HAEM - Platelets, Clotting and Coagulation/Anticoagulation Flashcards

1
Q

What leads to platelet adhesion after endothelium is damaged?

A

Exposure of collage and vWF

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2
Q

What does platelet adhesion lead to

A

Degranulation of platelets –> release ADP

Synthesise PG TXA2 –> VC + aggregation

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3
Q

What does ADP do at site of endothelial damage

A

Stimulates platelet aggregation

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4
Q

What activates the clotting cascade?

A

Receptors on platelet surface

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5
Q

Mode of action aspirin

A

Irreversibly inhibits COX1

Preventing conversioon of AA –> endoperoxidases such as PGI2 and TXA2

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6
Q

What can’t anucleate platelets form, PGI2 or TXAs

A

TXAs

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7
Q

Causes of thrombocytopenia - reduced production (3)

A

Aplastic anaemia
Marrow infiltration
Marrow suppression

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8
Q

Causes of thrombocytopenia - excess destruction (5)

A
ITP
Autoimmune - SLE, CLL, virus
TTP
HUS 
Sequestriation - hypersplenism
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9
Q

PS thrombocytopenia (4)

A

Mucocutaneous bleeding
Bruising/purpura skin
Epistaxis/menorrhagia
Major haemorrhage (rare)

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10
Q

Cause ITP - children

A

Virus/imms

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11
Q

Cause ITP - adults

A

Autoimmune

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12
Q

Ix ITP (3)

A

FBC - thrombocytopenia ONLY
BM - norm/incr megacaryocyte
Platelet ab +ve 70%

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13
Q

Mx ITP - kids

A

No Tx necess

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14
Q

Mx ITP - adults

A

1st line = CCS
IVIG
Splenectomy = 2nd line

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15
Q

What does PT test (prothrombin time)

A

Extrinsic pathway

VII X, V, II + I

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16
Q

When is PT prolonged (2)

A

Liver disease

If pt is on Warfarin

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17
Q

What is INR

A

Ratio of pt’s PT to norm control

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18
Q

Norm INR range

A

0.9-1.1

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19
Q

Which drug dosing is IR used for

A

Warfarin

20
Q

What does APTT test

A

Intrinsic pathways

21
Q

Which factors are tested APTT

A
XII
XI
IX 
VIII = extrinsic 
X
V
II
I = common
22
Q

Which drug monitoring is APTT used for

A

Unfractioned heparin

23
Q

Which conditions are APTT raised in?

A

Haemophilia
vWD
Liver disease
DICs

24
Q

What does thrombin time

A

Adition of thrombin to pt plasma

25
Q

What pathway is tested in Thrombin time

A
Common pathway 
X 
V 
II
I
26
Q

What prolongs thrombin time

A

Fibrinogen deficiency
or abnorm fct
or inhibits
e.g. heparin

27
Q

What is INR

A

Ratio of patients PT to normal control

28
Q

What is APTT

A

Activated partial thromboplastin time

Addition of surface activator to plasma

29
Q

Which clotting factors are produced by the liver? (6)

A
I - fibroinogen 
II - prothrombin 
IV
V
VI
VII
30
Q

What happens if any clotting factors produced by the liver decrease

A

INR increases

31
Q

What is required for Vit K absorption and why

A

Bile salts

As is fat soluble

32
Q

Vit K dependent factors (6)

A
II
VII
IX
X
Protein C
Protein S
33
Q

Where is Vit K absorbed

A

Upper ileum

34
Q

Where is Vit K stored

A

Liver

35
Q

What is protamine

A

antidote to heparin

36
Q

What are the 4 mechanisms haemostasis occurs by

A

Behavioural (compression + elevation)
Vascular spasm
Platelet plug (rapid response)
Fibrin clot

37
Q

What are the 4 control mechanisms in the clotting pathway?

A

Physical separation
Protein C inhibitory pathway
Antithrombin 3
Fibrinolysis

38
Q

What is protein C generated by

A

Vit K

39
Q

What is protein C activated by?

A

Thrombin

40
Q

What does protein C do once activated

A

Acts w/ co-factor S to induce fibrinolysis

Destroys 5 + 8 meaning no more thrombin made + inhibits stabilization of fibrin clot

41
Q

Which control mechanism does heparin enhance?

A

Antithrombin 3

42
Q

How does fibrinolysis work

A

Plasminogen –> plasmin (by tPA)

Plasmin breaks down fibrinogen + fibrin –> d-dimer

43
Q

How is t-PA release stimulated

A

Thrombin + APC (activated protein C)

44
Q

What happens to the deficiency of fibrinolysis in severe trauma

A

Efficiency is enhanced

–> hyperfibrinolysis

45
Q

What viscosity platelets are ideal

A

sticky

46
Q

Signs of VIt K deficiency

A

Increased PT

Haemorrhage

47
Q

Causes of Vit K deficiencies (3)

A

Malabsorptive conditions
Cholestatic jaundice ( no bile salts)
ABx - gut flora disturbance