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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
2 functions of VWF in haemostasis?
1. binding to collagen and capturing platelets | 2. stabilising factor VIII
26
what type of inheritance pattern is VWD?
autosomal
27
two types of VWD?
1. deficiency of VWF | 2. VWF with abnormal function
28
disorders of primary haemostasis - the vessel wall | - causes of issues with the vessel wall
1. inherited (Rare) -> Hereditary Hemorrhagic Telangiectasia , Ehlers-danlos syndrome, other connective tissue disorders 2. acquired -> steroids, ageing "senile purpura", vasculitis, scurvy
29
clinical features of disorders of primary haemostasis?
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
30
what causes petechiae?
bleeding under the skin
31
what happens when glass applied to purpura?
don't blanch
32
when do you see petechiae?
in thrombocytopenia
33
what disease can severe VWD present like?
haemophilia
34
tests for disorders of primary haemostasis? (4)
1. platelet count and morphology 2. bleeding time 3. assays of VWF 4. clinical observation
35
what tests come back normal in VWD?
PT and APTT, except in more severe VWD where FVIII is low
36
treatment of abnormal haemostasis: for failure of production/function
1. Replace missing factor/platelets e.g. VWF containing concentrates - > prophylactic - > therapeutic
37
treatment of abnormal haemostasis: for immune destruction
1. immunosuprresion e.g. prednisolone | 2. splenectomy for ITP
38
treatment of abnormal haemostasis: for increased consumption
1. treat cause | 2. replace as necessary
39
additional haemostatic treatments
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
40
who is desmopressin useful in treating?
mild disorder cases
41
what is the roles of coagulation (chemically)
to generate thrombin | -> this converts fibrinogen into fibrin
42
4 causes of coagulation factor deficiencies
hereditary acquired dilution increased consumption
43
hereditary causes of disorders of coag?
1. factor VIII/IX -> haemophilia A/B
44
acquired causes of disorders of coag?
1. liver disease | 2. Anticoagulant drugs (warfarin, DOACs)
45
dilution causes of disorders of coag?
blood transfusion (also acquired)
46
increased consumption causes of disorders of coag?
- acquired 1. DIC (common) 2. immune (ABs, rare) DIC = Disseminated intravascular coagulation
47
what deficiency occurs in haemophilia A?
factor VIII deficiency
48
what deficiency occurs in haemophilia B?
factor IX deficiency
49
coagulation disorders which aren't haemophilia are what?
rare | autosomal recessive
50
what does haemophilia do to fibrin?
unable to generate it -> no stabilisation of platelet plug
51
elbow hallmark of haemophilia?
haemarthrosis (bleeding into joints) | -> prophylactic replacement therapy in developed countries prevents development
52
what does chronic haemarthrosis lead to?
muscle wasting
53
what type of injection should be avoided in haemophilia?
intramuscular | -> leads to extensive haematoma
54
is the bleeding in haemophilia compatible with life?
yes
55
where do you see spontaneous bleeding in haemophilia?
the joints and muscles
56
what other factor (other than VIII and IX) can cause coag deficiences?
factor II (prothrombin)
57
is absence of prothrombin compatible with life?
no
58
what does factor XI deficiency lead to?
- bleed after trauma but not spontaneously
59
what does factor XII deficiency lead to?
- no change in bleeding
60
why does liver failure lead to acquired coagulation disorder?
- most coagulation factors are synthesised in the liver
61
why does dilution lead to acquired coagulation disorder?
- RBC transfusions no longer contain plasma | - major haemorrhage requires transfusion of plasma as well as red cells and platelets
62
what is disseminated intravascular coagulation?
- generalised not localised activation of coagulation tissue
63
problem with disseminated intravascular coagulation?
TF that normally doesn't come into contact with factor VIIa binds to it and leads to widespread unregulated coagulation
64
what can trigger disseminated intravascular coagulation?
1. sepsis 2. major tissue damage e.g. cancer 3. inflammation
65
what happens as a result of DIC to coag factors?
their widespread consumption and depletion | -> leads to thromboyctopenia
66
How can you test for DIC?
look for raised D dimer (breakdown product of fibrin)
67
what can deposition of fibrin cause?
1. organ failure | 2. shearing of the RBC in vessels its deposited in -> red cell fragmentation
68
how to treat DIC immediately?
give FFP and platelets (supportive treatment)
69
how to fix DIC?
treat underlying cause
70
clinical features of coagulation disorders (4)
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
disorders | pattern of bleeding in platelet/vasc vs coag?
p/v: superficial bleeding into skin + mucosal membranes | C: bleeding into deep muscles, muscles, joints
72
disorders | onset of bleeding in platelet/vasc vs coag?
p/v: immediately after injury | c: delayed but severe bleeding after injury. Bleeding is often prolonged
73
tests for coagulation disorders (3 types)
screening tests coagulation factor assay tests for inhibitors
74
screening tests for coag disorders:
PT APTT full blood count (platelets)
75
causes of prolonged APTT and PT (4)
1. liver disease 2. anticoagulant drugs 3. DIC 4. dilution following red cell transfusion
76
how to treat ITP
splenectomy
77
how to replace coagulation factors (4)
1. FFP 2. cryoprecipitate 3. factor concentrates 4. recombinant FVIII and FIX
78
what coag factors are in FFP?
all of them
79
what coag factors are in cryoprecipitate?
fibrinogen FVII VWF FXIII
80
novel treatments for haemophilia
1. gene therapy for A and B | 2. bispecific antibodies for A
81
how do bispecific ABs treat haemophilia A?
binds FIXa and FX | mimics procoagulant function of FVII
82
How do disorders of thrombosis present (venous)? (2)
1. PE | 2. DVT
83
symptoms of PE (6)
1. tachycardia 2. hypoxia 3. shortness of breath 4. chest pain 5. haemoptysis 6. sudden death
84
symptoms of DVT (6)
1. painful leg 2. swelling 3. red 4. warm 5. may embolise to lungs 6. post thrombotic syndromes
85
2 examples of arterial thrombosis
1. CVD | 2. rupture of cholesterol-platelet-rich plaques
86
what is thrombosis?
intravascular inappropriate coagulation. Can be venous or arterial. Obstructs flow and may embolise to lungs.
87
virchows triad indicates what?
the 3 contributory faxctors to thrombosis
88
what is virchows triad?
1. blood - dominant in VT 2. vessel wall - dominant in AT 3. blood flow - both AT and VT
89
what term refers to an increase risk of VT?
thrombophilia
90
features of thrombophilia
1. young age thrombosis 2. spontaneous thrombosis 3. multiple thromboses 4. thrombosis whilst anticoagulated
91
causes of thrombosis
1. coagulant factors | 2. platelets
92
factors that can be raised to cause thrombosis
1. factor VIII 2. Factor II 3. factor V leiden 4. myeloproliferative disorders
93
factor V leiden causes what?
increased activity due to activated protein C resistance
94
what anticoagulant proteins can be reduced to cause thrombosis?
1. antithrombin 2. protein C 2. protein S
95
states that cause increase coagulation factors and platelets
1. surgery 2. cancer 3. pregnancy
96
what is the cofactor of protein C
protein S
97
what does protein C do?
inactivate FVa and FVIIIa
98
what does anti-thrombin inactivate?
FIIa and FXa
99
is factor V leiden a high risk condition for thrombosis?
not necessarily. Tends to cause issues when accompanied by other risk factors e.g. pregnancy. OCP. long haul travel
100
order of significance of excess/deficiency for causing thrmobosis
1. antithrombin deficiency 2. protein C/S deficiency 3. coagulation factor excess
101
what can inflammatory states alter expression of?
endothelial protein C receptor and thrombomodulin receptor
102
things that can cause blood flow stasis
1. pregnancy 2. long haul travel 3. surgery
103
treatment of VT
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
what type of clots are most likely to grow and embolise
fresh ones -> need to focus treatment on these
105
which cells produce heparin?
mast cells
106
how are long chain - unfractionated - heparins given?
IV administration
107
how are LMW heparins given?
subcutaneous administration
108
action of unfractionated heparin
enhancement of antithrombin -> inactivation of thrombin -> inactivation FXa (-> inactivation FIXa, FXIa, FXIIa)
109
why does LMW heparin have less in the way of antithrombin activity than long chain heparins?
wrap around antithrombin only, not FXa like the longer chains do
110
what does unfractionated heparin do to APTT?
prolongs it
111
Do we monitor APTT for LMWH heparin?
normally doesn't require monitoring- doesn't really affect APTT If necessary measure anti-Xa levels to assess degree of anticoagulation
112
how does warfarin work as an anticoagulant?
blocks recycling of vitamin K | -> vita K dependent factors (II, VII, IX, X, protein C, protein S) not activated via gamma carboxylation
113
how can you reverse effects of warfarin?
vit K administration - takes hours | - rapidly reversed by infusion of coagulation factors e.g. by PCC or FFP
114
side effects of the anticoagulants?
1. bleedings 2. skin necrosis 3. purple toe syndrome 4. embryopathy = chondrodysplasia punctata
115
why can skin necrosis occur when on warfarin?
Due to severe protein c deficiency Occurs 2/3 days after starting warfarin -> thrombosis predominantly in adipose tissues
116
why can purple toe syndrome occur when on warfarin?
1. disrupted atheromatous plaques bleed | - > cholesterol emboli lodge in extremeties
117
what is observed in chondrodysplasia punctata
1. early fusion of epiphyses | 2. warfarin is teratogenic in 1st trimester
118
what is used to monitor warfarin?
INR
119
unanticogulated normal INR is what?
1
120
target INR for warfarin patients
2-3
121
causes of warfarin resistance
1. lack of compliamce 2. diet with ++ vit K 3. increased metabolism Cyt P450 (CYP2C9) 4. reduced binding (VKORC1)
122
warfarin vs DOACS | onsent/offest
W: slow D: rapid
123
warfarin vs DOACS | dosing
W: variable D: fixed
124
warfarin vs DOACS | food effect
W: yes D: no
125
warfarin vs DOACS | interactions
W: many D: few
126
warfarin vs DOACS | monitoring required
W: yes D: No
127
warfarin vs DOACS | renal dependence
W: No D: some
128
warfarin vs DOACS | reversibility
W: vitamin K/PCCs D: specific antidotes available for dabigatran and in development for FXa inhibitors
129
DOAC bleeding risk
- lower than for warfarin generally | - particularly for intracranial bleeding which is biggest worry
130
initial treatment of VT to minimise clot extension
DOAC/LMWH for first few days | -> follow with DOAC/warfarin
131
treatment to reduce risk of recurrence of VT
DOAC or warfarin
132
treatment for atrial fibrillation
DOAC/warfarin
133
treatment for mechanical prosthetic heart valve
warfarin | _DOACs ineffective and should be avoided_
134
thromboprophylaxis following surgery
LMWH or DOAC
135
thromboprophylaxis during pregnancy
LMWH -> DOACs not safe as they cross the placenta

BRS Year 2 (110 decks)

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