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Laura young Flashcards

1
Q

Where do platelets come from and how do they get into the blood?

A

They bud of megakaryocytes. They are located next to the bone marrow sinusoidal endothelial cells and extend filopodia into the capillaries. 4000 platelets/ megakaryocyte

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2
Q

What is in platelets?

A

Alpha granules that contain fibrinogen, factor V, vWF, fibronectin

Dense granulse: ADP, Ca2+, Mg2+, serotonin, nucleotides

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3
Q

What is primary and secondary haemostasis?

A

Primary - platelet plug at the site of vessel injury

Secondary - formation of fibrin

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4
Q

What is the process of primary haemostasis?

A

Constriction of the vessel wall.

Platelets become activated and aggregate the site of injury, forming a temporary loose plug.

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5
Q

What happens to a platelet when it becomes activated?

A

It changes from round to pointy with filopodia. It releases granules. Forms surface for coagulation pathway.

The released granules recruit more platelets.

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6
Q

How do platelets form a plug?

A

Endothelial cells produce vasodilators (NO). Damage stops this production.

Injury exposes collagen, which circulating vWBF binds. The platelet binds to vWBF with GP-1B-V-IX.

The platelet get pulled into the wound in a rolling motion and the platelet activates.

The activated platelets change shape and release their granules to attract more platelets (ADP, TxA2) and cause vasoconstriction (serotonin, ADP and TxA2).

The shape change also exposes integrin alpha-2bB3, which binds to other platelets via fibrinogen.

Clotting pathway then starts on the platelet surface. Platelets released some factors in the coagulation pathway.

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7
Q

What is the function of thromboxane A2?

A

It is produced by platelets and it decreases cAMP levels, which increases platelet Ca2+ and results in granule release and platelet activation. This is reduced by prostacyclin produced by intact endothelial cells.

Aspirin blocks COX, which is involved in production of TxA2.

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8
Q

What changes the number of platelets in the blood?

A

Decrease production - virus infection, drugs, bone marrow failure

Increase destruction - immune thrombocytopenia, DIC

Increase production - myeloproliferative disease - polycythaemia vera, essential thrombocythemia, primary myelofibrosis

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9
Q

What is thrombocytopenia?

A

Decreased platelets.

Recurrent epistaxis and easy bruising. Petechiae

Caused by anthing that reduces the number of megakaryocytes:

Decrease production- viruses or drugs, BM failure.

Increased destruction - immune thrombocytopenia (antibodies bind -> opsonisation), disseminated intravascular coagulation, glandular fever (caused by EBV)

Other: hypersplenism (pool of platelets in spleen)

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10
Q

What is immune thrombocytopenia?

A

Antibodies bind platelets -> opsonisation. With reduced platelet production.

Treat with prednisone. Remove spleen.
Thrombopoietin receptor agonist treatment.

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11
Q

What is haemostasis and thrombosis?

A

Normal situation where a blood clot is formed to heal vascular damage.

Thrombosis is the unnecessary formation of a clot.

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12
Q

What is the start of the extrinsic pathway?

A

Tissue factor and Factor VIIa

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13
Q

Where is tissue factor expressed?

A

On the subenothelial tissues. Exposed with tissue damage.

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14
Q

What are calcium and phospholipids required for?

A

Required on the platelet membrane to stabilize the proteins on the platelet membrane.

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15
Q

Where does fibrinogen come from?

A

It is in the plasma. Links together to form fibrin.

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16
Q

What inhibits the first complex?

A

Tissue factor pathway inhibitor (TFPI) - inhibits factor VII, TF

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17
Q

What do protein C and S inhibit?

A

Factor VIII and factor V

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18
Q

What does anti-thrombin do?

A

Inhibits Xa, IXa and thrombin

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19
Q

What does Factor XIII do and what activates it?

A

Cross-links the fibrin molecules and is activated by thrombin (factor IIa). Creates the D-dimers by cross-linking.

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20
Q

What are the functions of thrombin?

A

Converts fibrinogen into fibrin.
Activates factors V, VIII, XI, XIII and protein C.
Platelet activation

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21
Q

What are the two classes of functional enzymes?

A

Proteases and co-factors.

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22
Q

What are the vitamin K dependent factors?

A

Factor II, VII, IX, X, protein C and protein S

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23
Q

What does vitamin K do?

A

Enables the factors to bind to the platelet membranes.

Controls folding of the factors GLA domains to allow them to bind to the platelet membrane.

It carboxylates the glutamate residues in the GLA domain. Also need Ca2+

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24
Q

How is vitamin K absorbed?

A

Vit K is a fat soluble vitamin that you need bile to absorb. Liver disease = no vit K absorption.

Give vitamin K to prevent haemorrhagic disease of the newborn.

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25
Q

Do natural inhibitors change the laboratory tests?

A

No - only function in the blood, don’t change the tests.

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26
Q

What can you do to determine if clots are breaking down?

A

Look for the D-dimers in the blood.

27
Q

How are clots broken down?

A

Plasminogen is cleaved to plasmin by tissue plasminogen activator.
Plasmin then breaks down clots. Gives of D-dimers.

28
Q

What factors are you looking at in an APTT?

A

All factors are involved except TF. But the ones you are assessing relative to a PR is factor XII, XI, IX and VIII

29
Q

How is an APTT performed?

A

You take a venous blood sample. Calcium is removed by citrate in the tube. Collect the plasma. Add phospholipids and an activator. Add calcium and measure time to clot formation

30
Q

What is the starting point of the PR ratio and what factors is it assessing?

A

It starts with the addition of heaps of TF, which favtor VII binds to activate factor X, which activates thrombin. No amplification step required because of the excess thrombin. Complex 1 is sufficient.

31
Q

What factors deficiency would prolong the PR?

A

VII, X, V, prothrmbin or fibrinogen

32
Q

What test would identify a co-factor deficiency?

A

Factor V - PR

Factor VIII - APTT

33
Q

What are the inhibitors of thrombin?

A

Heparin

Dabigitran

34
Q

How does a thrombin clotting time work?

A

Add activated thrombin and see how quickly it converts fibrinogen into fibrin.

This is a check for inhibitors of thrombin

35
Q

What prolongs the APTT 1+1?

A

Lupus anticoagulant
Heparin
Dabigatran
Autoimmune antibodies against factors- usually factor VIII

36
Q

How do lupus anticoagulants work?

A

There are antibodies in the plasma that bind to phospholipids. In the lab this is an inhibitor but in the body there is too much phospholipid to have any effect.

37
Q

How does heparin prolong the APTT 1+1?

A

It upregulates antithrombin

38
Q

Hoe do you determine if a prolonged APTT 1+1 is caused by heparin?

A

Use protamine, which inhibits heparin

39
Q

How does dabigatram work?

A

Direct inhibitor of thrombin.

40
Q

How do you differentiate between a lupus anticoagulant and a dabigatran inhibition?

A

Use the TCT

41
Q

Which is more sensitive PT or APTT?

A

PT, so you may have a slow PT and normal APTT with mild II, X, V

42
Q

What is the cause of a prolonged APTT and PR?

A

Multiple factor deficiency or a deficiency of either X, II, or V

43
Q

What does a prolonged TCT indicate?

A

A thrombin inhibitor or a deficiency of fibringogen

44
Q

What are the most common causes of multiple factor deficiencies?

A

Bleeding - loss of coagulation factors and dilation of fluids.
Warfarin or vitamkin K deficiency (II, VII, IX, X)
DIC - depletion of clotting factors
Liver disease

45
Q

Most common causes of prolonged APTT and PT?

A

Warfarin
Vitamin K deficiency
Liver disease

46
Q

How does warfarin work?

A

It inhibits the recycling of vitamin K.

47
Q

What may be the issue with a prolonged APTT bt normal PT?

A

Factor VIII or IX deficiency - haemophillia - sequence factors

Administer recombinant

48
Q

What is von willebrand’s disease?

A

vWBF binds to factor 8 in the circulation and stabilises it. So a deficiency in vWF can cause both platelet and factor VIII deficiency

49
Q

What can cause DIC?

A

Meningicoccal septicaemia

50
Q

What are the three components of virchow’s triad and some examples of those?

A

Blood stasis
Hypercoagulability
Vascular injury

Vascular injury - artherlosclerotic plug -MI
Trauma
Thrombosis

Stasis
Post operative
Economy class syndrome
Pressure from a catheter or tumour
Increased viscosity from polycythaemia, dehydration, or EPO.

Hypercoagulability: increased procoagulants, decreased inhibitors

51
Q

What are the two manifestations of a deep vein thrombosis?

A

Clot in lower legs

Pulmonary embolism

52
Q

How do you diagnose DVT?

A

Clinical symptoms:
DVT: Leg swelling, pain, oedema.

Look for D-dimers if low risk and then ultrasound if present. Go direct to ultrasound if high risk.

D-dimer is good for ruling out but not for identifying.

53
Q

What is the risk with a proximal DVT?

A

Pulmonary embolism - 50% will progress without treatment.

54
Q

How do you diagnose chest pain?

A

Symptoms of:
SOB
Pleuritic pain
Haemoptysis

Signs:
Tachycardia
Tachypnoea
Hypoxia

Positive D-dimer

CT-scan CT pulmonary angigraphy

55
Q

What happens in massive PE?

A

Sudden death (15%)
Mortality (>50%)
Hypotension
severe right heat strain due to back pressure from pulmonary arteries

56
Q

How do you treat massive DVT and PE?

A

Initially: Low molecular weight inhibits Xa through antithrombin. Suncutaneous. Fast response to treatment.

Warfarin at the same time but has a slow response.

TPA to break down clot

57
Q

What is thrombophilioa?

A

Tendency to develop clots
Manifests as venous thromboembolism (DVT or PE)
Inherited or acquired

58
Q

What are some causes of thrombophilia?

A

Abnormal inhibitor function:
Resistance to activated protein C (factor V leiden)

Deficiency of inhibitors:
Antithrombin, protein C and protein S deficiency

Increased factor levels:
Elevated factor II
Elevated VIII

59
Q

What is factor V leiden?

A

Point mutation in factor V.

Protein C can’t bind and inhibit the mutated factor V -> higher factor V levels.

60
Q

What do you need to be careful with regarding warfarin?

A

Drug interactions: antibiotics, anticonvulsants.

INR

61
Q

What are two direct acting anticoagulants?

A

Dadbigatran - thrombin
Revaroxaban - Xa

Less chance of intracranial haemorrhage compared to warfarin.

62
Q

What tests will ivaroxaban prolong?

A

PT

APTT to a less extent

63
Q

What tests will dabigatran prolong?

A

TCT, APTT and PT

BII (14 decks)

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