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Y3 Haematology > Platelet Physiology & Investigations > Flashcards

Platelet Physiology & Investigations Flashcards

1
Q

Where does platelet synthesis occur and by what mechanism?

A

Bone marrow

Megakaryocyte buds off peripheral cytoplasm

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2
Q

What is haemostasis?

A

Physiological mechanism to stop bleeding and maintain BV patency

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3
Q

Where are coagulation factors synthesised? What happens to them after synthesis?

A

Liver hepatocytes

Circulate in inactivated form

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4
Q

What is the lifespan of a PLT? What is the clinical significance of this?

A

7-10 days

If on antiplatelet agent, stop 7 days before elective surgery otherwise bleeding risk

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5
Q

Platelets have no ____

A

Nucleus

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6
Q

What initiates primary haemostasis?

A

Endothelial damage

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7
Q

What vitamin deficiency increases the risk of endothelial damage?

A

Vitamin C scurvy

Decreased collagen synthesis

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8
Q

What age group is a risk factor for endothelial damage and why?

A

Elderly
Increased fragility

(Why bruising is more common in elderly)

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9
Q

What is primary haemostasis?

A

Platelet plug formation

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10
Q

What is secondary haemostasis?

A

Fibrin clot formation

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11
Q

What are the 3 main steps of primary haemostasis?

A

Adhesion
Aggregation
Activation

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12
Q

Endothelial damage exposes ____ and _____

A

Collagen and Von Willebrand Factor

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13
Q

Endothelial damage causes the endothelium to release _____ which initiates secondary haemostasis

A

Tissue factor TF

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14
Q

What is the function of glycoprotein 1b in primary haemostasis?

A

Involved in platelet adhesion to collagen and VWF

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15
Q

In platelet adhesion in primary haemostasis, what do platelets do next?

A

Release granules to attract more platelets

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16
Q

In primary haemostasis, what granules do platelets release to attract more platelets?

A

ADP, thromboxane A2 and thrombin

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17
Q

What is the function of GPIIbIIIa and fibrinogen in primary haemostasis?

A

Platelet aggregation (clumping)

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18
Q

In platelet activation in primary haemostasis, platelets change their ____ to expose more of their phospholipid surface and ADP receptors

A

shape

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19
Q

In secondary haemostasis, platelets secretes ____ which binds to the platelet phospholipid membrane and attracts clotting factors?

A

Calcium

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20
Q

What is the function of tissue factor in secondary haemostasis?

A

Activates factor VII to VIIa

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21
Q

What are the 3 steps of secondary haemostasis?

A

Initiation
Amplification
Propagation

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22
Q

In the initiation step of secondary haemostasis, the TF/VIIa complex activates _______. It converts ____ to ____.

A

In the initiation step of secondary haemostasis, the TF/VIIa complex activates V/Xa. It converts II to IIa.

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23
Q

What are factor I, Ia, II and IIa also known as?

A

I fibrinogen
Ia fibrin
II prothrombin
IIa thrombin

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24
Q

In the propagation step of secondary haemostasis, thrombin converts _____ to _____

A

I to Ia

Fibrinogen to fibrin

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25
Q

In the amplification step of secondary haemostasis, thrombin activates _____, which also activates ______. This is referred to as the thrombin burst.

A

In the amplification step of secondary haemostasis, thrombin activates VIII/IXa, which also activates V/Xa. This is referred to as the thrombin burst.

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26
Q

Where is vitamin K absorbed? What is required for its absorption?

A

Upper intestine
Fat soluble
Bile salts

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27
Q

What is the function of vitamin K?

A

Activates factor II, VII, IX and X and protein C and S via carboxylation

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28
Q

How many factors require vitamin K to be activated?

A

4

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29
Q

Where are platelets removed?

A

Spleen

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30
Q

In fibrinolysis, ______ converts ______ to ______. It converts _____ to _______

A

In fibrinolysis, tPA converts PLASMINOGEN to PLASMIN. It converts FIBRIN to FIBRIN DEGRADATION PRODUCTS

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31
Q

What is the most clinically important fibrin degradation product? (Since it is the one that gets measured to assess fibrinolysis)

A

D-dimers

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32
Q

Protein C, protein S and anti-thrombin III are all ______

A

Natural anticoagulants

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33
Q

What is the action of anti-thrombin III?

A

Negative effect on:

  • thrombin
  • TF/VIIa
  • V/Xa
  • VIII/IXa
34
Q

What is the action of protein C and S?

A

Negative effect on V/Xa and VIII/IXa

Basically stop thrombin activation and propagation

35
Q

What test is a measure of primary haemostasis?

A

Platelet count

36
Q

What test is a measure of initiation and amplification of secondary haemostasis?

A

Prothombin time PT initiation

Activated partial thromboplastin time APTT amplification

37
Q

What is a normal platelet count?

A

150 - 400

38
Q

What factors are tested by PT?

A

I, II, V, VII, X

39
Q

What factors are tested by APTT?

A

VIII, IX, or VWD

Also XI and XII but not clinically important

40
Q

What are the potential causes of a raised APTT but normal PT?

A
  • Factor VIII problem
  • Factor IX problem
  • APS (interferes with test)
  • VWD (decreases factor VIII)
41
Q

What are the potential causes of a raised PT and APTT?

How can you differentiate the causes?

A
  • DIC
  • Cirrhosis
  • Vitamin K deficiency
  • DIC; low platelets, clinical history of cause eg RTA
  • Cirrhosis; low platelets + low albumin, +-alcohol history
  • Vitamin K deficiency; intake, absorption or vitamin K antagonist history
42
Q

Where are purpura most commonly found? How are they distinguished from other rashes on exam?

A

Commonest on lower limb

Non-blanching

43
Q

Name 5 anticoagulants

A 
Heparin
Warfarin
Apixaban
Rivaroxaban
Dabigatran
44
Q

Name 2 antiplatelets

A

Asprin

Clopidogrel

45
Q

What is the drug mechanism of heparin?

A

Potentiates natural anticoagulant anti-thrombin

46
Q

What is the drug mechanism of warfarin?

A

Vitamin K antagonist; makes protein C/S, factor II, VII, IX, X non-functional

47
Q

What is the mechanism of rivaroxaban and apixaban in?

A

Xa inhibitor

48
Q

What is the mechanism of dabigatran?

A

Direct thrombin inhibitor

49
Q

What are the 2 forms of heparin? What routes are they given?

A

Unfractioned IV

LMWH SC

50
Q

What routes is warfarin given?

A

I don’t know

51
Q

What route is Xa inhibitors eg rivaroxaban and apixaban given?

A

PO

52
Q

What route is dabigatran given?

A

PO

53
Q

What drug class is warfarin in? What do all drugs in that class do?

A

Coumarins

All inhibit vit K

54
Q

What effect does heparin have on APTT and PT?

A

Raised APTT

+- Raised PT

55
Q

What are the differences between heparin and warfarin’s:

  • Time to produce effect
  • Therapeutic window-
  • Monitoring
  • Effecting secondary haemostasis
A
  • Heparin has immediate effect, warfarin takes 1 wk
  • Both have narrow therapeutic window
  • Unfractioned heparin monitored by APTT, LMWH not monitored (by Xa assay if needed), warfarin monitored by INR
  • Both stop secondary haemostasis
56
Q

How do the half lives of unfractioned and LMWH compare, how does this effect clinical practice?

A

Unfractioned heparin half life 30 min
LMWH half life 1 day

If need to use anticoagulant in a patient with a high bleeding risk- use unfractioned heparin since reverse quicker

57
Q

What are the side effects of heparin?

A
  • Bleeding
  • OP long term
  • HITT autoimmune thrombocytopenia with thrombosis
58
Q

How is heparin reversed in a severe bleed

A

Protamine sulfate

59
Q

How is warfarin metabolised?

A

CYP450 enzymes

60
Q

Which anticoagulant should be taken at the same time every day?

A

Warfarin

61
Q

Warfarin has a variable response so requires different ____ in different patients

A

doses

62
Q

What are the side effects of warfarin?

A
  • Bruising
  • Bleeding; epistaxis, haematuria, GI, ICH
  • Decreased BP
63
Q

Why is warfarin not used in the acute management of thrombosis?

A

Inhibits protein C and S so patients are prothrombotic for 1st week before anticoagulant effect kicks in

64
Q

What does INR stand for? What test is it based on? What drug does it monitor?

A

International normalised ratio
PT
Warfarin

65
Q

How is warfarin reversed if immediate reversal is needed?

A

Factor concentrate + IV / PO vit K

66
Q

How is warfarin reversed if a patient has a mildly increased INR?

A

Miss a few doses

67
Q

How long does vitamin K take to reverse warfarin?

A

6 hours

68
Q

How are Xa inhibitors eg rivaroxaban and apixaban monitored?

A

Not monitored

69
Q

Newer oral anticoagulants such as Xa inhibitors and dabigatran require no monitoring, have _____ side effects and _____ drug interactions. However, it is not possible to ______.

A

Newer oral anticoagulants such as Xa inhibitors and dabigatran require no monitoring, have LESS side effects and LESS drug interactions. However, it is not possible to REVERSE THEM.

70
Q

What is used more commonly; Xa inhibitors eg apixaban and rivaroxaban or dabigatran?

A

Xa inhibitors

71
Q

What are the indications for anticoagulants and how long should they be used for in these scenarios?

A

Single VTE = 6 months
Recurred VTE = lifelong
AF = lifelong

72
Q

AF causes stasis in the ____

A

Left atrium

73
Q

What are the indications for antiplatelets?

A

Arterial thrombosis

74
Q

What part of haemostasis do antiplatelets act in?

A

Primary haemostasis; prevent platelet aggregation

75
Q

What is the mechanism of aspirin?

A

Cyclo-oxygenase inhibitors - stop thromboxane A2 production which decreases platelet activatoin

76
Q

What are the side effects of aspirin?

A

Bleed
PUD (due to blocking PG synthesis)
Bronchospasm (due to blocking PG synthesis)

77
Q

The antiplatelet abciximab is a GP IIb/IIIa inhibitor, it is only used as an IV infusion in ______

A

Heart surgery

78
Q

What is the mechanism of clopidogrel and prasugrel?

A

ADP antagonist

79
Q

What is the main reason LMWH is used over unfractioned heparin?

A

Requires more monitoring

80
Q

Atherosclerosis causes endothelial damage. Foamy _____ produce cholesterol rich plaques. _____ plaques are hyalinised or calcified and cause angina or intermittent claudication. ______ plaque rupture in ACS or stroke initiates ______.

A

Atherosclerosis causes endothelial damage. Foamy MACROPHAGES produce cholesterol rich plaques. STABLE plaques are hyalinised or calcified and cause angina or intermittent claudication. UNSTABLE plaque rupture in ACS or stroke initiates HAEMOSTASIS.

81
Q

What hormone regulates PLT production?

A

Thrombopoietin

Y3 Haematology (15 decks)

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