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PHRM 844 Module #2 > VTE Introduction > Flashcards

VTE Introduction Flashcards

1
Q

Pathophysiology

A

venous thrombi are formed in areas of slow/disturbed flow; stasis blood promotes thrombus –> decreased clotting factor clearance
venous thrombi composed of RBCs, fibrin, and few platelets

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2
Q

Symptoms result when

A

flow is obstructed
vascular tissue wall becomes inflamed (i.e. surgical procedure/traumatic injury)
thrombus occurs and affects venous blood flow
emboli occur and enter pulmonary circulation
not all DVTs lead to PEs but all PEs come from DVTs

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3
Q

3 main things contributing to a blood clot in our pts (virchow’s triad)

A

hypercoagulable state - abnormalities of clotting components (i.e. pregnancy or cancer)
circulatory stasis - abnormalities in blood flow, occurs during long periods of immobility
endothelial injury - abnormality of surfaces in contact with blood flow (i.e. injury of blood vessel)

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4
Q

Postthrombotic syndrome

A

long-term complications of DVT caused by damage to venous valves - chronic venous obstruction, caused by venous hypertension, chronic pain and swelling, stasis ulcers, development of infection

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5
Q

DVT risk factors

A

age > 40 yrs
family history of DVT
heart failure
immobilization > 10 days
malignancy
myocardial infarction
obesity
othopedic injury
oral contraceptive/estrogen
paralysis
postoperative state
pregnany
prior DVT
varicose veins

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6
Q

Nonpharmacologic treatment

A

baseline monitoring
DVT: bed rest (w/ appropriate anticoagulation), elevation of feet, pain management, compression stockings
PE: oxygen, mechanical ventilation, compression stockings

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7
Q

Unfractionated heparin

A

rapid, parenteral antigoagulant (most often given as continuous infusion)
variable dose response –> need for aPTT monitoring (time that represents how long it takes the bood to form a clot) - goal 1.5-2.5 time control
AEs: bleeding, thrombocytopenia

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8
Q

Weight based dosing for unfractionated heparin

A

monitor aPTT at baseline 6 hours after dose or with each dosage change (for 1st 24hrs); check daily after first day
lower the aPTT is, necessitates an increase in the dose
more elevated aPTT, need to decrease rate or hold infusion for short period of time

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9
Q

Heparin associated thrombocytopenia (HAT)

A

non-immune mediated
mild decrease in platelets
occurs around 48-72 hours after administration of heparin
transient, do not need to stop heparin

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10
Q

Heparin induced thrombocytopenia (HIT)

A

immune mediated
thrombotic complications
occurs between 7-14 days
one of 2 things to recognize HIT: platelets drop >50% from baseline OR <100,000/mm3

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11
Q

HIT management

A

STOP all heparin products
give alternate anticoagulant
do NOT give platelet infusions
do NOT give warfarin until platelet count > 150,000
evaluate for thrombosis

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12
Q

Low molecular weight heparin

A

advantages over UFH:
reduced protein binding - good bioavailability, predictable dose response (don’t need to monitor aTTPs)
longer plasma half-life - once or twice daily dosing
smaller molecule - improved SQ absorption
less effect of platelets and endothelium - reduced incidence of HIT and possibly bleeding

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13
Q

Monitoring Anti Xa levels

A

measures plasma heparin; consider for children, severe kidney failure, obesity, long courses, pregnancy

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14
Q

Fondaparinux

A

use: prophylaxis following THA, TKA, hip replacement, or abdominal surgery; treatment of DVT or PE (1st med used)

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15
Q

Fondaparinux considerations

A

do not use if have renal function (CrCl < 30 mL/min)
do not use for prophylaxis with low body weight (<50 kg)
can be used in HIT
no routine monitoring for therapeutic efficacy; can monitor anti-Xa levels
pregnancy category B (safe to use)

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16
Q

IV direct thrombin inhibitors

A

all three are reserved for pts diagnosed with HIT
lepirudin
bivalirudin
argatroban (adjust dose based on hepatic impairment; elevated INR, overlap with warfarin until INR >/= 4)

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17
Q

NOACs/DOACs

A

direct thrombin inhibitor: dabigatran etexilate
factor Xa inhibitors: rivaroxaban, apixaban, edoxaban, betrixaban

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18
Q

Labeled use - postoperative prophylaxis

A

knee or hip replacment surgery

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19
Q

Labeled use - non-valvular atrial fibrillation

A

prevention of stroke and systemic embolism in pts with non-valvular atrial fibrillation

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20
Q

Labeled use - DVT treatment

A

treatment of a DVT
need to put on an anticoagulant very quickly

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21
Q

Labeled use - PE treatment

A

treatment of pulmonary embolism
need to put on an anticoagulant very quickly

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22
Q

Labeled use - Indefinite anticoagulation (secondary prevention of recurrent DVT and/or PE)

A

reduction in risk of recurrence of DVT and PE following initial 6 months of treatment for them

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23
Q

Labeled use - VTE prophylaxis

A

prophylaxis of VTE in adults hospitalized for an acute medical illness

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24
Q

NOAC approved indications - postoperative prophylaxis

A

dabigatran, rivaroxaban, apixaban

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25
NOAC approved indications - non-valvular atrial fibrillation
dabigatran, rivaroxaban, apixaban, edoxaban
26
NOAC approved indications - DVT/PE treatment
dabigatran, rivaroxaban, apixaban, edoxaban
27
NOAC approved indications - secondary prevention of recurrent DVT/PE
rivaroxaban, apixaban
28
NOAC approved indications - VTE prophylaxis
rivaroxaban, betrixaban
29
Warfarin available doses
1, 2, 2.5, 3, 4, 5, 6, 7.5, 10 all tabs scored, meant to split in half as needed
30
Challenges of warfarin
narrow therapeutic window (range considered to be safe is very close to the range considered to be unsafe) considerable inter-subject variability (have to individualize warfarin dosing) drug and diet interactions labs difficult to standardize (INR monitoring is standardized) good PK/PD understanding by both patient/provider
31
Warfarin MOA
does not effect circulating factors or previously formed thrombi (stops body from making new ones) inhibits enzymes responsible for cyclic conversion of vit K inhibit synthesis of vit K dependent clotting factors - factors II, VII, IX, X, protein C and S
32
PK/PD and half-lives of warfarin
anticoagulant effect within 24hrs, peak effect 72-96 hours, duration of action from single dose 2-5 days hepatically metabolized by CYP450; enantiomer S metabolized by CYP2C9, 2C19, 2C18 and R metabolized by CYP1A2 and CYP3A4 - lots of drug interactions
33
Genetic variances - VKORC1
VKORC1 is the reductase enzyme that forms the active form of vit K that then converts vit K into vit K dependent clotting factors 1639A and 1173T: decreased VKOR production 1639A: increased warfarin sensitivity (lower dose needed) 1639G: increased warfarin resistance (higher dose needed) more *2/*3 - more sensitive more *1/*2 - more resistant
34
Who should be tested for warfarin?
3 requirements need to be met: 1. patient is warfarin naive 2. genetic test results are available before teh 6th dose 3. pt is at a high risk of bleeding if INR is elevated if a single one is not met, do NOT offer warfarin genetic testing
35
Warfarin drug interactions
increase INR: erythromycin, metronidazole, amiodarone, alcohol, anabolic steroids, fluconazole, isoniazid, ciprofloxacin, bactrim, propafenone, liver disease decrease INR: rifampin, cholestyramine, carbamazepine
36
Food drug interactions
vit K reverses warfarin activity consistency is key
37
Alcohol and warfarin
acute EtOH: increase anticoagulant effect of warfarin by inhibiting its metabolism (increase INR) chronic EtOH w/o liver damage: enhances warfarin metabolism by inducing hepatic enzymes --> decreases the effect of warfarin (decrease INR) chronic EtOH w/ liver damage: due to lack of hepatic enzymes, increased anticoagulant effect (increase INR)
38
Antiplatelet use in VTE
limited role in VTE ASA: consideration for CHA2-DS-VASc score 1 dipyridamole: consider concomitant use with warfarin with prosthetic heart valves concomitant use with anticoagulants and increased risk of bleeding
39
VTE bleeding management
discontinue med, apply manual compression, maintain BP, surgical or radiological intervention, blood products +/- PCC +/- antidotes consider: activated charcoal
40
Protamine sulfate: UFH and LMWH antidote
protamine sulfate binds UFH and LMWH to inhibit their further ability to cause anticoagulation AEs: hypotension, bradycardia
41
Idacruzimab
MOA: direct binder to dabigatran (higher affinity than dabigatran to thrombin) ADR: delirium, HA, hypokalemia, constipation, pneumonia, fever monitoring schedule: baseline aPTT --> repeat in 2 hours --> every 12 hours until normal
42
Andexanet alfa
MOA: binds and sequesters FXa inhibitors need to consider when last dose of those meds was given and what the last dose was to determine if we use the low or high dose ADR: local site indusion rxn, DVT, ischemic stroke, AMI, PE, UTI, pnuemonia no specific monitoring parameters
43
Warfarin: bleeding management
dependent on INR and presence/absence of bleeding vit K, fresh frozen plasma, prothrombin complex concentrate INR 4.5-10 + NO evidence of bleeding: avoid vit K INR > 10 + NO evidence of bleeding: PO vit K major bleeding: PCC preferred over FFP
44
Warfarin reversal
rapid (complete): PCC fast (partial): FFP prompt: IV vit K slow: PO vit K very slow: omit warfarin (no vit K)
45
VTE prophylaxis
without prophylaxis: VTE incidence 5-15% in medical pts without prophylaxis: VTE incidence 40-80% in surgical pts VTE prophylaxis options: UFH, LMWH, factor Xa inhibitors, vit K antagonists
46
Risk stratification - low risk < 10%
minor surgery fully ambulatory medical pts no specific pharmacologic therapy recommended early and aggressive ambulation
47
Risk stratification - moderate 10-40%
most non-orthopedic surgery pts acutely ill medical pts
48
Risk stratification - high 40-80%
major orthopedic surgery major trauma spinal cord injury
49
Moderate VTE risk treatment
general surgery pts: UFH, LMWH, and factor Xa inhibitor recommended; continue prophylaxis up to 28 days after hospital discharge acutely ill medical pts: UFH, LMWH, fondaparinux, rivaroxaban, betrixaban all apprpriate; UFH, LMWH, and fondaparinux have no specific recommendations for post discharge VTE prophylaxis duration
50
High VTE risk treatment
orthopedic surgery (hip/knee replacement pts) - LMWH, fondaparinux, rivaroxaban, apixaban, dabigatran (hip), UFH or vit K continue >/= 10-14 days postop
51
High bleeding risk
mechanical prophylaxis preferred: intermittent pneumatic compression devices, venous foot pumps, graduated compression stockings
52
CHA2DS-VAS and HAS-BLED
afib increases risk of stroke or systemic VTE by 5 fold - anticoagulant therapy reduces risk of stroke and all-cause mortality CHA2DS2-VAC: risk factors for stroke or systemic VTE HAS-BLED: risk factors for bleeding
53
Score interpretations
CHA2DS2-VAS: >/=2 - oral anticoagulation; 1 - no antithrombotic therapy OR oral anticoagulant OR antiplatelet HAS-BLED: >/=3 - high risk of bleeding, caution and regular monitoring of pt are recommended
54
CHA2DS2-VASc congestive heart failure score
1
55
CHA2DS2-VASc hypertension score
1
56
CHA2DS2-VASc age >/= 75 years score
2
57
CHA2DS2-VASc diabetes score
1
58
CHA2DS2-VASc stroke/TIA score
2
59
CHA2DS2-VASc vascular disease score
1
60
CHA2DS2-VASc age 65-74 years score
1
61
CHA2DS2-VASc female score
1
62
HAS-BLED hypertension score
1
63
HAS-BLED abnormal renal and liver function score
1 point each
64
HAS-BLED stroke score
1
65
HAS-BLED bleeding tendency/predisposition score
1
66
HAS-BLED labile INRs (if on warfarin) score
1
67
HAS-BLED age > 65 years score
1
68
HAS-BLED drugs or EtOH score
1 or 2

PHRM 844 Module #2 (23 decks)

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