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haemostasis Flashcards

coagulopathy: compare the clinical features of bleeding due to different causes, and explain the principles of management of disorders of haemostasis

1
Q

elements of a significant bleeding history: epistaxis (nosebleeding)

A

epistaxis not stopped by 10 mins compression, or requiring medical attention/transfusion

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2
Q

elements of a significant bleeding history: cutaneous haemorrhage or bruising

A

cutaneous haemorrhage or bruising occur without apparent trauma (especially multiple or large)

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3
Q

elements of a significant bleeding history: prolonged bleeding

A

prolonged bleeding (>15 mins) from trivial wounds, or in oral cavity or recurring spontaneously in 7 days after wound (spontaneous GI bleeding leading to anaemia)

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4
Q

elements of a significant bleeding history: menorrhagia

A

menorrhagia requiring treatment or leading to anaemia, not due to structural lesions of the uterus

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5
Q

elements of a significant bleeding history: heavy, prolonged or recurrent bleeding

A

heavy, prolonged or recurrent bleeding after surgery or dental extractions

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6
Q

stages of haemostatic plug formation in response to injury

A

vessel constriction -> formation of unstable platelet plug (platelet adhesion and aggregation) -> stabilisation of plug with fibrin (blood coagulation) -> dissolution of clot and vessel repair (fibrinolysis)

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7
Q

2 general causes of abnormal haemostasis

A

lack of a specific factor, defective function of specific factor

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8
Q

2 causes of lack of a specific factor

A

failure of production (congenital or acquired), increased consumption or clearance

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9
Q

2 causes of a defective function of a specific factor

A

genetic defect, acquired defect (drugs, synthetic defect, inhibition)

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10
Q

what is exposed, triggering primary haemostasis, which isn’t normally; what binds and via what (platelet adhesion and aggregation)

A

collagen in subendothelium, which platelets (via GlpIa/vWF) and vWF bind to (platelet adhesion), causing exposure of GlpIIb/IIIa (platelets then aggregate and stick to each other)

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11
Q

what can be disordered in primary haemostasis

A

platelets, vWF, vessel wall

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12
Q

2 disorders of primary haemostasis associated with platelet adhesion and aggregation

A

thrombocytopenia (low platelet numbers presenting as petechiae (only if thrombocytopenia, not vWD)), impaired function of platelets

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13
Q

2 causes of thrombocytopenia

A

bone marrow failure (e.g. leukaemia, B12 deficiency (megaloblastic anaemia)), accelerated clearance (immune e.g. ITP, DIC)

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14
Q

describe process of auto-ITP (auto-immune thrombocytopenic purpura)

A

antiplatelet antibodies bind to sensitised platelet, which is then engulfed by a splenic macrophage

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15
Q

3 mechanisms and causes of thrombocytopenia

A

failure of platelet production by megakaryoctes, shortened half life of platelets, increased pooling of platelets in enlarged spleen (hypersplenism) and shortened half life

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16
Q

2 causes of impaired function of platelets

A

hereditary absence of glycoproteins or storage granules, acquired due to drugs e.g. aspirin, NSAIDs, copidogrel

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17
Q

what platelet surface glycoprotein is impaired by Glanzmann’s thrombasthenia

A

GpII/IIIa (recessive)

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18
Q

what platelet surface glycoprotein is impaired by Bernard Soulier syndrome

A

GpIb

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19
Q

what is impaired by storage pool disease

A

issue with contents or relase of dense granules, containing ADP, ATP, serotonin and Ca2+

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20
Q

cause of disorder of vWF

A

vW disease (autosomal; if severe, haemophoilia-like bleeding due to FVIII deficiency)

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21
Q

2 causes of vW disease

A

hereditary decrease of quantity and/or function (common), acquired due to antibody (rare)

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22
Q

2 functions of vWF in haemostasis

A

binding to collagen and capturing platelets, stabilising FVIII (FVIII may be low if vWF is very low)

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23
Q

3 types of hereditary vWF

A

type 1 or 3 (deficiency of vWF; type 1 not enough, type 3 (recessive) none at all), type 2 (vWF with abnormal function)

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24
Q

2 causes of disorder of vessel wall

A

inherited (rare), acquired

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25
2 rare inherited conditions causing vessel wall disorder
hereditary haemorrhagic telangiectasia, Ehlers-Danlos syndrome, other connective tissue disorders
26
4 causes of acquired vessel wall disorders
scurvy, steroid therapy (thins connective tissue of small vessels, so more likely to bleed), ageing (senile purura), vasculitis
27
what type of bleeding is associated with disorders of primary haemostasis
immediate, prolonged, epistaxes, mucocutaneous, menorrhagia, easy bruising
28
4 tests for disorders of primary haemostasis
platelet count and morphology, bleeding time (not sensitive or specific so recreated as PFA100 in lab), assays of vWF, clinical observation
29
what is clotting factor I
fibrinogen
30
what is clotting factor II
prothrombin
31
what is clotting factor III
tissue factor (TF)
32
what is clotting factor IV
calcium ions (Ca2+)
33
what is clotting factor VI
activated factor V (Va)
34
what clotting factors require a post-translational vitamin K dependent modification
factors II, VII, IX and X
35
what clotting factors are not serine proteases
V, VIII, XIII
36
what factors are co-factors
V, VIII
37
what factor is a transglutamidase
XIII
38
where is phospholipid derived from
activated platelet membrane
39
what does the fibrin mesh do
binds and stabilises platelet plug and other cells
40
what is the instrinsic pathway of blood coagulation in secondary haemostasis
XII->XIIa, which activates XI->XIa, which activates IX->IXa, which, along with VIIIa, phospholipids and Ca2+, activates X->Xa
41
what is the extrinsic pathway of blood coagulation in secondary haemostasis
tissue factor, released due to vessel damage, along with VIIa and Ca2+, activates IX->IXa (instrinsic pathway) or X->Xa
42
what is the common pathway of blood coagulation in secondary haemostasis
Xa, along with Va, phospholipids and Ca2+, activates prothrombin->thrombin (IIa), which activates fibrinogen->fibrin. and XIII->XIIIa. XIIIa converts fibrin to crosslinked fibrin
43
shape of normal thrombogram (thrombin generation over time by coagulation cascade)
TF trigger, before rapid rise in thrombin generation (minutes), before peaking and an equally rapid decline in generation, before rate slows
44
shape of haemophilia A (FVIII) thrombogram (thrombin generation over time by coagulation cascade)
TF trigger, then very slow rise in thrombin levels, before peaking at a much lower level than normal after a longer period of time, followed by a slow decrease in thrombin levels
45
what can be disordered in secondary haemostasis
any coagulation factor that results in failure of thrombin generation, and hence fibrin formation
46
what vessels require secondary haemostasis
larger vessels, as a primary platelet plug would fall apart
47
what is haemophilia
failure to generate fibrin to stabilise platelet plug
48
2 causes of deficiency of coagulation factor production
hereditary, acquired
49
2 hereditary haemophilias causing a deficiency of coagulation factor production, and corresponding coagulation factor
haemophilia A (FVIII), haemophilia B (FIX)
50
what pathway do both haemophilia types affect
intrinsic pathway
51
are all coagulation factor deficiencies the same
no
52
compatibility with life and symptoms of haemophilia (FVIII and FIX deficiency)
severe but compatible with life; spontaneous joint and muscle bleeding (X-linked so affect males more)
53
compatibility with life of prothrombin (FII) deficiency
lethal (die in utero)
54
symptoms of FXI deficiency
bleed after trauma but not spontaneously
55
symptoms of FXII deficiency
no excess bleeding at all
56
3 causes of acquired coagulation disorder (much more common than hereditary)
liver disease, dilution, anticoagulant drugs (e.g. warfarin)
57
why does liver failure lead to decreased production of coagulation factors
most coagulation factors are synthesised in the liver
58
how does dilution occur, leading to an acquired coagulation disorder
red cell transfusions no longer contain plasma (major transfusions require plasma as well as erythrocytes and platelets)
59
2 acquired causes of increased consumption of coagulation factors, leading to coagulation disorder
disseminated intravascular coagulation (DIC), immune (auto-antibodies)
60
what activates disseminated intravascular coagulation (DIC), and what is consumed
generalised unregulated activation of coagulation by TF, consuming and depleting coagulation factors, platelets and fibrinogen (activates fibrinolysis as well); can't be switched off but can treat underlying cause (e.g. deliver baby), or through replacement
61
what is disseminated intravascular coagulation (DIC) associated with, and what does it lead to
associated with sepsis, major tissue damage and inflammation, with deposition of fibrin causing organ failure
62
5 clinical symptoms of bleeding in coagulation disorders
superficial cuts do not bleed (platelets present), bruising is common but nosebleeds are rare, spontaneous bleeding is deep into muscles and joints, bleeding after trauma may be delayed and is prolonged, frequently restarts after stopping
63
what is a hallmark of haemophilia
haemarthrosis (haemorrhage into joint space)
64
what route of administration should be avoided in patients with coagulation disorders
intramuscular injections
65
seriousness of haemophilia
very without treatment, as simply by cutting a lip someone could bleed to death
66
platelet/vascular defect bleeding vs coagulation defect bleeding
platelet/vascular: superficial bleeding into skin and mucosal membranes, with bleeding immediately after injury; coagulation: bleeding into deep tissues, muscles and joints, with bleeding delayed, severe and prolonged after injury
67
3 tests for coagulation disorders
screening tests (clotting screen), factor assays (e.g. for FVIII etc.), test for inhibitors
68
3 screening tests for coagulation disorders
prothrombin time (PT), activated partial thromboplastin time (APTT), full blood count (platelets)
69
what factor deficiencies are detected by prolonged APTT (activated partial thromboplastin time) in haemophilia (intrinsic pathway)
FXII, XI, VIII, IX (and V, X, II) until fibrin strand forms
70
what factor deficiencies are detected by PT (prothrombin time) (extrinsic pathway)
FVIIa (and V, X, II) until fibrin strand forms; if high due to warfarin, treat with vitamin K injections
71
8 bleeding disorders not detected by routine clotting tests, so history and screening tests important
mild factor deficiencies, vWF, FXIII deficiency (crosslinking), platelet disorders, excessive fibrinolysis, vessel wall disorders, metabolic disorders (e.g. uraemia), thrombotic disorders
72
2 causes of fibrinolysis disorders
hereditary, acquired
73
hereditary cause of fibrinolysis disorders
antiplasmin deficiency
74
2 acquired causes of fibrinolysis disorders
drugs e.g. tPA (tissue plasminogen activator "clot buster"), disseminated intravascular coagulation (DIC)
75
haemophilia inheritance pattern
sex-linked (X-linked) recessive disorder (affected males below normal range, carrier females vary due to lyonization); FVIII normal range is 0.5-1.5 iu/ml
76
vWD inheritance pattern
autosomal dominant disorder (type 2, type 1 are autosomal dominant, type 3 is autosomal recessive)
77
other common bleeding disorders (all the rest e.g. V deficiency, X deficiency etc.) inheritance pattern
autosomal recessive so much less common
78
2 ways abnormal haemostasis due to failure of production/function is treated
replace missing factor/platelets, stop drugs
79
2 ways to replace missing factor/platelets in abnormal haemostasis due to failure of production/function
prophylactic, therapeutic
80
2 ways abnormal haemostasis due to immune destruction is treated
immunosuppression (prednisolone), splenectomy for ITP (immune thrombocytopenic purpura)
81
2 ways abnormal haemostasis by increased consumption is treated
treat cause (e.g. of DIC), replace as necessary
82
4 factor replacement therapies
plasma, cryoprecipitate, factor concentrates, recombinant forms
83
what coagulation factors does plasma contain
all
84
what coagulation factors does cryoprecipitate contain
fibrinogen, FVIII, vWF, FXIII
85
what factor concentrates are available
all but FV
86
what coagulation factors are present in prothrombin complex concentrates (PCCs)
FII, VII, IX, X (used to reverse warfarin)
87
what 2 coagulation factors have recombinant forms
FVIII, FIX
88
what can gene therapy be used to treat
haemophilia (B>A)
89
2 other treatments of haemostatic disorders causing bleeding
platelet replacement therapy (pooled platelet concentrates available), novel approaches (e.g. bispecific antibody, anti TFPI (tissue factor pathway inhibitor) antibody, antithrombin RNAi)
90
3 additional haemostatic treatments
DDAVP (desmopressin), tranexamic acid, fibrin glue/spray
91
how does desmopressin (DDAVP) work
vasopressin derivative, causing a 2-5 fold rise in vWF and FVIII (FVIII>vWF) by releasing endogenous stores, so only useful in mild disorders
92
how does tranexamic acid work
inhibits fibrinolysis by competing with fibrin for binding of TPA (tissue plasminogen activator)
93
distribution of tranexamic acid
wide as crosses placenta, but low concentration in breast milk
94
treatment of vWD
intermediate purity vWF/FVIII concentrates, DDAVP, tranexamic acid

Y2 MCD Haematology (20 decks)

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