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J Haem > Thrombosis > Flashcards

Thrombosis Flashcards

1
Q

what is the thrombus made of in arterial thrombosis

A

platelets

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2
Q

when atherosclerotic plaques rupture what is exposed

what does this cause

A

collagen and von Willebrand factor exposed = platelet aggregation and platelet plug formation

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3
Q

why does hypertension and smoking cause increased risk of arterial thrombosis

A

both damage the vessel walls = more susceptible to platelet aggregation

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4
Q

management of arterial thrombosis

A 
anti platelet (aspirin) bc arterial thrombosis = platelet rich thrombus 
decrease risk factors - hypertension, smoking etc
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5
Q

what is the thrombus made of in venous thrombosis

A

fibrin

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6
Q

what are the 3 potential problems that can cause venous thrombosis

A

hypercoagulability
stasis
vessel wall

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7
Q

how does pregnancy/puerperium/COCP increase risk of venous thrombosis

A

estrogen increases clotting factors to decrease risk of bleeding at childbirth

= hypercoagulability

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8
Q

how does thrombophilia increase risk of venous thrombosis

A

coagulation problem (ie no natural anticoags or increased coagulation) = hypercoagulability = fibrin thrombosis

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9
Q

how does paralysis increase risk of venous thrombosis

A

paralysis = immobility = stasis of venous blood

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10
Q

how does long haul flights increase risk of venous thrombosis

A

long haul flights = immobility = stasis of venous blood

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11
Q

how does surgery (lower leg ortho) increase risk of venous thrombosis

A

immobility = stasis of venous blood

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12
Q

how does smoking increase risk of venous thrombosis

A

vessel wall damage

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13
Q

how does previous clot increase risk of venous thrombosis

A

vessel wall damage

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14
Q

Virchow’s triad

A

hypercoagulability
stasis
vessel wall

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15
Q

presentation of DVT

A

unilateral lower limb
hot swollen tender
pitting oedema

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16
Q

differential of DVT

A

cellulitis

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17
Q

why does pitting oedema occur in DVT

A

blood cant get back to heart so fluid leaks into legs

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18
Q

investigations for DVT

A

doppler US

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19
Q

what test can you do to rule out DVT, but isn’t diagnostic bc high in lots of things

A

d-dimers

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20
Q

prevention of DVT if risk factors

A

compression stockings
early mobilization
anti-coags - LMWH

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21
Q

complication of untreated DVT

A

PE

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22
Q

presentation of PE

A

pleuritic chest pain
hypoxia
SOB

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23
Q

ECG of PE

A

S1Q3T3

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24
Q

investigations for PE

A

V/Q scan (looking for mismatch)

ECG - for S1Q3T3

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25
Q

what arrhythmia is a risk factor for venous thrombosis

why

what can it cause

A

AF
= venous stasis in heart (LA)

can cause a stroke if the clot embolises

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26
Q

drug management of venous thrombosis

A

anti-coags (LMWH, warfarin, new anticoags) - bc problem is coagulation, not platelets (like arterieal thrombosis)

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27
Q

what is the most common type of thrombophilia

A

factor V leiden

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28
Q

types of thrombophilia other than factor V leiden

A

prothrombin mutation
antithrombin deficiency
protein C deficiency
protein S deficiency

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29
Q

what type of thrombosis (arterial or venous) does thrombophilia cause

A

venous

bc thrombophilia = coagulation problem (ie no natural anticoags or increased coagulation) = fibrin thrombosis

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30
Q

recurrent DVTs

Fx

A

consider thrombophilia

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31
Q

management of thrombophilia

A

avoid DVT risk factors - COCP, smoking

consider long term anti-coag if recurrent

32
Q

how does someone get thrombophilia

A

hereditary

33
Q

is antiphospholipid syndrome acquired or hereditary

A

acquired

34
Q

what type of condition is antiphospholipid syndrome

A

autoimmune

35
Q

is primary or secondary haemostasis the problem in antiphospholipid syndrome
hence what type of thrombosis occurs

A

both primary and secondary haemostasis

= arterial and venous thrombosis

36
Q

management of antiphospholipid syndrome

A

antiplatelet (aspirin) - to stop primary haemostasis problem
AND
anticoag (LMWH, warfarin) - to stop secondary haemostasis problem

37
Q

what are the natural anti coagulants that satisfy most peoples need to stop coagulation

A

antithrombin
protein S
protein C

38
Q

indications for anti coagulant drugs

A

venous thrombosis eg DVT

atrial fibrillation - stroke prophylaxis

39
Q

which scoring system to you use to assess risk of stroke in AF

A

CHA2DS2VAC score

40
Q

side effects of anti coagulants

A

increased bleeding risk

41
Q

how long before surgery should you stop warfarin

A

5 days

42
Q

indications for warfarin over NOAC (2)

A

renal failure

patient scared to try new drugs

43
Q

how does warfarin work

A

inhibits vit K = decreased activation of clotting factors = decreased coagulation

44
Q

drugs interactions with warfarin (3)

A

cranberry juice
grapefruit
alcohol (liver problems)

45
Q

what is the initial effect of warfarin
what is the long term effect of warfarin (after a week)

clinical significance of this

A

initially - causes coagulation (decreases protein C and S)
long term - causes anti-coagulation

put on heparin instead of warfarin if you need immediate effects

46
Q

con of warfarin

A

needs monitoring, low therapeutic index

47
Q

what happens if warfarin dose too high

A

bleeding risk

48
Q

what happens if warfarin dose too low

A

thrombosis risk

49
Q

how do you monitor warfarin dose to make sure its not too high or too low
how often

A

INR - based on PT but comparable between hospitals
prothrombin time - measures extrinsic pathway (TF/VIIa)

can be weekly or 3 monthly, just depends

50
Q

INR aim for warfarin therapy

A

x2-3 normal

51
Q

management of bleed caused by warfarin therapy (4 stages depending on how severe and INR)

A

1 - nothing
2 - stop warfarin
3 - vit K PO- reverse anti coag effects of warfarin (warfarin inhibits vit K)
4 - clotting factors (II, VII, IX, X) form donor blood

52
Q

how fast does giving clotting factors work to helping bleed by warfarin

indication for this

A

immediately!!

indicated if life threatening emergency

53
Q

how fast does giving vit K work to helping bleed by warfarin

indication for this

A

6 hours

if not life threatening, but high INR

54
Q

how fast does stopping warfarin work to helping bleed by warfarin

indication for this

A

3 days

if only minor bleed and INR slightly high

55
Q

indication for heparin over warfarin

A

when immediate anti coag effects required (warfarin is delayed by 1 week)

56
Q

types of heparin

how are they administered

A

LMWH SC

unfractionated heparin IV

57
Q

drug class of dalteparin

A

LMWH

58
Q

is LMWH or unfractionated heparin used more

indications for the other
why

A

LMWH used more

unfractionated heparin - high risk of bleeding AND thrombosis (eg pregnancy)
bc has a short half life (30mins) = if bleeding starts can come of fit quickly

59
Q

do you need to monitor warfarin

A

yes - INR

60
Q

do you need to monitor LMWH

A

no

61
Q

do you need to monitor unfractionated heparin

A

no

62
Q

management of bleed caused by heparin therapy

A

stop heparin - if unfractionated will be out of system in 30 mins
protamine - only if severe bleeding

63
Q

why are NOACs preferred over warfarin

A

no monitoring needed bc normal therapeutic range

less durg interactions than warfarin

64
Q

what annual check do you need to do if on new anticoags (NOACs)

A

annual renal function checks

65
Q

contraindications to NOACs

A

renal failure

66
Q

NOACs

example of oral Xa inhibitor

A

rivaroxaban

the ‘-Xa bans’ block factor Xa (bans it)

67
Q

how does rivaroxaban work

A

oral Xa inhibitor = blocks Xa = no thrombin formation

68
Q

drug class of rivaroxaban

A

oral Xa inhibitor class of NOACs

69
Q

what type of thrombosis are anti platelet drugs used for

A

arterial thrombosis - caused by platelet aggregation

70
Q

aspirin drug class

A

anti platelet

71
Q

side effects of anti platelets

A

bleeding risk

72
Q

management of serious bleed caused by anti platelet

A

stop anti platelet

platelet transfusion

73
Q

how long before surgery should you stop an antiplatelet

A

1 week

bc life span of platelet is 7-10 days

74
Q

what does aspirin inhibit inside the platelets

what does this cause

A

cyclo-oxygenase
decreased prostaglandins
decreased platelet aggregation

75
Q

aspirin in directly decreased prostaglandins, what side effect can this cause (2)

A

GI ulceration

bronchospasm

76
Q

mechanism of clopidogrel

what does this cause

A

ADP receptor antagonist

decreased platelet aggregation (need ADP for this)

77
Q

clopidogrel drug class

A

anti platelet

J Haem (12 decks)

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