Thrombosis Flashcards
what is the thrombus made of in arterial thrombosis
platelets
when atherosclerotic plaques rupture what is exposed
what does this cause
collagen and von Willebrand factor exposed = platelet aggregation and platelet plug formation
why does hypertension and smoking cause increased risk of arterial thrombosis
both damage the vessel walls = more susceptible to platelet aggregation
management of arterial thrombosis
anti platelet (aspirin) bc arterial thrombosis = platelet rich thrombus decrease risk factors - hypertension, smoking etc
what is the thrombus made of in venous thrombosis
fibrin
what are the 3 potential problems that can cause venous thrombosis
hypercoagulability
stasis
vessel wall
how does pregnancy/puerperium/COCP increase risk of venous thrombosis
estrogen increases clotting factors to decrease risk of bleeding at childbirth
= hypercoagulability
how does thrombophilia increase risk of venous thrombosis
coagulation problem (ie no natural anticoags or increased coagulation) = hypercoagulability = fibrin thrombosis
how does paralysis increase risk of venous thrombosis
paralysis = immobility = stasis of venous blood
how does long haul flights increase risk of venous thrombosis
long haul flights = immobility = stasis of venous blood
how does surgery (lower leg ortho) increase risk of venous thrombosis
immobility = stasis of venous blood
how does smoking increase risk of venous thrombosis
vessel wall damage
how does previous clot increase risk of venous thrombosis
vessel wall damage
Virchow’s triad
hypercoagulability
stasis
vessel wall
presentation of DVT
unilateral lower limb
hot swollen tender
pitting oedema
differential of DVT
cellulitis
why does pitting oedema occur in DVT
blood cant get back to heart so fluid leaks into legs
investigations for DVT
doppler US
what test can you do to rule out DVT, but isn’t diagnostic bc high in lots of things
d-dimers
prevention of DVT if risk factors
compression stockings
early mobilization
anti-coags - LMWH
complication of untreated DVT
PE
presentation of PE
pleuritic chest pain
hypoxia
SOB
ECG of PE
S1Q3T3
investigations for PE
V/Q scan (looking for mismatch)
ECG - for S1Q3T3
what arrhythmia is a risk factor for venous thrombosis
why
what can it cause
AF
= venous stasis in heart (LA)
can cause a stroke if the clot embolises
drug management of venous thrombosis
anti-coags (LMWH, warfarin, new anticoags) - bc problem is coagulation, not platelets (like arterieal thrombosis)
what is the most common type of thrombophilia
factor V leiden
types of thrombophilia other than factor V leiden
prothrombin mutation
antithrombin deficiency
protein C deficiency
protein S deficiency
what type of thrombosis (arterial or venous) does thrombophilia cause
venous
bc thrombophilia = coagulation problem (ie no natural anticoags or increased coagulation) = fibrin thrombosis
recurrent DVTs
Fx
consider thrombophilia
management of thrombophilia
avoid DVT risk factors - COCP, smoking
consider long term anti-coag if recurrent
how does someone get thrombophilia
hereditary
is antiphospholipid syndrome acquired or hereditary
acquired
what type of condition is antiphospholipid syndrome
autoimmune
is primary or secondary haemostasis the problem in antiphospholipid syndrome
hence what type of thrombosis occurs
both primary and secondary haemostasis
= arterial and venous thrombosis
management of antiphospholipid syndrome
antiplatelet (aspirin) - to stop primary haemostasis problem
AND
anticoag (LMWH, warfarin) - to stop secondary haemostasis problem
what are the natural anti coagulants that satisfy most peoples need to stop coagulation
antithrombin
protein S
protein C
indications for anti coagulant drugs
venous thrombosis eg DVT
atrial fibrillation - stroke prophylaxis
which scoring system to you use to assess risk of stroke in AF
CHA2DS2VAC score
side effects of anti coagulants
increased bleeding risk
how long before surgery should you stop warfarin
5 days
indications for warfarin over NOAC (2)
renal failure
patient scared to try new drugs
how does warfarin work
inhibits vit K = decreased activation of clotting factors = decreased coagulation
drugs interactions with warfarin (3)
cranberry juice
grapefruit
alcohol (liver problems)
what is the initial effect of warfarin
what is the long term effect of warfarin (after a week)
clinical significance of this
initially - causes coagulation (decreases protein C and S)
long term - causes anti-coagulation
put on heparin instead of warfarin if you need immediate effects
con of warfarin
needs monitoring, low therapeutic index
what happens if warfarin dose too high
bleeding risk
what happens if warfarin dose too low
thrombosis risk
how do you monitor warfarin dose to make sure its not too high or too low
how often
INR - based on PT but comparable between hospitals
prothrombin time - measures extrinsic pathway (TF/VIIa)
can be weekly or 3 monthly, just depends
INR aim for warfarin therapy
x2-3 normal
management of bleed caused by warfarin therapy (4 stages depending on how severe and INR)
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
how fast does giving clotting factors work to helping bleed by warfarin
indication for this
immediately!!
indicated if life threatening emergency
how fast does giving vit K work to helping bleed by warfarin
indication for this
6 hours
if not life threatening, but high INR
how fast does stopping warfarin work to helping bleed by warfarin
indication for this
3 days
if only minor bleed and INR slightly high
indication for heparin over warfarin
when immediate anti coag effects required (warfarin is delayed by 1 week)
types of heparin
how are they administered
LMWH SC
unfractionated heparin IV
drug class of dalteparin
LMWH
is LMWH or unfractionated heparin used more
indications for the other
why
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
do you need to monitor warfarin
yes - INR
do you need to monitor LMWH
no
do you need to monitor unfractionated heparin
no
management of bleed caused by heparin therapy
stop heparin - if unfractionated will be out of system in 30 mins
protamine - only if severe bleeding
why are NOACs preferred over warfarin
no monitoring needed bc normal therapeutic range
less durg interactions than warfarin
what annual check do you need to do if on new anticoags (NOACs)
annual renal function checks
contraindications to NOACs
renal failure
NOACs
example of oral Xa inhibitor
rivaroxaban
the ‘-Xa bans’ block factor Xa (bans it)
how does rivaroxaban work
oral Xa inhibitor = blocks Xa = no thrombin formation
drug class of rivaroxaban
oral Xa inhibitor class of NOACs
what type of thrombosis are anti platelet drugs used for
arterial thrombosis - caused by platelet aggregation
aspirin drug class
anti platelet
side effects of anti platelets
bleeding risk
management of serious bleed caused by anti platelet
stop anti platelet
platelet transfusion
how long before surgery should you stop an antiplatelet
1 week
bc life span of platelet is 7-10 days
what does aspirin inhibit inside the platelets
what does this cause
cyclo-oxygenase
decreased prostaglandins
decreased platelet aggregation
aspirin in directly decreased prostaglandins, what side effect can this cause (2)
GI ulceration
bronchospasm
mechanism of clopidogrel
what does this cause
ADP receptor antagonist
decreased platelet aggregation (need ADP for this)
clopidogrel drug class
anti platelet
