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Bleeding Disorders and Thrombosis Flashcards

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1
Q

Bleeding disorders can be due to _______

A

failure of platelet plug formation or failure of fibrin clot formation

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2
Q

Failure of platelet plug formation can be due to ________

A

vascular disorders
thrombocytopenia (low platelets)
platelet functional defects

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3
Q

Vascular disorders can be hereditary e.g. ___1____ or acquired e.g. __2__ , __2___, ___2___

A

1) Marfans

2) HSP, vit C deficiency, ageing process where collagen is lost

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4
Q

What is the commonest cause of primary haemostatic failure?

A

thrombocytopenia (low platelets)

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5
Q

Is Thrombocytopenia more commonly hereditary or acquired?

A

acquired

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6
Q

What is thrombocytopenia and platelet function defects disorders clinical features?

A

characterised by mucosal bleeding: epistaxes, GI bleeding, conjunctival bleeding and menorrhagia
also get spontaneous bruising and purpura

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7
Q

Thrombocytopenia is either due to ______ or ______

A

reduced production or increased destruction (more common)

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8
Q

Causes of increased platelet destruction?

A

coagulopathy, immune thrombocytopenic purpura (ITP) or hypersplenism

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9
Q

What is the commonest cause of thrombocytopenia?

A

ITP

immune thrombocytopenic purpura - an autoimmune disorder

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10
Q

Are platelet functional defects more commonly acquired or hereditary?

A

acquired

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11
Q

Causes of acquired platelet defects?

A

drugs e.g. aspirin, NSAIDs

uraemia of renal failure

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12
Q

Hereditary cause of platelet defect?

A

VWF deficiency

autosomal dominant with variable severity

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13
Q

Investigations for platelet plug function?

A

platelet count

no easy test for other components of primary haemostasis

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14
Q

Does failure of fibrin clot formation have a characteristic clinical syndrome?

A

no

unlike platelet plug where there is a characteristic syndrome

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15
Q

Failure of fibrin clot formation can be due to _______

A

multiple factor deficiencies or single factor deficiencies

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16
Q

What will happen to the PT and APTT in multiple factor deficiencies?

A

Both PT and APTT will be prolonged

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17
Q

What are some causes of multiple clotting factor deficiency?

A

Liver failure
Vit K deficiency
Disseminated intravascular coagulation

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18
Q

Why does liver failure cause a multiple clotting factor deficiency?

A

All coagulation factors are synthesised in hepatocytes so this is reduced in liver failure

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19
Q

Why does Vit K deficiency cause a multiple clotting factor deficiency?

A

Factors II, VII, IX and X are carboxylated by Vit K which is essential for function

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20
Q

How do we get vitamin K?

A

Vit K is found in green leafy vegetables but can also be synthesised by gut bacteria, it requires bile salts for absorption

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21
Q

Causes of Vit K deficiency?

A

poor diet, malabsorption, obstructive jaundice (stops bile salts needed for absorption getting to gut) e.g. cancer of pancreas head or gallstones, Vit K antagonists e.g. warfarin, haemorrhagic disease of the newborn

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22
Q

Explain what haemorrhagic disease of the newborn is and how we prevent it?

A

new babies have low Vit K esp if specifically breast fed and can develop HDN which can be prevented by administering Vit K to all neonates after birth

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23
Q

Explain how DIC arises?

A

Systemic activation of coagulation

widespread intravascular coagulation

organ dysfunction (which causes more inflammation and coagulation activation)

the person then also has a bleeding tendency after initial thrombosis because fibrinolysis is increased and also there is consumption of clotting factors

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24
Q

What things can trigger DIC?

A 
malignancy
sepsis 
AHTR 
placental abruption 
snake bite
trauma 
burns 
surgery
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25
Clinical features of DIC?
patient is usually shocked and ill they may be bleeding from their mouth, nose, venipuncture site, widespread ecchymoses (looks kind of like bruising as basically bleeding under the skin) thrombotic events can involves any organ but skin, brain, kidneys are most common
26
Management of DIC?
treat underlying cause and intensive support | transfusions to replace losses - platelets, plasma, cryoprecipitate
27
What will happen to PT and APTT in haemophilia?
normal PT, prolonged APTT (because only that side of coagulation cascade is being affected by the single factor deficiency)
28
What is haemophilia?
X linked, hereditary disorder in which abnormally prolonged bleeding recurs episodically at one or a few sites on occasion
29
What is more common, haemophilia A or B?
A is five times more common than B
30
Haemophilia A is caused by deficiency of factor ____
VIII
31
Haemophilia B is caused by deficiency of factor _______
IX
32
What severity of haemophilia is most common?
severe because most mutations cause complete knock out of the gene
33
Clinical features of severe haemophilia?
recurrent haemarthroses (usually in larger joints that are used a lot e.g. ankle and knee) , recurrent soft tissue bleeds e.g. bruising in toddlers, prolonged bleeding after dental extraction, surgery and invasive procedures
34
Complications of haemophilia when treatment was unavailable?
used to lead to loss of joint function because of recurrent bleeds
35
What is a target joint in reference to haemophilia?
a joint that patients tend to get recurrent bleeds due to a past bad bleed
36
Treatment of haemophilia?
can now treat with IV factor VIII or IX injections
37
White thrombus?
arterial thrombus
38
Arterial thrombi are _____ rich
platelet
39
Red thrombus?
venous thrombus
40
Venous thrombi are _____ rich
fibrin
41
What are the three components of Virchow's triad?
stasis, vessel wall damage (degeneration of valves), hypercoagulability
42
Is VTE common?
yes very common, particularly in elderly
43
List 10 risk factors for VTE?
``` age obesity pregnancy puerperium oestrogen therapy previous PE/ DVT trauma/ surgery paralysis infection thrombophilia ```
44
What is the most important risk factor for VTE?
history of previous DVT/ VTE
45
Define thrombophilia?
familial or acquired disorders of the haemostatic mechanism which are likely to predispose to thrombus the main mechanism is through decreased anticoagulant activity
46
List 5 hereditary thrombophilias?
``` Factor V Leiden (most common) Prothrombin 20210 mutation anti-thrombin deficiency protein C deficiency Protein S deficiency ```
47
Who should you consider screening for hereditary thrombophilia?
``` venous thrombosis < 45 years old recurrent venous thrombosis unusual venous thrombosis FH of venous thrombosis FH of thrombophilia ```
48
Management of hereditary thrombophilia?
advice on avoiding risk .eg. avoid the COCP short term prophylaxis to prevent thrombotic events during known periods of risk long term anticoagulation if recurrent thrombotic events
49
Name an acquired thrombophilia?
antiphospholipid syndrome
50
Main features of APS?
recurrent venous and arterial thrombosis, recurrent fetal loss, mild thrombocytopenia
51
Antibodies for APS?
lupus anticoagulant, anticardiolipin
52
What may APS be associated with?
other autoimmune diseases
53
What is the main mechanism for thrombophilia?
decreased anticoagulant activity
54
What is meant by the extrinsic, intrinsic and final common pathway?
extrinsic pathway- Tissue factor binding to factor 7 which causes activation of 5 and 10 final common pathway- 5 and 10 activates prothrombin then get thrombin then fibrinogen forms the clot intrinsic pathway- thrombin activates factors 8 and 9 which activates more 5 and 10 in a positive feedback loop
55
What pathway is affected if only the PT is increased?
extrinsic pathway
56
What pathway is affected if only the APTT is increased?
intrinsic
57
What condition can cause symptoms of primary haemostasis but also a prolonged APTT and why?
VWF disease because VWF has main role in primary haemostasis but it also carries factor 8 so can affect APTT
58
What things can cause a prolonged APTT only?
``` Haemophilia A (factor 8 deficiency) Haemophilia B (factor 9 deficiency) 11 or 12 deficiency (less clinically relevant but can lead to v long APTT) Heparin (common cause of prolonged APTT as switches off thrombin- lots of heparin will affect both PT and APTT but APTT tends to most affected) APS (artefact where antibody prolongs APTT but doesn’t actually cause bleeding disorder) ```
59
Why does APS cause prolonged APTT?
an artefact- the APTT isn't actually prolonged because it is a clotting disorder, the antibodies mess with the test
60
2 indications for anticoagulants?
``` venous thrombosis atrial fibrillation (takes into account the majority of patients on anticoagulant drugs in Tayside) ```
61
Anticoagulant drugs target _________
the formation of the fibrin clot
62
MOA of heparin?
potentiates the action of antithrombin
63
How is heparin given?
IV or subcut
64
How quickly does heparin have effect? Where does it tend to be used?
has immediate effect tends therefore to be used acutely in hospital not used so much long term because it needs injected
65
What two forms does heparin come in?
unfractionated (older) | LMWH
66
What does heparin do to the APTT and PT?
prolongs both but APTT is much more sensitive so usually first to appear prolonged and more significant
67
What should be used for monitoring effect of heparin?
APTT
68
What type of heparin tends to be used more and why? What is the use for the other less used version?
LMWH tends to be used more because it requires less monitoring unfractionated heparin is shorter acting and easier to reverse it has a role when want to be able to switch off quickly e.g. in patient with both high risk of thrombosis or bleeding when going to surgery
69
3 complications of heparin?
bleeding, heparin induced thrombocytopenia, osteoporosis with long term used (although heparin is generally not used long term)
70
Describe heparin reversal?
can just stop the heparin as it has a short t 1/2 in severe bleeding can given protamine sulphate this completely reverses unfractionated heparin and partially reverses LMWH
71
What type of anticoagulant is warfarin?
coumarin
72
How does warfarin and all other coumarin anticoagulants work?
inhibition of vitamin K meaning it stops factor 2, 7, 9 and 10 working (1972)
73
Why does someone need to be given heparin when they are initially started on warfarin?
warfarin also causes a drop in protein C and S which at first can cause an initial increased risk of thrombosis but as the drug has time to work this risk drops
74
How is warfarin taken?
oral drug
75
What happens to the PT and APTT with warfarin?
both are prolonged because it affects multiple clotting factors
76
Why does warfarin need close monitoring?
it has a narrow therapeutic window
77
What ratio is used to monitor warfarin and why?
INR - used because unlike PT it is standardised so is the same everywhere (PT can differ from lab to lab depending on what chemicals they use)
78
Describe warfarin and interactions?
warfarin has many drug interactions because it is metabolised by cytochrome P450, some of these reactions can be quire dangerous warfarin can also interact with some foods and alcohol
79
Describe bleeding as mild and severe side effects of warfarin?
mild: bruising, epistaxis, haematuria severe: GI, intracerebral, significant Hb drop
80
Describe reversal of warfarin?
NICE guidelines: - If major bleeding - give prothrombin complex concentrate and vitamin K - If INR >8 and no or minor bleeding give vitamin K and omit warfarin - If INR 5-8 and minor bleeding, give vitamin K, omit warfarin - If INR 5-8 and no bleeding omit warfarin for 1-2 days and restart at lower dose
81
Why are the new anticoagulants better?
they require less monitoring than heparin and warfarin they are more direct because they directly inhibit clotting factors all have less drug interactions than heparin and warfarin they all have recently had specific antidotes developed
82
MOA of Dabigatran?
a direct thrombin inhibitor
83
Which DOAC is a direct thrombin inhibitor?
dabigatran
84
MOA of edoxaban, rivaroxaban, apixaban?
factor X inhibitors (Xa in name for factor Xa)
85
Why does Dabigatran tend to be used less?
it is really excreted and can therefore cause a decline in renal function in the elderly
86
Describe how atherosclerosis occurs? What may stable atherosclerotic plaques cause?
occurs when there is damage to the endothelium, recruitment of foamy macrophages rich in cholesterol occurs, and plaques rich in cholesterol form stable atherosclerotic plaques are hyalnised and calcified and may cause angina and intermittent claudication
87
Describe how atherosclerosis can lead to arterial thrombosis?
unstable atherosclerotic plaques can rupture, platelets will then be recruited which causes acute thrombosis there is sudden onset of symptoms e.g. MI or stroke
88
Why can antiplatlets be helpful in those with atherosclerosis?
reduce risk of thrombosis and vessel occlusion because if a plaque does rupture the anti platelets reduce the chance of platelets adhering to it
89
What chemicals can cause aggregation of platelets? How do platelets attach to each other?
ADP and thromboxane A2 cause platelet aggregation | platelets attach to each other via GP IIbIIIa and fibrinogen
90
What is the MOA of aspirin?
inhibits cycle-oxygenase which is necessary to produce thromboxane A2 (thromboxane A2 causes platelet aggregation)
91
What is the MOA of clopidogrel and plasugrel?
ADP receptor antagonists (ADP causes platelet aggregation)
92
Is dipyridamole commonly used as antiplatelet?
no | the use of aspirin, clopidogrel and plasugrel is more common
93
What is the MOA of dipyridamole?
phosphodiesterase inhibitor reduces production of cAMP which is a second messenger in platelet activation
94
How long do anti-platelet drugs affect platelet function?
once a platelet is exposed they are affected for their whole life span (7-10 days)
95
How long before elective surgery should you stop antiplatelets?
7 days prior
96
If there is serious bleeding how can you reverse anti platelets?
platelet transfusion

Haematology (12 decks)

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