Acute VTE therapy Flashcards

(44 cards)

1
Q

General approach to acute VTE therapy

A

1) diagnosis of VTE: objective tests
2) how stable is the pt
3) do they need IVC filter
4) in vs out pt
5) selection of therapy
6) do they need stockings?

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2
Q

When would someone need to get an immediate removal of clot

A

PE: with RF for poor prognosis (hypotension, brady (low HR), shock —— could go into organ failure)

DVT with limb gangrene —- possible amputation

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3
Q

Methods of clot removal

A

1) pharmacological : thrombolysis (dissolve clot)
2) pulmonary embolectomy: indicated if CI to thrombolysis (active bleeding) OR failed thrombolysis therapy

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4
Q

What is an IVC filter

A

Filter that goes into IVC and blocks and parts of DVT that may fall off
- stops them from reaching lungs

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5
Q

When is an IVC filter indicated

A

1) pt with absolute CI to anticoagulation+ have DVT (ex// major active bleed, major bleeding disorder, platelets < 30 x 10^9)

2) pt survived major PE but wouldn’t survive 2nd

3) Pt has recurrent VTEs despite anticoag therapy

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6
Q

When would a pt with a VTE automatically be admitted to hospital ?

A

hypotension, hypoxemia or tachycardia (increased HR)
—- aka if unstable

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7
Q

What risk tool do we use to determine whether to treat VTE in or out pt

A

PESI score
- looks at age, sex, cancer, HR, T, RR, O2 levels

—-low risk < 66— can treat outpt
—— if older than 66— automatically high risk (treat in hospital)

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8
Q

What is defined as a rapid anticoagulant

A

something that becomes effective with 1 hour
— normally SC or IV (PO—- riva or apix)

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9
Q

How many days of overlap bw rapid and warfarin do we need to get adequate protection?

A

at least 5 days + 2 consecutive INR 24 hours apart that are > 2
- if using warfarin for long term therapy—- need to start when start Rapid+ have a 5 day overlap

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10
Q

What is a good duration for rapid therapy

A

5-7 days as long as being followed up with LT anticoag after for at least 3mths

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11
Q

What is the approximate bleed risk on UFH

A

2-5 %: increases if recent surgery, trauma, F, old, malignancy

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12
Q

T or F: About 30% of pt on UFH will experience thrombocytopenia

A

T: can be directly or indirectly caused

directly: heparin binds to platelets + causes clumps (common + little worry)

indirectly: immune mediated HIT (PF4 + heparin; body makes AB —- cause platelet aggregation + activation —- pro thrombosis state)

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13
Q

What are the main SEs of UFH

A

bleeding
HIT
osteoporosis: not common
—- heparin binds to blasts— activate clasts
—- only seen with LT > 6mths of use

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14
Q

How common is HIT with UFH use

A

< 5%

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15
Q

What to monitor when looking for HIT

A

sudden drop in platelets in first 5 days of UFH use
—- is happens: stop heparin + start fonda

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16
Q

Advantages of UFH

A

IV admin: if bleed, can suddenly stop

antidote: protamine sulphate (1mg/100 units of heparin; max 50mg)

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17
Q

How is IV UFH dosed

A

weight based initial dose + infusion rate

  • initial bolus of 80-100units/kg + infusion rate of 17-20 units/kg/hour

—- check apTT in 4-6 hours to adjust dose if needed (if high——- lower dose)

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18
Q

Negatives of UFH

A

required monitoring — apTT
— need to be in pt (IV )
— requires blood draws

no SC dosing in Canada

19
Q

What needs to be monitored with UFH

A

CBC + platelets at baseline + at 2 weeks

apTT at baseline + every so often based on protocol

20
Q

What meds are LMWHs

A

dalt, tinza, enox

21
Q

T or F: LMWH is better than UFH

A

F- there was a study that showed decreased risk of bleeds/mortality but HAD a lot of bias

—- therefore both considered equally effective

22
Q

Dalt dosing

A

200 units/kg SC daily
if > 100kg: 100 units/kg SC BID

23
Q

Tinzaparin dosing

A

175units/kg SC daily

24
Q

Enoxaparin BID dosing

A

1.0mg/kg SC BID

25
T or F: we should use the 1.5mg/kg SC QD enoxaparin dosing over the BID dosing for VTE
F- not been studies in acute VTE treatment in comparison to UFH
26
T or F: protamine sulphate can be used as an antidote for LMWH
T- but not as effective; 60% reversal because LMWH are SC not IV
27
T or F: the rate of major bleeds with LMWH is lower than with UFH
F- equal
28
T or F: the rates of thrombocytopenia are lower with LMWH than UFH
T — lower rates —can’t use if history of HIT though
29
T or F: LMWH is safe in pregnancy
T- preferred agent; can use UFH though too
30
At what creatinine clearance is LMWH CI
< 30
31
Why do LMWH have less risk of thrombocytopenia + osteo compared to UFH
shorter chain —- less nonspecific binding to shit
32
What is the biggest advantage of LMWH to UFH
convenience —- less monitoring , SC once daily; don’t need to be in hospital
33
What assay can we use to monitor LMWH therapy
Anti-factor Xa—- don’t do it often though — not great evidence for values + how to adjust based on values
34
What do we have to check at baseline when starting LMWH
CBC, platelets, PT/INR, aPPT and Scr
35
What has to be monitored every 5-10 days during first 2 weeks of LMWH therapy
CBCs
36
When is the only real time we use fondaparinux
If history of HIT — similar efficacy to LMWH (only 2 studies) — similar risk of bleeds - no antidote - renal impairment — don’t use
37
Fonda dosing
7.5mg once daily if > 100: 10mg < 50: 2.5mg
38
Efficacy of Riva vs W
study showed equal efficacy (in prevention of recurrent VTE) —- Time in therapeutic target for W was longer than normal though (60 vs 70%) —- Riva showed decreased bleeding risk (but open label) sooooooo bias ?? study also had multiple checkin + FU points—- not normal for riva but have with W (INR) —- may have less adherence with riva in really life
39
T or F: cost of Riva + W are about the same
Riva; ODB covers 6 mths with LU 444 —— after you have to pay —— if have no insurance or even do: still costs more than W
40
T or F: Edoxaban + Dabigatran are equally effective in preventing VTE as Riva (we have plenty of evidence on both)
F- —- little evidence for E + D ++++ in the studies they showed benefit of them WHEN OVERLAPPED with LMWH
41
INR target for W
2.5 (2-3)
42
T or F: elastic compression stockings can be used to prevent PTS
F- no evidence that starting them earlier helps prevent PTS; may helps with symptoms of PTS
43
Impact of alcohol on INR
elevates INR — alcohol inhibits warfarin metabolism —- increasing concentration —- increase efficacy
44
Impact of smoking on W
Increases Cl—- induces metabolism —- INR decrease + may need a higher dose of W