Haemostasis Intro Flashcards

1
Q

what is haemostasis

A

the arrest of bleeding and the maintenance of vascular patency

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2
Q

what does haemostasis need to be

A

always ready
prompt response to reduce blood loss
localised response
protection against unwanted thrombosis

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3
Q

what constitutes primary homeostasis

A

the formation of a platelet plug

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4
Q

what is secondary homeostasis

A

the formation of a fibrin clot (more stable meshwork)

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5
Q

what happens after secondary haemostasis

A

fibrinolysis and anticoagulant defences to re-establish blood flow in the vessel

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6
Q

how are platelets made

A

bud of megakaryocytes in the bone marrow

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7
Q

what is the lifespan of platelets

A

7-10 days in the circulation (as have no nucleus)

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8
Q

what is the structure of platelets

A

small anucleate discs

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9
Q

how are platelets directed to a site of injury

A

endothelial (vessel wall) damage exposes collagen and releases von willebrand factor (+other proteins) to which platelets have receptors= bind to site of injury

platelets then secrete chemicals which auses aggregation at this site

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10
Q

what might cause a failure of platelet plug formation (primary haemostasis)

A

vascular (e.g. if collagen deficient)
platelets (reduced number- thrombocytopenia, or reduced function- e.g. on aspirin or NSAIDs)
von willebrand factor (e.g. inherited deficiency)

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11
Q

what can cause a collagen deficiency resulting in primary haemostasis problems

A

old age

scurvy (vit c needed to make collagen)

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12
Q

what are the potential consequences of platelet plug formation failure

A

spontaneous bruising and purpura
mucosal bleeding (epistaxes, GI, blood blisters in mouth, conjunctival haemorrhages, menorrhagia)
intracranial haemorrhage
retinal haemorrhages

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13
Q

where does purpura usually affect

A

lower limbs (as gravity big influence, pulls blood out of vessels)

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14
Q

does purpura blanch

A

no

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15
Q

why do more women with VWF deficiency present

A

affects men and women equally but women more likely to present with menorrhagia

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16
Q

what screening test for primary haemostasis

A

platelet count

17
Q

where does the fibrin clot form

A

on the platelet plug surface

18
Q

how does the fibrin clot form

A

platelets full of phospholipids which are negatively charged
platelets release calcium which is positively charged and sits on the cell surface
this attracts the clotting factors

tissue factor (CF7) attracted first which starts haemostasis and activates CF 5 and 10 (initiation phase) 
prothrombin activated into thrombin (by factors 5 and 10) (propagation stage)
thrombin cleaves fibrinogen into fibrin 

thrombin also activates CF 8 and 9 (amplification stage) which activate CF 5 and 10 creating positive feedback mechanism allowing fast clot formation

19
Q

what can cause failure of fibrin clot formation (secondary haemostasis)

A
single clotting factor deficiency (usually hereditary e.g. haemophilia)
multiple clotting factor deficiency (usually acquired e.g. DIC) 
increased fibrinolysis (usually part of complex coaguloplathy e.g. DIC)
20
Q

which single clotting deficiencies are more common

A
haemophilia A (CF 8) most common 
haemophilia B (CF 9) less common
21
Q

why do you have multiple CF deficiency in DIC

A

as making so many and then breaking down so many clots

22
Q

how does fibrinolysis happen

A

plasminogen converted to plasmin by tissue plasminogen activator (tPA)

fibrin then broken down into fibrin degradation products by plasmin

23
Q

what test can measure fibrin degradation products

A

D dimers

24
Q

what are the consequences of fibrin clot formation failure (problems with secondary haemostasis)

A

no classic clinical syndrome
can be combined with primary haemostasis failure

pattern of bleeding depends on:

  • single/ multiple factors affected (single e.g. haemophilia, affects joints in certain pattern. multiple e.g. DIC)
  • the clotting factors involved
25
Q

what happens to clotting factors in DIC

A

all used up

26
Q

what screening tests for fibrin clot formation (secondary haemostasis)

A
prothrombin time (uses citrate to analyse factors 7, 5, 10 and thrombin) 
activated partial thromboplastin time (analyses factors 8 and 9 (which in turn activate 5 and 10) 

e.g. if missing factor 8/0 then APTT will be increased by PT normal

27
Q

how do NSAIDs affect haemostasis

A

interfere with platelet function affecting primary haemostasis

28
Q

how do warfarin and NOAC affect haemostasis

A

affect secondary hameostasis

29
Q

what does anti-thrombin do

A

neutralises thombin, tissue factor (CF 7), CF 5, 10, 8 and 9

30
Q

how can you assess previous haemostasis from Hx

A
bleeding/ bruising 
duration (if lifelong)
previous surgery/ dental procedure, how long were you nleeding for afterwards 
Drug Hx
FHx
exam
31
Q

what is serine protease inhibitor

A

antithrombin- naturally occurring anti coagulant

32
Q

what are protein C and protein S

A

naturally occurring anticoagulants

switch off CF 8 and 8

33
Q

what does thrombomodulin do

A

modulates the function of thrombin to increase protein C and protein S which in turn deactivate CF 5 and 8, cause anti coagulation

34
Q

what is thrombophilia

A

increased tendency to develop venous thrombosis (e.g. DVT, PE)

35
Q

what can cause thrombophilia

A

deficiency of naturally occurring anticoagulants (serine protease inhibitors (anti thrombin), protein C and protein S (thombomodulin)