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thrombosis Flashcards

1
Q

What is Thrombosis?

A

Solid mass of blood formed within the cardiovascular system involving the interaction of endothelial cells, platelets and the coagulation cascade that
impedes blood flow

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2
Q

what is haemostasis?

A

Haemostasis is the normal physiological process of coagulation to prevent bleeding

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3
Q

where does thrombosis occur?

A

Arterial & venous thrombosis

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4
Q

arterial thrombosis

what do they mostly result from?
are they platelet-rich? colour?
block which arteries?

what are they mostly due to? what does this lead to?

A

Mostly result from atheroma rupture (MI, stroke)
Platelet-rich “white” thrombosis
Block downstream arteries

Mostly due to atheroscelrosis hence plaques build up within interior of the vessel which rupture + thrombosis can occur which can block or impede blood flow

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5
Q

Venous thrombosis
what does it result from?
are they platelet rich? colour?
where could it go?

A

Result from stasis or a hypercoagulant state (DVT)
Platelet-poor “red” thrombus
May move to lungs

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6
Q

What makes blood clot?

the 4 key components

A 
Four key components:
Endothelium
Platelets
Coagulation
Fibrinolysis (to resolve clot)
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7
Q

What is normal hameostasis?

what does it respond to?
what happens? 2 different main processes? what happens in the end?

A

Response to injury
Vessel constriction
↓
Formation of unstable platelet plug
(primary haemostasis) platelet adhesion
platelet aggregation
↓
Stabilisation of the plug with fibrin
(secondary haemostasis) blood coagulation
↓
Dissolution of clot and vessel repair
fibrinolysis

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8
Q

Platelets + coagulation

what causes this? (2)
what is primary haemostasis? (3)
what is secondary haemostasis? (2)

A

Tissue damage OR inflammation

primary hameostasis
platelet -> activated platelet (adhere, activate + aggeregate)

secondary haemostasis
fibrinogen -> fibrin (coagulation)

Both process happen together for clot

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9
Q

Importance of charged phospholipds on platelets

A

to allow coagulation to occur hence will lead to fibrin formation

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10
Q

coagulation + fibrinolysis

what do endothelila cells release? to what? what does this convert? what does this do?

A

endothelial cell will release tPA to plasminogen which is converted to potent plasmin -> breaks down fibrin into fibrin fragments + D-dimers

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11
Q

Blood coagulation inhibitors

name 2 different inhibitors and what they inactivate

A

Antithrombin III -> switch off the X to XA and thrombin’s activity

Protein c + s leads to activated protein C -> inactivates VIIIa and VA hence no amplification process

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12
Q

Deep vein thrombosis (DVT)
symptoms (5)

What do they all reflect?

A 
Pain & tenderness of veins
Limb swelling 
Superficial venous distension
Increased skin temperature 
Skin discoloration

All reflect obstruction to the venous drainage

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13
Q

Involvement of valves in clot formation

what do valves do in veins?
what do contraction of muscles do?

how do clots form in this situation?

A

Valves in veins prevent backflow of blood
Contraction of nearby muscles squashes veins, acting as a pump to return blood to the heart

Clot formation happens when instead of strong upsurge of blood to the heart, it can eddy around valves hence more stasis and more risk of clot formation therefore can cause thrombosis + obstruction of blood flow

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14
Q

Virchow’s Triad

3 things that develop a venous thrombus?

A

Development of a venous thrombus depends on:

Changes in normal blood flow (stasis)
Alterations in the constituents of the blood (hypercoagulability)
Damage to the endothelial layer (extrinsic pathway will activate thrombosis)

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15
Q

Stasis

different reasons? (7)

A

Prolonged immobility e.g. surgery, travel
Stroke
Cardiac failure
Pelvic obstruction
Dehydration
Hyperviscosity
Polycythaemia -> increased RBC hence increased viscoscity of the blood and decreased blood flow

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16
Q

Hypercoagulabilty

what does this mean? what is there less of and more of?

A

Alterations in the constituents of blood components
HENCE

LESS Fibrinolytic factors, anticoagulant proteins/activity
MORE Coagulation factors, platelets

17
Q

LESS Fibrinolytic factors, anticoagulant proteins/activity example

what defiency? what mututaion is this? effect of this?

A

e.g. ATIII deficiency
Protein C and Protein S deficiencies
FV Leiden mutation is a thrombophilia (resistance to the anticoagulant complex - activated protein C APC)
hence as protein c can’t break it down, it leads to amplification process

18
Q

MORE Coagulation factors, platelets

such as?

A

Malignancy increases clotting factors

e.g. tissue factor, FXa, thrombin

19
Q

Fate of venous thrombosis: lungs

small? large?

A

if small thrombosis, can be asymptomatic

if large can lead to obstructuion + rapid death

20
Q

Proximal DVT

where? what is there risk of?

A

above knee

Higher risk of pulmonary embolism and post-thrombotic syndrome (pain, swelling, maybe even ulcers)

21
Q

Distal DVT
where?
risk of?

A

below knee
Rarely cause pulmonary embolism
Rarely cause post-thrombotic syndrome

22
Q

Post thrombotic syndrome

results from?
what does it reduce?
what does it increase?
how does risk increase?
symtoms?
A 
Chronic complication develops in 20-50% of DVT  patients
Results from venous hypertension
Reduces calf muscle perfusion
Increases tissue permeability 
Risk increases with obesity and age
Pain, swelling, oedema
Redness
Thickening of skin
Ulcers in 5-10%
23
Q

Anti-coagulants

what do they do? examples?

A

prevent clots

e.g. warfarin, heparin, direct oral anticoagulants

24
Q

Thrombolytics/Fibrinolytics reverse

what do they do? examples

A

break down clots

e.g. plasminogen activators, streptokinase

25
Q

Treatment of VTE
Cardiovascularly stable with acute VTE

what do you do? what drugs do you give?

A

Anticoagulate
Immediate anticoagulant effect
Heparin then warfarin/DOAC or immediate DOAC - Rivaroxaban or apixaban

26
Q

Treatment of VTE
Circulatory collapse due to PE

what do you do differently in this case? what drugs do you give?

A

Thrombolysis
Alteplase (tissue plasminogen activator)
Streptokinase
Followed by heparin and warfarin or other - prevent recurrence

27
Q

Investigations pre-treatment

what other tests than clot test do you do?
what are the clot tests?

A

Clotting screen
Prothrombin time (INR)
Partial thromboplastin time
Thrombin time

Full blood count

Urea and electrolytes
usually part of routine screen – to know creatinine clearance

Liver function tests
If clinical suspicion of liver disease

28
Q

New(ish) anticoagulants

3 drug types
name the drugs

A

Indirect Xa inhibitors - enhance antithrombin
Fondaparinux
Idraparinux

Direct Xa inhibitors ORAL
Rivaroxaban
Apixaban

Direct thrombin inhibitors ORAL
Dabigatran

29
Q

Bleeding complications from anticoagulants (3)

occurs with which drugs?

A

eyes
arm
brain

can occur with older anti-coagulants like warfarin

Blood (7 decks)

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