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Endo, Cardio and Neuro > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

what is the purpose of haemostasis?

A

prevention of blood loss from intact vessels
arrest bleeding from injured vessels
enable tissue repair

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2
Q

what is haemostasis?

A

cellular and biochemical processes that enables both the specific and regulated cessation of bleeding in response to vascular insult

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3
Q

describe the mechanisms of haemostasis

A

vessel constriction
formulation of unstable platelet plug
stabilisation of plug with fibrin
vessel repair and dissolution of clot

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4
Q

what is primary haemostasis?

A

unstable platelet plug

platelet adhesion, aggregation to limit blood loss and provides surface for coagulation

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5
Q

what is secondary haemostasis?

A

stabilisation of platelet plug (fibrin)

blood coagulation to stop blood flow

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6
Q

what is fibrinolysis in haemostasis?

A

final stage of haemostasis - vessel repair and dissolution of clot
restores vessel integrity

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7
Q

what is the importance of understanding haemostasis?

A 
diagnose/treat bleeding disorders
control bleeding in normal individuals
identify risk factors for fibrinolysis
treat thrombotic disorders
monitor treatment for bleeding/thrombotic disorders
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8
Q

how does platelet adhesion occur?

A

adheres to collagen in vessel wall
GlpIa receptor direct bonding
GlpIb receptor via Von Willebrand Factor

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9
Q

how does platelet aggregation occur?

A

platelets release ADP, fibrinogen and thromboxane A2 after they are activated
express GlpIIb/IIIa for adhesion of other platelets via fibrinogen and Ca2+

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10
Q

what conditions cause thrombocytopenia?

A 
bone marrow failure (leukaemia, b12 deficiency)
accelerated clearance (immune ITP, disseminated intravascular coagulation)
pooling and destruction in splenomegaly
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11
Q

what conditions cause impaired platelet function?

A

hereditary absence of glycoproteins or storage granules

latrogenic - aspirin, NSAIDs, clopidogrel

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12
Q

what is immune thrombocytopenic purpura? ITP

A

antiplatelet autoantibodies bind to sensitised platelets
macrophages then bind to the platelets and destroy them (spleen)
this causes low platelet count

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13
Q

what are some hereditary platelet defects?

A

Glanzmanns thrombasthenia - absence of GlpIIb/IIIa
bernard soulier syndrome - absence of GlpIb
storage pool disease - absence of dense or alpha granules

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14
Q

what is aspirins MOA?

A

binds irreversibly to cyclooxygenase
inhibits thromboxane A2 synthesis
therefore prevents platelet aggregation
effects last around 7 days

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15
Q

what is clopidogrels MOA?

A

irreversibly blocks ADP receptor (P2Y12) on platelet cell membrane
therefore platelets cannot be activated to cause aggregation

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16
Q

what are the functions of von willebrand factor?

A

binding to collagen and capturing platelets

stabilising factor VIII

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17
Q

what is von willebrand disease?

A

hereditary autosomal dominant disease causing failure of primary haemostasis
deficiency of VWF (type 1&3)
VWF with abnormal function (type 2)

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18
Q

what are some causes of vessel wall disorders?

A 
hereditary haemorrhagic telangiectasia
ehlers danlos syndome
steroid therapy
ageing
vasculitis
scurvy
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19
Q

how does typical primary haemostasis bleeding present?

A 
immediate
prolonged bleeding from cuts
prolonged nose bleeds, gum bleeding
menorrhagia
ecchymosis - easy and spontaneous bruises
prolonged bleeds after trauma/surgery
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20
Q

what specific symptom occurs for thrombocytopenia?

A

petechiae - bleeding under skin

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21
Q

what disorders cause purpura as a symptom?

A

platelet or vascular disorders (thrombocytopenia pupura)

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22
Q

what tests are used in diagnosis of primary haemostasis disorders?

A 
platelet count and morphology 
PFA100 (platelet function analysis - bleeding time)
assays of VWF
clinical observation
PT and aPTT
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23
Q

what tests are usually normal in primary haemostasis disorders?

A

PT and aPTT

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24
Q

how do you treat failure of production/function platelet disorders?

A

replace missing platelets/factor e.g VWF prophylactically or therapeutically
stop aspirin/nsaids

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25
how do you treat immune destruction of platelets?
immunosuppression | splenectomy for ITP
26
how do you treat increased consumption of platelets?
treat underlying cause | replacement
27
how can desmopressin be used to treat primary haemostatic abnormalities?
causes 2-5 fold increase of VWF and factor VIII | releases endogenous stores therefore only used in mild disorders
28
how is tranexamic acid used?
traumatic bleeds, strokes | antifibrinolytic
29
when are fibrin glues/sprays used?
during surgeries
30
what is the overall role/end goal of coagulation in haemostasis?
generate thrombin IIa to convert fibrinogen to fibrin
31
what are the acquired causes of factor deficiencies?
liver disease | anticoagulant drugs - warfarin, DOACs
32
what are the hereditary causes of factor deficiency?
haemophilia A/B (VIII/IX)
33
what are the causes of dilution coagulopathy?
blood transfusions
34
what are the causes for increased consumption coagulopathy?
disseminated intravascular coagulation DIC | immune autoantibodies
35
what is haemarthrosis?
spontaneous joint bleeding causes long term chronic muscle wasting prophylaxis from around 9mths age
36
what does a deficiency of factor II cause?
incompatibility with life - prothrombin is necessary
37
what does a deficiency of factor XI cause?
bleeds after trauma no spontaneous bleeding
38
what does a deficiency of factor XII cause?
no bleeding
39
what factors aren't produced in the liver?
VWF (endothelium), factor V (platelets)
40
what is disseminated intravascular coagulation?
generalised activation of coagulation - tissue factor consumes and depletes coagulation factors platelets consumed - thrombocytopenia fibrinolysis depletes fibrinogen causing raised D-dimer and red cell fragmentation deposition of fibrin in vessels causes organ failure risk of sepsis, cancer, obstetric disorders
41
different types of factor replacement therapy
Fresh Frozen Plasma Cryoprecipitate Factor Concentrates Recombinate forms of FVIII and FIX
42
FFP
contains all Coagulation factors
43
cryoprecipitate
Fibrinogen, Factor VIII (8), XIII and VWF
44
factor concentrates
Concentrates available for all factors except factor V. | Prothrombin complex concentrates (PCCs) Factors II, VII, IX, X
45
whn are recombinant forms of FVIII and FIX used?
‘On Demand’ to treat bleeds | Prophylaxis to prevent bleeds
46
disorders of thrombosis present with
pulmonary embolism | deep vein thrombosis
47
pulmonary embolism symptoms
``` Tachycardia Hypoxia Shortness of breath Chest pain Haemoptysis Sudden death ```
48
features of DVT
``` Painful leg Swelling Red Warm May embolise to lungs Post thrombotic syndrome ```
49
What is thrombosis
inappropriate intravascular coagulation Venous (or arterial) Obstructs flow May embolise to lungs
50
What is Virchow's triad
``` Three contibutory factors to thrombosis Blood (dominant in venous) Vessel wall (dominant in arterial) Blood flow (both) ```
51
what is indicative of thrombosis
Thrombosis at young age ‘spontaneous thrombosis’ Multiple thromboses Thrombosis whilst anti-coagulated
52
anticoagulant proteins
antithrombin protein C protein S
53
risk factors of venous thrombosis
age] genetic environmental
54
prevention of thrombosis
prophylactic anticoagulant therapy
55
acquired causes of coagulopathy
liver failure anticoagulant drugs dilution increased consumption -DIC
56
blood test sign of DIC
raised D-dimer | red cell fragmentation
57
clinical features of coagulation disorders
``` superficial cuts dont bleed bruising common, nosebleeds rare spontaneous bleeds are deep - joints etc bleeding after trauma may be late and prolonged bleeding frewuently restarts ```
58
differences between platelet/vascular and coagulation disorders
platelet - superficial bleeds, immediate bleeds | coagulation - deep bleeds, prolonged but delayed
59
tests for coagulation disorders
clotting screen - APTT, PT, FBC coagulation factor assays tests for inhibitors
60
what does APTT measure
intrinsic pathway
61
what does PT measure
extrinsic factor VII via tissue factor pathway
62
prolonged APTT indicates
``` haemophilia A/B factor XI deficiency or XII (no bleeds) ```
63
prolonged PT indicates
factor VII deficiency
64
prolonged APTT and PT
``` liver disease anticoagulant drugs DIC dilution factor X, II, V (common pathway) deficiencies ```
65
treatments for failure of production
replaces as necessary | stop drugs e.g nsaids, aspirin
66
treatments for immune destruction
immunosuppresion - prednisolone | splenectomy - ITP
67
treatments for increased ocnsumption
treat cause | replace as necessary
68
how to reduce recurrence of thrombosis
lower procoagulants - DOACs, warfarin | increase anticoags - heparin

Endo, Cardio and Neuro (22 decks)

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