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B4W2 > THE COAGULATION SYSTEM > Flashcards

THE COAGULATION SYSTEM Flashcards

1
Q

what is haemostasis?

A

the process of forming a clot to stop the bleeding whilst still maintaining blood flow in the rest of the vessel

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2
Q

what is thrombosis? how can this cause an embolism?

A

a formation of a blood clot that prevents blood flow, causing hypoxia and tissue damage.
if the clot dislodges then it can form an embolism

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3
Q

Outline the 3 stages of haemostasis

A
  1. vascular spasm
  2. platelet plug formation/primary haemostasis
  3. coagulation/secondary haemostasis
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4
Q

what happens during vasuclar spasm?

A

damaged blood vessels constrict, reducing blood flow in the damaged area and reducing the amount of blood lost.

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5
Q

where do platelets come from?
how long is their life span?
how are they destroyed?

A

small fragments of megakaryocyte cytoplasm
5-9 days
Kupffer cells in the liver or phagocytosis in the spleen

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6
Q

Why don’t platelets have a nucleus? what is the implication of this?

A

as they are just chunks of cytoplasm.

they can’t produce anything new so they must contain all the factors required for their function.

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7
Q

describe platelet ultrastructure?

A

they have surface-connected canalicular systems. microtubules, alpha granules, dense granules, glycogen fragments and mitochondria

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8
Q

what is the function of microtubules in platelets?

A

they allow them to change shape and release granules

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9
Q

what are alpha granules?

A

these are dense granules that contain lots of proteins

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10
Q

what are dense granules? do we have more or less in platelets compared to alpha granules?

A

we have 2-7 in each platelet, way less than alpha granules

they contain vasoconstrictive agents, platelet agonists, calcium and magnesium

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11
Q

what are calcium and magnesium critical for?

A

integrin function

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12
Q

what do dense granules look like under a microscope?

A

a dense core surrounded by a halo

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13
Q

what receptors do platelets have on their membranes?

A

agonist and glycoprotein receptors

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14
Q

what happens because of damage to the endothelial layer of blood walls?

A

the sub endothelial layer is exposed, exposing collagen fibres and von Willebran factors

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15
Q

how do platelets adhere to the sub endothelial layer of blood vessel walls?

A

platelets adhere to exposed collagen fibres with help of vWF due to shear stress. Blood flow then rolls the platelets along the sub-endothelium, promoting more glycoprotein and vWF associations. this creates firmer adhesion

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16
Q

what is shear stress?

A

platelets are smaller than other blood cells so tend to travel along the edges of blood vessel walls and therefore travel at a higher pressure.

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17
Q

what happens once a platelet has adhered to the sub-endothelium?

A

this initiates platelet activation and aggregation resulting in granule release, conformational changes, stronger adhesion

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18
Q

describe platelet aggregation?

A

a platelet monolayer forms on the exposed subendothelial layer. the activated platelets monolayer releases platelet agonists and adhesive proteins which recruits further platelets. the newly recruited platelets are attracted and change shape to allow for greater platelet-platelet interactions= temporary plug

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19
Q

why don’t platelets bind to healthy cells?

A

as these secrete substances to prevent adhesion. e.g. nitric oxide and prostaglandin

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20
Q

outline secondary haemostasis

A

a coagulation cascade can be initiated by either trauma (extrinsic) or internal damage to the vessel wall (intrinsic)

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21
Q

what is the result of the coagulation cascade?

A

a gelatinous, but robust clot made up on a mesh of fibrin in which platelets and blood cells are trapped

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22
Q

describe the intrinsic coagulation pathway?

A

damage of the vessel wall activates factor 12 which then goes on to activate factor 9. factor 9 then forms a complex with factor 8 and this goes on to activate factor 10

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23
Q

describe the extrinsic coagulation pathway

A

after trauma to extravascular cells, factor 3 is released which activate factor 7. the factor 3 and 7 complex then goes on to activate factor 10

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24
Q

why is it important that the extrinsic pathway is simpler?

A

so we can initiate the coagulation cascade sooner after trauma

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25
Q

describe the common coagulation cascade pathway

A

factor 10 then activates prothrombin to produce thrombin. thrombin then acts as an enzyme (along with Ca2+) to convert fribrinogen to fibrin. fibrin and factor 13 form a cross-linked mesh work that captures blood cells

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26
Q

What is Tissue Factor Pathway Inhibitor?

A

an anticoagulant expressed and released by all endothelial cells. this prevents activation of factor 10 and the active of factor 7 complex

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27
Q

what is Anti-Thrombin?

A

this binds directly to thrombin, factor 9, factor 10 and factor 11.

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28
Q

describe the process and results expected of platelet aggregometry

A

shine light through platelet rich plasma. inactive platelets will make the plasma cloudy whereas active platelets that clump together will form clots and allow more light through. It forms an S shaped curve. the small notch is where platelets change shape and get a little more cloudy just before they aggregate

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29
Q

Describe the process of the coagulation test

A

you take plasma with no blood cells and put it in a cuvette with a metal ball. the machine spins the plasma and makes the ball fly around the cuvette. We add certain reagents to initiate the coagulation cascade and time how long it takes for the plasma to coagulate, form a gel and for the ball to stop moving

30
Q

What is prothrombin time?

A

it measures how long it takes for blood to clot down the extrinsic pathway

31
Q

what is partial thromboplastin time?

A

it measures how long it takes for blood to clot down the intrinsic pathway

32
Q

What does a prolonged prothrombin time but normal partial thromboplastin time suggest?

A

liver disease due to decreased vitamin K

33
Q

what does a prolonged partial thromboplastin time but normal prothrombin time suggest?

A

defects in factors 8,9,10 11 or von Willebrands disease

34
Q

what does a prolonged partial thromboplastin and prothrombin time suggest?/

A

defects downstream of the intrinsic and extrinsic pathways… defects in factor 10/ liver disease

35
Q

What is thrombocytopenia?

A

a condition of low circulating platelets.

36
Q

what is primary thrombocytopenia?

A

where the low platelet count occurs spontaneously for no reason

37
Q

what is immune thrombocytopenia?

A

platelets have many glycoproteins so an anti-viral effect could produce antibodies that are specific to a platelet glycoprotein so these platelets could be opsonised and cleared out of circulation by our own immune system

38
Q

how does thrombocytopenia present when mild and when severe?

A 
mild= petechia (small haemorrhages) which appear as a rash
severe= extensive hematomas and cerebral haemorrhages
39
Q

What is Glanzmann’s Thrombasthenia? What causes it?

A

an autosomal recessive bleeding syndrome affecting the megakaryocyte lineage and is characterised by a lack of platelet aggregation.

specific mutations lead to changes in expression and/or function of glycoprotein 2b or 3a

40
Q

what can be symptoms of Glanzmann’s Thrombasthenia?

A

mild e.g. bleeding gums

severe e.g. severe haemorrhages

41
Q

what is haemophilia? who suffers from it?

A

a recessive sex-linked X chromosome disorder so the vast majority of sufferers are male.

42
Q

What is haemophilia A caused by? what is haemophilia B caused by?

A

A- deficiency in factor 8

B- deficiency in factor 9

43
Q

Describe the mechanism of aspirin

A

it inhibits platelet cylcooxygense which prevents the formation of thromboxane A2 which prevents platelet activation and aggregation

44
Q

what are some anti thrombotic drugs?

A

aspirin and clopidogrel

45
Q

Why must patients take aspirin every day if using as anti-thrombotic drugs?

A

as platelets only have a lifespan of 5-9 days so its important that all the platelets are inhibited, including new ones

46
Q

what happens when aspirin inhibits COX1?

A

it prevents thromboxane synthesis

47
Q

what happens when aspirin inhibits COX 2?

A

it has an anti-inflammatory effect which, in turn, can also have an anti-thrombotic effect

48
Q

What are indications of aspirin?

A

ischemic stroke, transient ishemic attacks, chronic stable angina, unstable angina, coronary stenting, acute myocardial infarction, prevention of MI

49
Q

What are side effects of aspirin?

A

GI bleeding, haemorrhage stroke

50
Q

what are low-dose and high-dose aspirin given for?

A

low dose- prevent problems by inhibiting platelet activity

high dise- treatment of symptoms

51
Q

Describe the mechanism of clopidogrel?

A

its a prodrug that is metabolised in the liver by CYP2C19 and prevents ADP binding to P2Y12 and activating platelet aggregation

52
Q

what are the indications of clopidogrel?

A

prevents blockages of coronary arterial stents, reduce thrombotic events in patients with recent MI, stroke or peripheral arterial disease

53
Q

what is the fatal side effect that can come with clopidogrel?

A

thrombotic thrombocytopenia purpura. when there’s an issue with breaking down vWF so they soak all the platelets up and the patient is left with no platelets and cannot activate any new platelets.

54
Q

what is the goal of anticoagulants?

A

to reduce the formation of fibrin

55
Q

what are the 2 ways in which anticoagulants can work?

A

inhibiting the synthesis of clotting factors

inhibiting the activity of clotting factors

56
Q

what is unfractionated heparin?

A

an anticoagulant that can bind to antithrombinand then bind to factor 10 and wrap around thrombin due to the long chains and binding sites. this holds them in place and deactivates them.

57
Q

why does heparin aim to deactivate factor 10?

A

as its the start of the common coagulation pathway

58
Q

what is low molecular weight heparin?

A

an anticoagulant that can bind to antithrombin and then bind to factor 10, deactivating it.

59
Q

What do we use unfractionated heparin for?

A

atrial fibrillation, treatments of embolisms and vacutainers (more severe cases)

60
Q

what do we use low molecular weight heparin for?

A

prophylaxis, unstable angina, pregnant women, anti thrombotic therapy

61
Q

what are the side effects of heparin?

A

bleeding, immune-induce thrombocytopenia, neurological injuries

62
Q

What is warfarin?

A

a vitamin K antagonist. it decreases the amount of reduced vitamin k which if required for clotting factor formation

63
Q

what are the side effects of warfarin?

A

bleeding, can’t be used in pregnancy/breast feeding, long term use can result I osteoporosis.

64
Q

how can we reverse the bleeding effects of warfarin?

A

with an injection of vitamin k

65
Q

what do platelets release in primary haemostasis after they stick to the wall?

A

thromboxane 2, seretonin, ADP

66
Q

why do platelets secrete thromboxane 2?

A

to stimulate platelet activation and increase aggregation

67
Q

why do platelets secrete serotonin?

A

it enhances vascular;ar spasm and enhances platelet aggregation

68
Q

why do platelets secrete ADP?

A

to cause further platelet activation and aggregation

69
Q

what is the role of calcium in the coagulation cascade?

A

to allow the clotting factors to work

70
Q

why when we take blood do we often use citrate?

A

as it removes free Ca2+ by binding to it and therefore prevents coagulation

B4W2 (11 decks)

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