Haemostasis and Thrombosis Flashcards Preview

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Flashcards in Haemostasis and Thrombosis Deck (60):
0

Describe haemostasis

Stopping of haemorrhage. Must act within seconds to prevent blood loss.

1

What enzyme in clotting allows the production of fibrin?

Thrombin

2

Describe what a thrombus is

A clot within the vascular system. Haemostasis in the wrong place.

3

Describe the process of haemostasis from the moment an artery is severed.

Severed artery contracts to decrease pressure downstream.

Primary haemostatic plug of activated platelets forms at the mouth, sticking to injured vessel and connective tissue outside.

Secondary haemostatic plug forms as fibrin filaments stabilise the platelet plug. Eventually becomes organised, replaced by granulation tissue and a tiny scar.

4

What stage of haemostasis is absent in patients with a low platelet count or non-functional platelets?

Primary haemostatic plug wont form

5

What stage of haemostasis will be absent in haemophiliacs?

Secondary haemostatic plug wont form

6

What activates platelets?

Collagen surfaces
Thrombin
ADP
Adrenaline
Some prostaglandins

7

What component of subendothelium allows platelets to adhere to it?

von Willebrand factor

8

What acts as a glue between platelets to allow aggregation?

Fibrinogen

9

What is secreted by platelets to allow a platelet plug to grow after adhesion and some aggregation?

Fibrinogen
ADP
Thromboxane A2

10

Describe the difference between the intrinsic and extrinsic pathways in clotting.

Intrinsic - involves factors contained in the blood. Triggered by a negative surface.

Extrinsic - needs a tissue factor (thromboplastin) from outside the blood. Released from damaged cells when blood is spilled.

11

Describe how platelets can pull together the sides of wounds.

As they die they pull filaments of fibrin by their actin-myosin system.

12

What methods stop clotting?

Dilution of clotting factors by blood flow
Natural anticoagulants which oppose fibrin formation e.g. Antithrombin iii, protein C, protein S

13

Describe fibrinolysis

Macrophages recognise and break down fibrin which is then destroyed by free floating enzymes.
Split products of fibrin inhibit blood clotting.

14

What enzyme is responsible for fibrinolysis and where is it produced?

Plasmin. Produced as plasminogen in the liver

15

Give some examples of plasminogen activators.

tPA
Streptokinase
Urokinase

16

Describe the function of plasminogen activators

Dissolve fibrin, and therefore thrombi and thromboemboli
Attack fibrinogen, causing general depletion.

17

Describe the features of the endothelium which oppose and favour blood clotting.

Oppose - secretes prostacyclin which inhibits platelet aggregation. Opposes thrombin. Favours fibrinolysis by secreting tPA and urokinase.

Favour - produces von Willebrand factor, favours coagulation cascade, opposes fibrinolysis

18

Describe a thrombus.

Forms within the heart or vessels from the constituents of the blood during life.
Caused when normal haemostatic mechanisms are turned on inappropriately.

19

What is Virchow's triad?

Changes to the vascular wall
Changes in blood flow
Changes in the blood

20

How many components are required from the Virchow's triad are required for a clot to form?

Two

21

What do platelets adhere to when the endothelium has been damaged?

von Willebrand factor
Factor VIII

22

Why don't platelet thrombi generally not grow in arteries?

Swift currents wash away the platelets and chemical mediators

23

Why is thrombosis more frequent in veins?

Slower flow
Ebbing due to valves
Pockets of stagnant blood around valves

24

Why is thrombi of the lower limbs common in pregnancy?

Two of Virchow's triad is present
Pressure on the pelvis increases stasis in the large veins
Blood is hypercoaguable

25

What clotting factor does smoking activate?

Hageman factor (XII)

26

What does pregnancy and recent surgery increase concentration of that causes hypercoaguability of blood?

Fibrinogen
Factor VIII

27

Describe the formation of a post-surgical thrombus.

Platelets in a vein concentrate along the endothelium because they are the smallest elements in blood
Platelets aggregate more easily
They catch in an eddy behind a valve, aggregate, settle on the wall, and other platelets stick.
Fibrin grows out of the platelet layer and traps red blood cells. The surface of the red layer is thrombogenic.

28

Describe lines of Zahn in a thrombus.

Layers of a thrombus that are visible to the naked eye.
Red - aggregation of red blood cells
White - aggregations of platelets.

29

Describe the difference between an occlusive and parietal thrombus.

Occlusive - fills and obstructs the lumen
Parietal - restricts the lumen of the vessel

30

What is the most important mechanism for limiting the spread of a thrombus?

Blood flow

31

Give the different possible fates of thrombi.

Resolution
Embolisation
Organisation (covered by cells, forms fibrous scars)
Recanalisation (new channels form through the thrombus)
Partial calcification

32

Where do occlusive thrombi tend to form?

Over an atherosclerotic plaque that has cracked open.

33

Describe the difference between thrombi and post-mortem clots?.

Thrombi - laminated by lines of Zahn (need blood flow to form). Opposed to intimal surface

Post mortem clot - rubbery and shiny, never laminated, never attached to intima.

34

Describe a vegetation

A thrombus on a cardiac valve.
Tends to occur on the left side as they are exposed to greater pressure and microtrauma.
Exposed subendothelium is thrombogenic and can become infected.

35

Where are the most dangerous sources of emboli?

Large veins of the lower limbs.
Femoral, iliac, popliteal

36

Describe how aspirin is antithrombogenic.

Irreversibly acetylates an enzyme of prostaglandin metabolism in platelets so they can't produce thromboxane A2.
Formation of a haemostatic plug is inhibited and bleeding time is prolonged.

37

Describe disseminated intravascular coagulation

Blood clots throughout the circulation which form as a complication of a primary event that triggers generalised clotting.
Is a combination of clotting and non clotting leading to thromboembolism and haemorrhage.
Clotting factors and platelets are used up by the widespread clotting, causing susceptibility to haemorrhage.

38

Give some circumstances which precipitate disseminated intravascular coagulation.

Sepsis - especially gram negative bacteria which produces endotoxin
Severe trauma - especially to the brain which has a large amount of thromboplastin
Complications of childbirth - amniotic fluid embolism, retained dead foetus
Shock
Tumour
Snake bite

39

Describe the signs of microvascular thrombosis and haemorrhage in disseminated intravascular coagulation.

Microvascular thrombosis - neurological impairment, gangrene of skin, renal failure, respiratory distress, gastrointestinal ulceration

Haemorrhage - intracerebral bleeding, petichiae, haematuria, epistaxis, GI bleeding

40

Describe microangiopathic haemolytic anaemia

Red blood cells can be traumatised by fibrin in the microthrombi

41

Describe an embolus

A solid, liquid or gas carried by the blood which is large enough to impact in a vascular lumen

42

Describe an embolism.

Impaction of an embolus. Can't occur in veins as blood flow is from small to large vessels.

43

Give an example of something which can form an embolus, aside from a thrombus fragment.

Body fat
Bone marrow
Atheromatous plaques
Tumours
Parasites
Debris

44

Where do emboli from the peripheral veins end up?

Lungs

45

Where do emboli from the right heart end up?

Lungs

46

Where do emboli from the left heart end up?

Anywhere in systemic circulation, especially the limbs.

47

Where do emboli from the aorta end up?

Anywhere in systemic circulation, especially the limbs.

48

Describe pulmonary emboli

Large emboli will become lodged astride the bifurcation of the pulmonary artery (saddle emboli). Usually lethal.
Small emboli with lodge further down in the lungs, and if they persist can cause pulmonary hypertension.

Approximately 80% arise in thrombi in deep veins of the thigh and popliteal vein.
They can be prevented by putting an umbrella shaped filter in the vena cava.

49

Why are thromboemboli often seen in the left heart?

Infarcts commonly affect the left ventricle which causes thrombosis.
Vegetations more common
Atrial fibrillation causes dilatation of the left atrium
Stagnation of blood which causes thrombi formation

50

Describe paradoxial emboli.

Arise in the systemic veins but embolise in the systemic arteries.
Small ones bypass the lungs through arterio-venous anastamoses in the pulmonary circuation
Large through defects in the interventricular septum or foramen ovale during coughing, lifting or straining as this can increase right heart pressure above the left.
Patients with a stroke are 4 times more likely to have this.

51

Describe an atheroma

Necrotic tissue in atherosclerotic plaques which is released when a plaque breaks open. Happens spontaneously during surgery or catheterisation.

52

Describe a transient ischaemic attack

Microscopic atheroembolism to the brain.
Episodes of neurologic dysfunction that appear suddenly then disappear. Usually from the carotid artery and left heart.
As they are small they break up before lasting harm is done.

53

Describe how fat and bone marrow emboli form.

Complication of bone fractures but can also form after liposuction.
Bone marrow fat cells break up, oil droplets coalesce and are sucked into venules torn by the fracture.

54

Describe the symptoms of a fat or bone marrow embolus.

Respiratory distress
Neurological symptoms
10-15% mortality
Emboli lodge in the lungs and some droplets pass through to the systemic circulation and organs (e.g. Brain/kidneys)

55

Describe how an air embolism could form.

Negative pressure in the chest and head veins forms on inspiration. They can draw air in if theres been trauma of the neck or chest.
During labour air can enter the uterus and be forced into open veins during uterine contraction.

56

Describe how air emboli can cause a problem in the heart.

Bubbles gather in the right heart as a frothy mass which stops circulation.

57

Describe the bends.

Body tissues and blood are saturated with gas at high pressure. If a diver resurfaces too quickly these are released as bubbles and act as emboli.

Treated with prompt recompression.

58

Why is nitrogen a particular problem in the bends?

Its fat soluble so can result in persistent bubbles in lipid-rich tissues.

59

Describe an amniotic fluid embolism.

A complication of labour and caesarian section.
Causes sudden respiratory distress and collapse.
Amniotic fluid enters the circulation through a tear in the amniotic membranes.
Microscopic emboli of foetal origin are found in the lungs (e.g. Meconium)
Symptoms and signs may occur secondary to disseminated intravascular coagulation