haemostasis Flashcards

1
Q

describe the actions of haemostasis after an artery is severed

A
  1. artery contracts and pressure decreases downstream
  2. primary haemostat plug forms out of platelets= v fragile and temporary (1min)
  3. secondary haemostat plug forms and firkin stabilises it (30 mins)
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2
Q

components that platelets are activated by

A

collagen surfaces
ADP (released by platelets and damaged RBC)
thromboxane (aggregates platelets)
thrombin (informs which clotting factors are activated)

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3
Q

action of platelets once activated

A
  1. stick to vWF on endothelial membrane
  2. aggregate other platelets to form a plug and bound by fibrinogen to form secondary plug
  3. change shape to stick spiny spheres
  4. factors excreted which aid growth of platelet plug e.g ADP or thomboxne
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4
Q

action of aspirin

A

it irreversibly acetylates an enzyme of prostogladin synthesis meaning platelets can’t produce thromboxane reducing coagulation

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5
Q

what does the intrinsic pathway of the clotting cascade involve

A

triggered by damaged blood vessel. contained in the blood. involves factors I, II, IX, X, XI, and XII

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6
Q

what des extrinsic pathway involve

A

trauma to extravascular cells. triggered by thromboplastin outside blood. involves factors I, II, VII, and X

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7
Q

learn clotting cascade

A

:)

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8
Q

cofactors needed by the clotting cascade

A

ca2+ and phospholipids act as cofactors for enzymes in these reaction
ALSO vit k required for synthesis of protein S and C (anticoagulants)

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9
Q

role of vascular wall in coagulation

A
contracts when vessel damage 
sub endothelium traps platelets 
also balances coagulation by secreting 
protein C=  anticoagulant 
plasminogen activator = fibrinolysis  
vWF= clotting
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10
Q

factors opposing clot

A

antithrombin III
protein C
protein S
also oppose it by dilution of clotting factors

if missing any of these leads to thrombosis

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11
Q

describe clot retraction

A

platelets die = cling to fibrin and pull on actin and myosin filaments together.

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12
Q

describe fibrinolysis

A
  1. plasminogen (inactive precursor circulating blood made in liver) is activated by tea (tissue plasminogen activator)
    = PLASMIN
  2. plasmin is an enzyme used by macrophages to break down fibrin
  3. increase in FDP (breakdown product of fibrin which is found very high in thrombosis
  4. eventually clot is replaced by granulation tissue and leaves a scar
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13
Q

how is fibrinolysis activated

A

activated by clotting cascade. fibrin increases activity of plasminogen activators. fibrinolytic activity drops after surgery increasing risk of DVT

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14
Q

what are streptokinase and urokinase and side effects

A

streptokinase (from streptococcus) and urokinase (from urea) are also plasminogen activators.
side effects of these drugs = bleeding e.g nose bleeds.
used to break down clots

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15
Q

what is haemophilia and effects

A

have platelets but lack clotting factors so can’t produce fibrin
easy bruising, haemorrhage after surgery and trauma.
may develop harm-arthritis from minor injuries
petechiae is also seen

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16
Q

what is haemophilia A

A

factor VIII deficiency - X linked and therefore affects males. treated by infusion of engineered factor VIII

17
Q

what is haemophilia B

A

reduction in factor IX = prolonged APTT. treated by infusion of engineered factor IX

18
Q

what is vonwillerbrands disease

A

reduced FVIII- leads to bleeding e.g nose bleeds, bruising,prlonged bleeding after trauma.
skin and mucosal associated bleeding - gums, bruising and epistaxis

19
Q

what is DIC

A

disseminated intravascular coagluation - activator of clotting which gets into blood forming clots. no disease in itself always occurs as a complication e.g sepsis or trauma

20
Q

treatment of DIC

A

treat underlying cause of DIC
if lots of bleeding because factors/ platelets have been consumed require transfusion
sometimes anticoagulant e.g herapin is needed

21
Q

causes of DIC

A

gangrene, renal failure, respiratory distress, haemorrhage

22
Q

signs of DIC

A

increased FDP’s e.g Ddimers in the blood as the fibrinolytic system is activated and damage to RBC as the move past thrombi

23
Q

screening tests

A

PT- measure extrinsic pathway (time to make prothrombin)
APPT- measures intrinsic common pathway - time to make partial thromboplastin
thrombin time
fibrinogen