

54
Q

What tests are needed if you are in warfarin?

A

PT/INR test

55
Q

What effect would a paracetamol overdose have on clotting tests?
Why?

A

PT raised
Paracetamol toxicity > liver failure
Prothrombin isn’t produced by the liver

56
Q

What is prothrombin a test on?

A

Extrinsic pathway
Clotting factors made by the liver

57
Q

What effect would a paracetamol overdose have on blood tests?

A

Raised PT
Raised ALT

58
Q

What effect would a paracetamol overdose have on ALT tests?
Why?

A

Increased ALT
Hepatocytes die due to paracetamol toxicity
ALT leaks out of the damaged cell membranes

59
Q

What is a paracetamol overdose treated with?

A

N-acetylcysteine

60
Q

Why are pregnant women predisposed to DVT?

A
  • Pregnancy blood is hypercoagulable
  • The baby can compress venous outflow from legs and cause venous stasis
61
Q

Why is low molecular weight heparin favoured over warfarin?

A

LMW heparins effective immediately
Warfarin takes a few days to become effective

62
Q

What type of inhibitor is aspirin?

A

Non-competitive

63
Q

What does aspirin do?

A
  • Irreversible inhibits cylcooxygenase (enzyme for prostaglandin synthesis)
  • platelets can’t produce thromboxane A2
  • reduced platelet aggregation
64
Q

What inhibits cyclooxgenase?

A

Aspirin - non competitively
Ibuprofen - competitively

65
Q

What does low molecular weight heparin do?

A

Irreversible complexes with and activates antithrombin III

66
Q

Bleeding time in aspirin

A

Prolonged

67
Q

What does cyclooxgenase cataylse?

A

Prostaglandin synthesis

68
Q

Where do the of thrombi that cause majority of pulmonary emboli arise from?

A

Deep veins of thigh + popliteal vein

69
Q

What is most likely cause of thrombi occurring in veins

A

Blood stasis

70
Q

What type of thrombi usually occur at site of endothelial injury?

A

Atrial and cardiac thrombi

Pathological Processes (14 decks)

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