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BRS Year 2 > CVR haemostasis and thrombosis > Flashcards

CVR haemostasis and thrombosis Flashcards

1
Q

what is haemostasis?

A
  • the cellular and biochemical process that enables the specific and regulated cessation of bleeding in response to vascular insult
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2
Q

what is haemostasis for?

A
  1. prevention of blood loss from intact vessels
  2. arrest bleeding from injured vessels
  3. enable tissue repair
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3
Q

blood coagulation video

A

https://www.youtube.com/watch?v=FNVvQ788wzk

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4
Q

what is secondary haemostasis?

A

stablisations of the plug with fibrin

  • > blood coagulation
  • > stops blood loss
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5
Q

what is primary haemostasis?

A

formations of an unstable platelet plug

  • > platelet adhesion
  • > platelet aggregation
  • –> limits blood loss + provides a surface for coagulation
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6
Q

what is fibrinolysis?

A

vessel repair and dissolution of clot

-> cell migration/proliferation & fibrinolysis

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7
Q

what must be balanced for normal haemostasis?

A

fibrinolytic factors & anticoag factors
vs
coagulant factors & platelets

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8
Q

reasons for lack of factors in coagulation cascade?

A

congenital and acquired causes for failed production

-> increased consumption/clearance

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9
Q

how does GlpIb bind platelets?

A

via VWF

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10
Q

how does GlpIa bind platelets?

A

directly

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11
Q

what does binding of platelet to GlpIb/GlpIa cause?

A

release of ADP and thromboxane

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12
Q

what is it called when you have low numbers of platelets?

A

thrombocytopenia

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13
Q

disorders of primary haemostasis - platelets

Causes of thrombocytopenia?

A
  1. bone marrow failure e.g. leukaemia, B12 deficiency
  2. Accelerated clearance e.g. Immune (Immune thrombocytopenic purpura), Disseminated intravascular coagulation
  3. platelets pooled and destroyed in an enlarged spleen
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14
Q

ITP explanation

A

antiplatelet ABs stick to sensitised platelet

- cleared by macrophages of reticulo-endothelial system in the spleen

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15
Q

reasons for impaired function of platelets (2)

A
  1. hereditary absence of glycoproteins or storage granules
    - > very rare
  2. acquired due to drugs e.g. aspirin, NSAIDs, clopidogrel (common)
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16
Q

what is observed in Glanzmann thrombothaenia?

A

absence of the GPIIb/IIIa receptor on platelets

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17
Q

what is observed in Bernard Soullier syndrome?

A

absence of GPIb receptors

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18
Q

what is storage pool disease?

A

disorders referring to reduction in the granular content of platelets (dense granules)

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19
Q

what drug class is widely used n the prevention and treatment of cardiovascular and cerebrovascular disease?

A

antiplatelet drugs

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20
Q

what is the mechanism of action of aspirin?

A

irreversibly blocks COX -> inhibits production of thromboxane A2

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21
Q

why isn’t prostacyclin production blocked by aspirin?

A

endothelial cells can still generate is

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22
Q

how longs do the effects of aspirin remain for?

A

7 days

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23
Q

how does clopidogrel work?

A

irreversibly blocks P2y12 (ADP receptor) on the platelet cell membrane

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24
Q

disorders of primary haemostasis - VWF

-> what can cause problems with VWF? (2)

A
  1. Hereditary decrease of quantity +/ function (common)

2. acquired due to AB (rare)

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25
Q

2 functions of VWF in haemostasis?

A
  1. binding to collagen and capturing platelets

2. stabilising factor VIII

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26
Q

what type of inheritance pattern is VWD?

A

autosomal

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27
Q

two types of VWD?

A
  1. deficiency of VWF

2. VWF with abnormal function

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28
Q

disorders of primary haemostasis - the vessel wall

- causes of issues with the vessel wall

A
  1. inherited (Rare) -> Hereditary Hemorrhagic Telangiectasia , Ehlers-danlos syndrome, other connective tissue disorders
  2. acquired -> steroids, ageing “senile purpura”, vasculitis, scurvy
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29
Q

clinical features of disorders of primary haemostasis?

A

bleeding features:

  1. immediate
  2. prolonged from cuts
  3. nose bleeds
  4. prolonged gum bleeding
  5. menorrhagia
  6. ecchymosis - spontaneous/easy
  7. prolonged bleeding after trauma/surgery
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30
Q

what causes petechiae?

A

bleeding under the skin

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31
Q

what happens when glass applied to purpura?

A

don’t blanch

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32
Q

when do you see petechiae?

A

in thrombocytopenia

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33
Q

what disease can severe VWD present like?

A

haemophilia

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34
Q

tests for disorders of primary haemostasis? (4)

A
  1. platelet count and morphology
  2. bleeding time
  3. assays of VWF
  4. clinical observation
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35
Q

what tests come back normal in VWD?

A

PT and APTT, except in more severe VWD where FVIII is low

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36
Q

treatment of abnormal haemostasis: for failure of production/function

A
  1. Replace missing factor/platelets e.g. VWF containing concentrates
    - > prophylactic
    - > therapeutic
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37
Q

treatment of abnormal haemostasis: for immune destruction

A
  1. immunosuprresion e.g. prednisolone

2. splenectomy for ITP

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38
Q

treatment of abnormal haemostasis: for increased consumption

A
  1. treat cause

2. replace as necessary

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39
Q

additional haemostatic treatments

A
  1. desmopressin -> 2-5 increase in VWF. Releases endogenous stores
  2. tranexamic acid
  3. fibrin glue/spray
  4. other approaches e.g. OCP for menorrhagia
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40
Q

who is desmopressin useful in treating?

A

mild disorder cases

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41
Q

what is the roles of coagulation (chemically)

A

to generate thrombin

-> this converts fibrinogen into fibrin

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42
Q

4 causes of coagulation factor deficiencies

A

hereditary
acquired
dilution
increased consumption

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43
Q

hereditary causes of disorders of coag?

A
  1. factor VIII/IX -> haemophilia A/B
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44
Q

acquired causes of disorders of coag?

A
  1. liver disease

2. Anticoagulant drugs (warfarin, DOACs)

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45
Q

dilution causes of disorders of coag?

A

blood transfusion (also acquired)

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46
Q

increased consumption causes of disorders of coag?

A
  • acquired
    1. DIC (common)
    2. immune (ABs, rare)

DIC = Disseminated intravascular coagulation

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47
Q

what deficiency occurs in haemophilia A?

A

factor VIII deficiency

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48
Q

what deficiency occurs in haemophilia B?

A

factor IX deficiency

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49
Q

coagulation disorders which aren’t haemophilia are what?

A

rare

autosomal recessive

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50
Q

what does haemophilia do to fibrin?

A

unable to generate it -> no stabilisation of platelet plug

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51
Q

elbow hallmark of haemophilia?

A

haemarthrosis (bleeding into joints)

-> prophylactic replacement therapy in developed countries prevents development

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52
Q

what does chronic haemarthrosis lead to?

A

muscle wasting

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53
Q

what type of injection should be avoided in haemophilia?

A

intramuscular

-> leads to extensive haematoma

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54
Q

is the bleeding in haemophilia compatible with life?

A

yes

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55
Q

where do you see spontaneous bleeding in haemophilia?

A

the joints and muscles

56
Q

what other factor (other than VIII and IX) can cause coag deficiences?

A

factor II (prothrombin)

57
Q

is absence of prothrombin compatible with life?

A

no

58
Q

what does factor XI deficiency lead to?

A
  • bleed after trauma but not spontaneously
59
Q

what does factor XII deficiency lead to?

A
  • no change in bleeding
60
Q

why does liver failure lead to acquired coagulation disorder?

A
  • most coagulation factors are synthesised in the liver
61
Q

why does dilution lead to acquired coagulation disorder?

A
  • RBC transfusions no longer contain plasma

- major haemorrhage requires transfusion of plasma as well as red cells and platelets

62
Q

what is disseminated intravascular coagulation?

A
  • generalised not localised activation of coagulation tissue
63
Q

problem with disseminated intravascular coagulation?

A

TF that normally doesn’t come into contact with factor VIIa binds to it and leads to widespread unregulated coagulation

64
Q

what can trigger disseminated intravascular coagulation?

A
  1. sepsis
  2. major tissue damage e.g. cancer
  3. inflammation
65
Q

what happens as a result of DIC to coag factors?

A

their widespread consumption and depletion

-> leads to thromboyctopenia

66
Q

How can you test for DIC?

A

look for raised D dimer (breakdown product of fibrin)

67
Q

what can deposition of fibrin cause?

A
  1. organ failure

2. shearing of the RBC in vessels its deposited in -> red cell fragmentation

68
Q

how to treat DIC immediately?

A

give FFP and platelets (supportive treatment)

69
Q

how to fix DIC?

A

treat underlying cause

70
Q

clinical features of coagulation disorders (4)

A
  1. superficial cuts don’t bleed
  2. bruising common, nosebleeds rare
  3. spotaneous bleeding is deep; into muscles and joints
  4. bleeding after trauma may be delayed and is prolonged
71
Q

disorders

pattern of bleeding in platelet/vasc vs coag?

A

p/v: superficial bleeding into skin + mucosal membranes

C: bleeding into deep muscles, muscles, joints

72
Q

disorders

onset of bleeding in platelet/vasc vs coag?

A

p/v: immediately after injury

c: delayed but severe bleeding after injury. Bleeding is often prolonged

73
Q

tests for coagulation disorders (3 types)

A

screening tests
coagulation factor assay
tests for inhibitors

74
Q

screening tests for coag disorders:

A

PT
APTT
full blood count (platelets)

75
Q

causes of prolonged APTT and PT (4)

A
  1. liver disease
  2. anticoagulant drugs
  3. DIC
  4. dilution following red cell transfusion
76
Q

how to treat ITP

A

splenectomy

77
Q

how to replace coagulation factors (4)

A
  1. FFP
  2. cryoprecipitate
  3. factor concentrates
  4. recombinant FVIII and FIX
78
Q

what coag factors are in FFP?

A

all of them

79
Q

what coag factors are in cryoprecipitate?

A

fibrinogen
FVII
VWF
FXIII

80
Q

novel treatments for haemophilia

A
  1. gene therapy for A and B

2. bispecific antibodies for A

81
Q

how do bispecific ABs treat haemophilia A?

A

binds FIXa and FX

mimics procoagulant function of FVII

82
Q

How do disorders of thrombosis present (venous)? (2)

A
  1. PE

2. DVT

83
Q

symptoms of PE (6)

A
  1. tachycardia
  2. hypoxia
  3. shortness of breath
  4. chest pain
  5. haemoptysis
  6. sudden death
84
Q

symptoms of DVT (6)

A
  1. painful leg
  2. swelling
  3. red
  4. warm
  5. may embolise to lungs
  6. post thrombotic syndromes
85
Q

2 examples of arterial thrombosis

A
  1. CVD

2. rupture of cholesterol-platelet-rich plaques

86
Q

what is thrombosis?

A

intravascular inappropriate coagulation. Can be venous or arterial. Obstructs flow and may embolise to lungs.

87
Q

virchows triad indicates what?

A

the 3 contributory faxctors to thrombosis

88
Q

what is virchows triad?

A
  1. blood - dominant in VT
  2. vessel wall - dominant in AT
  3. blood flow - both AT and VT
89
Q

what term refers to an increase risk of VT?

A

thrombophilia

90
Q

features of thrombophilia

A
  1. young age thrombosis
  2. spontaneous thrombosis
  3. multiple thromboses
  4. thrombosis whilst anticoagulated
91
Q

causes of thrombosis

A
  1. coagulant factors

2. platelets

92
Q

factors that can be raised to cause thrombosis

A
  1. factor VIII
  2. Factor II
  3. factor V leiden
  4. myeloproliferative disorders
93
Q

factor V leiden causes what?

A

increased activity due to activated protein C resistance

94
Q

what anticoagulant proteins can be reduced to cause thrombosis?

A
  1. antithrombin
  2. protein C
  3. protein S
95
Q

states that cause increase coagulation factors and platelets

A
  1. surgery
  2. cancer
  3. pregnancy
96
Q

what is the cofactor of protein C

A

protein S

97
Q

what does protein C do?

A

inactivate FVa and FVIIIa

98
Q

what does anti-thrombin inactivate?

A

FIIa and FXa

99
Q

is factor V leiden a high risk condition for thrombosis?

A

not necessarily. Tends to cause issues when accompanied by other risk factors e.g. pregnancy. OCP. long haul travel

100
Q

order of significance of excess/deficiency for causing thrmobosis

A
  1. antithrombin deficiency
  2. protein C/S deficiency
  3. coagulation factor excess
101
Q

what can inflammatory states alter expression of?

A

endothelial protein C receptor and thrombomodulin receptor

102
Q

things that can cause blood flow stasis

A
  1. pregnancy
  2. long haul travel
  3. surgery
103
Q

treatment of VT

A

prevention - prophylactic therapy + assess and prevent risks

reduce risk of recurrence/extension:

  • lower procoagulant factors e.g. warfarin, DOACs
  • increase anticoagulant activity e.g. heparin
104
Q

what type of clots are most likely to grow and embolise

A

fresh ones -> need to focus treatment on these

105
Q

which cells produce heparin?

A

mast cells

106
Q

how are long chain - unfractionated - heparins given?

A

IV administration

107
Q

how are LMW heparins given?

A

subcutaneous administration

108
Q

action of unfractionated heparin

A

enhancement of antithrombin
-> inactivation of thrombin
-> inactivation FXa
(-> inactivation FIXa, FXIa, FXIIa)

109
Q

why does LMW heparin have less in the way of antithrombin activity than long chain heparins?

A

wrap around antithrombin only, not FXa like the longer chains do

110
Q

what does unfractionated heparin do to APTT?

A

prolongs it

111
Q

Do we monitor APTT for LMWH heparin?

A

normally doesn’t require monitoring- doesn’t really affect APTT
If necessary measure anti-Xa levels to assess degree of anticoagulation

112
Q

how does warfarin work as an anticoagulant?

A

blocks recycling of vitamin K

-> vita K dependent factors (II, VII, IX, X, protein C, protein S) not activated via gamma carboxylation

113
Q

how can you reverse effects of warfarin?

A

vit K administration - takes hours

- rapidly reversed by infusion of coagulation factors e.g. by PCC or FFP

114
Q

side effects of the anticoagulants?

A
  1. bleedings
  2. skin necrosis
  3. purple toe syndrome
  4. embryopathy = chondrodysplasia punctata
115
Q

why can skin necrosis occur when on warfarin?

A

Due to severe protein c deficiency
Occurs 2/3 days after starting warfarin
-> thrombosis predominantly in adipose tissues

116
Q

why can purple toe syndrome occur when on warfarin?

A
  1. disrupted atheromatous plaques bleed

- > cholesterol emboli lodge in extremeties

117
Q

what is observed in chondrodysplasia punctata

A
  1. early fusion of epiphyses

2. warfarin is teratogenic in 1st trimester

118
Q

what is used to monitor warfarin?

A

INR

119
Q

unanticogulated normal INR is what?

A

1

120
Q

target INR for warfarin patients

A

2-3

121
Q

causes of warfarin resistance

A
  1. lack of compliamce
  2. diet with ++ vit K
  3. increased metabolism Cyt P450 (CYP2C9)
  4. reduced binding (VKORC1)
122
Q

warfarin vs DOACS

onsent/offest

A

W: slow
D: rapid

123
Q

warfarin vs DOACS

dosing

A

W: variable
D: fixed

124
Q

warfarin vs DOACS

food effect

A

W: yes
D: no

125
Q

warfarin vs DOACS

interactions

A

W: many
D: few

126
Q

warfarin vs DOACS

monitoring required

A

W: yes
D: No

127
Q

warfarin vs DOACS

renal dependence

A

W: No
D: some

128
Q

warfarin vs DOACS

reversibility

A

W: vitamin K/PCCs
D: specific antidotes available for dabigatran and in development for FXa inhibitors

129
Q

DOAC bleeding risk

A
  • lower than for warfarin generally

- particularly for intracranial bleeding which is biggest worry

130
Q

initial treatment of VT to minimise clot extension

A

DOAC/LMWH for first few days

-> follow with DOAC/warfarin

131
Q

treatment to reduce risk of recurrence of VT

A

DOAC or warfarin

132
Q

treatment for atrial fibrillation

A

DOAC/warfarin

133
Q

treatment for mechanical prosthetic heart valve

A

warfarin

DOACs ineffective and should be avoided

134
Q

thromboprophylaxis following surgery

A

LMWH or DOAC

135
Q

thromboprophylaxis during pregnancy

A

LMWH -> DOACs not safe as they cross the placenta

BRS Year 2 (110 decks)

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