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PHAR253 > VTE/PE > Flashcards

VTE/PE Flashcards

1
Q

Why is VTE and PE so important?

A

VTE is a major cause of morbidity & mortality
-more deaths than breast cancer, HIV, and vehicle accidents combined
-50% attributed to hospitalization
10% of hospital deaths due to PE
average cost per VTE=$10k-$30k
affects approximately 100,000 Canadians/yr

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2
Q

True or false: VTE treatment and prophylaxis is the same as atrial fibrillation or secondary prevention of MI/stroke

A

false
not the same

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3
Q

Provide some characteristics of veins.

A

returns blood to the heart for re-oxygenation
thinner walled than arteries
elastic (variably widens as blood passes through)
lower shear rate than arteries
one-way valves close to prevent backflow (damage=pooling)

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4
Q

Differentiate between a venous thrombus and an arterial thrombus.

A

venous thrombus
-formed without damaging vessel wall
-held together mostly by fibrin, less platelet
-leads to VTE (DVT/PE)
arterial thrombus
-formed from rupture of atherosclerotic plaque
-held together by mostly platelets, less fibrin
-leads to ACS, stroke, or PAD

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5
Q

What is a venous thromboembolism?

A

results from clot formation within venous circulation
mainly develops in lower extremities
-majority in calf veins
-minority in arms, brain, GI tract, liver

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6
Q

After a venous thrombus is formed, what are some possibilities that could occur next?

A

lyse
obstruct venous circulation
embolize
combination of the above

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7
Q

Briefly describe the physiology of coagulation.

A

central to the coagulation is the generation of thrombin
-factor IIa
thrombin is made from prothrombin by factor Xa
prothrombin–>thrombin–>fibrinogen–>fibrin clot

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8
Q

What is Virchows triad?

A

risk factors for VTE
-stasis
-vessel wall injury
-hypercoagulability

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9
Q

Describe circulatory stasis as a risk factor for VTE.

A

bed rest/immobility (prolonged)
heart failure (class III-IV)
varicose veins (controversial)
atrial fibrillation

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10
Q

Describe vascular damage as a risk factor for VTE.

A

previous VTE
bacterial infection (sepsis)
prosthetic implants
peripheral vascular disease
trauma
surgery (mainly hips and knees)

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11
Q

Describe hypercoagulability as a risk factor for VTE.

A

medications
use of oral contraceptives
malignancy
inherited thrombophilias (factor V leiden gene)
advanced age >60 (esp >75)
obesity (esp >50)
protein C or S deficiency
smoking

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12
Q

Describe pregnancy as a risk factor for VTE.

A

5-10x increase during pregnancy
15-35x increase during early postpartum (6-12wks)

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13
Q

What are some medications that increase the risk for VTE?

A

estrogen
-CHC has RR of 2 but ARI is 0.04% and NNH is 2500
SERMS (tamoxifen/raloxifen)
chemotherapy
older antipsychotics
erythropoeitin

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14
Q

What is the clinical presentation of VTE?

A

often asymptomatic
symptoms are often non-specific
-diagnosis is difficult
-requires assessment of risk factors and lab/imaging

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15
Q

What are the symptoms of DVT?

A

leg pain (90%)
tenderness
ankle edema
calf swelling
dilated veins
dusky discolouration

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16
Q

What are the symptoms of PE?

A

sudden, unexplained SoB
tachypnea
tachycardia
unexplained chest pain/discomfort
cough
hemoptysis
fever
cyanosis
syncope
sense of impending doom

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17
Q

What are the complications of VTE?

A

recurrence rates are high
post-thrombotic syndrome
venous ulcers
chronic thromboembolic pulmonary hypertension (CTEPH)

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18
Q

Describe PTS as a complication of VTE.

A

sx: chronic pain, edema, fatigue, and leg ulcers
20-50% of DVT sufferers will develop within 3-6mo
possible treatment: compression stockings
-ankle to knee
-30 to 40mmHg at ankle at onset of DVT
-may decrease incidence of PTS

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19
Q

Describe venous skin ulcers as a complication of VTE.

A

results from venous insufficiency, leading to pooling of blood
major cause of chronic wounds
lack of proper blood flow

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20
Q

Describe CTEPH as a complication of VTE.

A

can occur after a PE
causes scarring in lungs
-narrows the arteries and leads to a permanent increase in pulmonary blood pressure, may lead to right-side HF
requires anti-coagulation for life

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21
Q

What are the ways that VTE is diagnosed?

A

lab tests
-D dimer increase
-ESR and WBC count increase
clinical prediction score
-Wells criteria
imaging
-compression, ultrasonography
-CT scan
-ventilation/perfusion scan

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22
Q

What are the goals of therapy for VTE?

A

prevent initial VTE
resolution of signs and symptoms
prevention of extension of VTE (prevention of PE in pts with DVT)
prevention of hemodynamic collapse and/or death
prevention of recurrence of VTE in select patients
prevent the development of CTEPH or PTS
reduce the risk of adverse effects from pharm treatment

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23
Q

What is PT?

A

prothrombin time
-measures the extrinsic and common pathway for coagulation (factor 10, 5, 7, 2)
-tests heparin

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24
Q

What is aPTT?

A

activated partial thromboplastin time
-measures the intrinsic and common pathways of coagulation
-longer time means less clotting
-tests heparin, not for LMWH

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25
Q

What does anti-Xa activity test for?

A

tests LMWH and heparin

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26
Q

What is the INR?

A

international normalized ratio
-standard measure of anticoagulant activity of warfarin
-only validated for warfarin, other anticoags will change it but does not accurately reflect it
-PT/PT reference

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27
Q

What is the difference between PT and aPTT?

A

both measure the intrinsic and common pathways but aPTT uses an activator to speed up clotting time, creating a narrower reference range to aim for (more sensitive)

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28
Q

What are the challenges of preventing and treating VTEs?

A

precise dosing of anticoagulants
monitoring properly
balance bleed risk vs clotting risk
bleeding is the predominant adverse event
-tends to increase with the intensity and duration of therapy
potential drug interactions
drug/disease interactions
patient issues: compliance, administration
clinician assessment and appropriate prophylaxis

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29
Q

What are the drugs used for VTE?

A

heparin
low molecular weight heparin
heparinoids (danaparoid)
glycosaminoglycan heparinoid (fondaparinux)
direct thrombin inhibitor (argatroban)
vitamin K antagonist (warfarin)
direct oral anticoagulants

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30
Q

What is the MOA of unfractionated heparin?

A

catalyzes antithrombin–>inactivates factor IIa and IXa, Xa, XIa & XIIa
prolongs aPTT
cannot bind to thrombin already in a clot
also binds to cells and other plasma proteins (unpredictable PK/PD)

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31
Q

What is the onset of effect for UFH?

A

IV: beings working immediately
SC: 30-60min

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32
Q

What is the duration of effect for UFH?

A

t1/2=1-2hrs
IV: continuous infusion to ensure level response
SC: 8hrs

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33
Q

What are the contraindications for UFH?

A

not absolute CI
active bleeding or conditions that increase bleed risk
-hemorrhagic stroke, severe HTN, active gastric ulcer, haemophilia
injuries and operations to brain, spinal cord, eyes/ears
severe thrombocytopenia
prior occurrence of HIT (this is an absolute CI)

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34
Q

Describe the dosing and administration of UFH.

A

IV or SC only
initial doses calculated using body weight
prophylaxis: 5000 units SC q8-12h
treatment:
-IV: LD 80 units/kg over 10min; then 18 units/kg/hr
-SC: 250 units/kg q12h
both: adjust dose until aPTT is 1.5-2.5x baseline

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35
Q

Does UFH have a wide or narrow therapeutic window?

A

narrow

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36
Q

How long is heparin used?

A

<7 days
-simultaneously given with warfarin
-discontinued once warfarin reaches target INR for 1-2 days

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37
Q

What are the common adverse effects of heparin?

A

minor bleeds
injection site reactions if subcut
transient, mild liver enzyme increase

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38
Q

What are the serious adverse effects of heparin?

A

heparin induced thrombocytopenia
major bleeds
hyperkalemia
skin necrosis
BMD decrease

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39
Q

What is the antidote to major bleeds from heparin?

A

IV protamine sulfate
-1 to 1.5mg neutralizes 100U of heparin if heparin was in last 29 minutes
-0.5 to 0.75mg neutralizes 100U of heparin if heparin was in last 30-120 minutes
-0.25 to 0.375mg neutralize 100U of heparin if heparin was given over 120 minutes ago

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40
Q

Describe heparin induced thrombocytopenia.

A

immune-mediated platelet aggregation reaction
-causes platelets to activate and stick together
-increased thrombotic and bleed risk
onset typically occurs 5-10 days after heparin initiation
depends on prior heparin exposure

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41
Q

Describe the 4T score.

A

thrombocytopenia:
-2 pts=>50% fall or nadir >20 x 10 to the 9/L
-1 pt=30-50% fall or nadir 10-19 x 10 to the 9/L
-0 pts=<30% fall or nadir <10 x 10 to the 9/L
timing of the decrease in platelet count:
-2 pts=days 5-10, or < day 1 with recent heparin (past 30d)
-1 pt=>day 10 or timing unclear, or <1 day if heparin exposure within past 30-100d
-0 pts=<day 4 (no recent heparin)
thrombosis or other sequelae:
-2 pts=proven thrombosis, skin necrosis, or systemic rxn
-1 pt=progressive, recurrent, or silent thrombosis, skin lesions
-0 pts=none
other causes of thrombocytopenia:
-2 pts=none evident
-1 pt=possible
-0 pts=definite
0-3 points= low probability (risk of HIT <1%)
4-5 points=intermediate probability (risk of HIT ~10%)
6-8 points=high probability (risk of HIT ~50%)

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42
Q

What is the treatment of HIT?

A

discontinue all sources of heparin
begin alternate anticoagulation
-warfarin initially unsuitable
-argatroban, fondaparinux, danaparoid, bivalirudin
-transition to warfarin once platelets restored and minimum x 5 days
-DOACs in stable pts with medium risk of bleed (rivaroxaban 15mg BID until platelets restored, 15mg BID x 21d then 20mg daily thereafter)

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43
Q

What are the drug interactions of UFH?

A

ACE/ARBs (hyperkalemia)
antiplatelets (increased anti-coagulation)
ASA/NSAIDs (increased anti-coagulation)
estrogens/progestins (pro-thrombotic)
herbs (194 have anti-coagulant properties)
potassium salts/sparing diuretics

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44
Q

Describe monitoring for UFH.

A

effectiveness
-must monitor aPTT (VTE tx, not prophylaxis)
-see validated nomograms
safety
-platelet count (get baseline if possible, if >4d of therapy then check qod until finished, if prev UFH exposure check at baseline and q24h)
-Hgb and hematocrit (baseline and q3d)
-potassium (only if high risk of hyperkalemia; baseline & q3d x 1wk)

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45
Q

Which are examples of low-molecular weight heparin?

A

enoxaparin
dalteparin
tinzaparin
nadroparin
all appear equal clinically in safety and efficacy
not interchangeable
different dosing regimens

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46
Q

What is the MOA of LMWH?

A

same as heparin but higher affinity for Xa
can affect aPTT
cannot bind to thrombin already in a clot
more predictable PK compared to UFH (allows for fixed doses and adjustment based on labs)

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47
Q

Which LMWH is of choice in the SHA?

A

tinzaparin
-prophylaxis and treatment of VTE
-dialysis line patency
enoxaparain used for acute ACS

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48
Q

What are the contraindications of LMWH?

A

same as UFH

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49
Q

Describe dosing and administration of LMWH.

A

subcut administration
prophylaxis:
-tinzaparin 75 units/kg
-okay down to CrCl 20ml/min
treatment:
-tinzaparin 175 units/kg
-okay down to CrCl of 30ml/min
dialysis line patency:
-tinzaparin 2500 units
no renal dose adjustment

50
Q

Describe LMWH use in pregnancy.

A

altered metabolism of LMWH throughout course of pregnancy, especially in the 3rd trimester
opinion differs:
-weight at the beginning and go
-weigh every trimester and adjust dose?
-anti Xa levels
-switch to UFH at 36 wks (SC q12h)

51
Q

What is the onset of effect for LMWH?

A

starts in one hour
peak anti-coagulation response in 3-5h

52
Q

What is the duration of effect for LMWH?

A

anti-Xa activity persists for 12-24h with a SC dose
half-life is only 3-6h

53
Q

What are the common adverse effects of LMWH?

A

same as UFH, but much lower incidence

54
Q

What are the serious adverse effects of LMWH?

A

same as UFH, but risk of HIT is dramatically lower

55
Q

What are the drug interactions of LMWH?

A

same as UFH

56
Q

Describe the monitoring for LMWH.

A

efficacy:
-cannot use aPTT
-monitoring anti-Xa levels not indicated unless obese, pregnant, renal insufficiency
safety:
-platelet count (baseline if possible, if on therapy for >4d then check qod until finished, previous heparin exposure get baseline and after 24h)
-Hgb and hematocrit
-potassium (only if high risk of hyperkalemia; baseline & q3d x 2 then weekly thereafter)
-renal function

57
Q

What is the MOA of heparinoids (danaparoid), glycosaminoglycan (fondaparinux), and direct thrombin inhibitor (argatroban)?

A

inhibits factor Xa (fondaparinux, danaparoid) or directly inhibits thrombin (argatroban)

58
Q

What is the indication for danaparoid?

A

prevention of DVT after surgery, or use in HIT

59
Q

What is the indication for fondaparinux?

A

same as LMWH, plus use in HIT

60
Q

What is the indication for argatroban?

A

anticoagulation in patients with HIT

61
Q

What are the advantages of fondaparinux?

A

no cases of HIT reported
possibly superior in preventing recurrent events
even less variability with dose-response
no monitoring
obesity dose better studied

62
Q

What are the disadvantages of fondaparinux?

A

possible increase in major bleeds with high doses
no antidote
longer half-life
can only use to CrCl of 30ml/min

63
Q

What are the advantages of danaparoid and argatroban?

A

specifically studied to treat HIT
no cases of HIT
no adjustment in obesity needed
can use in severe renal impairment

64
Q

What are the disadvantages of danaparoid and argatroban?

A

no antidote
limited pregnancy experience

65
Q

What is the MOA of warfarin?

A

vitamin K antagonist
interferes with production of clotting factors dependent on vitamin K (X, IX, VII, II) and protein C and S

66
Q

What is the onset of effect for warfarin?

A

not immediate (must clear vitamin K clotting factors from circulation)
takes 2-7 days (avg 3-5)
offset also takes a similar time

67
Q

What are the contraindications to warfarin?

A

pregnancy
high risk of bleed where benefit of anticoagulation is less than risk of bleeding
previous skin reaction to warfarin

68
Q

What are the options for initiating warfarin?

A

option 1: begin at 2-3mg OD x 2d
option 2: begin at 5mg OD x 2d
option 3: beging at 10mg OD x 2d
then adjust dose on day 3

69
Q

How do we deal with subtherapeutic or supratherapeutic INRs?

A

step 1:
-determine indication and target INR
-any symptoms of high or low INR?
step 2:
-if no issues above; is the pt at risk of having those issues develop?
step 3:
-determine if sub/supratherapeutic INR is from a permanent or transient cause

70
Q

Describe the bridge to warfarin therapy.

A

delayed onset
must assess how critical rapid anti-coagulation is needed
starting warfarin:
-initiate warfarin and UFH or LMWH simultaneously
-overlap for at least 5 days AND until INR is >2 for 2d

71
Q

When do we bridge to warfarin therapy?

A

during initial treatment of VTE
for prevention of VTE after high-risk procedure
for a patient at high risk of VTE or arterial emboli undergoing surgery

72
Q

Describe bridging off warfarin therapy.

A

warfarin has a delayed offset
must assess risk of thrombosis for stopping anticoagulation vs bleed risk for continuing during surgeries
-stop warfarin 3-5 days prior; wait until INR drops <1.5
-begin UFH or LMWH once INR <2
–>stop UFH 4-5h before surgery; LMWH 24hrs
-resume UFH or LMWH 24hrs after surgery, alongside warfarin

73
Q

What are the common side effects of warfarin?

A

minor bleeds (gums, shaving, cuts, bruises)
abdominal cramps
diarrhea
nausea
skin reactions, hives (rare but not serious)

74
Q

What are the serious side effects of warfarin?

A

major bleeds
-intracranial hemorrhage
purple toe syndrome
skin necrosis

75
Q

What are the 8 major classes of interacting drugs for warfarin?

A

antibiotics
antifungals
antidepressants
antiplatelets
amiodarone
anti-inflammatory agents
acetaminophen
alternative remedies
corticosteroids
any 2C9 inhibitor/inducer will have strong effect
648 documented food and drug interactions
acute drugs most risky

76
Q

Describe the antibiotic-warfarin interaction.

A

all impact warfarin by decrease in vitamin K
some also inhibit warfarin metabolism significantly
-ciprofloxacin
-clarithromycin
-erythromycin
-metronidazole
-TMP/SMX

77
Q

How do we manage drug interactions for warfarin?

A

empiric dose adjustment to warfarin is often more risky and unpredictable than the DI
check INR again in 4-6 days and adjust dose in response
some warfarin DIs cannot be monitor for
-NSAID, antiplatelet, hormone therapy
-must balance risk of bleed or clot with benefit of therapy

78
Q

Describe monitoring for warfarin.

A

safety/efficacy
-signs of major bleeds
-INR on day 3 & 5–>twice weekly x 1wk–>weekly until stable for 2 wks–>q2w until stable x 1 month–>monthly
-check in 4-6d after dose change or other issue

79
Q

What are some clinical tips regarding warfarin?

A

warfarin thrives on consistency
-many DIs
-many food interactions
easiest piece of advice to give patients:
-dont start any new meds/OTC/herbals or make any drastic changes in your diet without consulting a pharmacist/MD

80
Q

What is the antidote for warfarin?

A

vitamin K
-bleed or extremely elevated INR (>10), vitamin K IV or oral is given
-2.5-5mg orally will reduce INR in 24-48hrs
if serious bleed, regardless of INR
-hold warfarin
-give vitamin K 5-10mg IV q12h
-give factor IV prothrombin complex or FPP

81
Q

What is the MOA of the DOACs?

A

rivaroxaban, apixaban, edoxaban
-inhibit factor Xa
dabigatran
-directly inhibits thrombin

82
Q

What is the onset of effect for the DOACs?

A

all achieve peak anti-coagulation in about 2hrs

83
Q

What is the duration of effect for the DOACs?

A

rivaroxaban: t1/2 9h
apixaban: t1/2 8-14h
dabigatran: t1/2 13h, up to 18h in renal impairment
edoxaban: t1/2 14h

84
Q

True or false: there are renal dose adjustments for the DOACs

A

false
its all or none

85
Q

What are the drug interactions of the DOACs?

A

antiplatelet properties (ASA, NSAIDs, antidepressants)
estrogens/progestins
strong 3A4 and P-gp inducers
-carbamezepine, phenytoin, rifampin, St Johns Wort
strong 3A4 and P-gp inhibitors
-ketoconazole, itraconazole, ritonavir, clarithromycin, fluconazole, dronedarone
strong 3A4 inhibitors
-HIV protease inhibitors
strong p-glycoprotein inhibitors
-cyclosporine

86
Q

Which DOACs are unaffected by the CYP drug interactions?

A

dabigatran and edoxaban

87
Q

True or false: dabigatran is unaffected by anything that raises pH

A

false
affected by anything that raises pH

88
Q

What is the dosing of the DOACs for prevention of VTE after TKR/THR?

A

rivaroxaban: 10mg daily
-35 days (hip), 14 days (knee)
apixaban: 2.5mg BID
-35 days (hip), 14 days (knee)
dabigatran: 110mg STAT, then 220mg daily
-35 days (hip), 10 days (knee)
-reduce to 150mg OD if >75yo
edoxaban: N/A

89
Q

What is the dosing of DOACs for VTE treatment?

A

rivaroxaban
-15mg BID CC x 3wks; then 20mg OD x 3-6months
apixaban
-10mg BID x 7d; then 5mg BID x 3-6months
dabigatran
-must receive 5-10d of SC anti-coag; then begin prevention dosing
edoxaban
-60mg OD (after bridging x 5-10d)
-<60kg: 30mg

90
Q

What is the dosing of DOACs for prevention of recurrent VTE?

A

rivaroxaban
-6 months after tx dose; 10-20mg daily with food
apixaban
-6 months after treatment dose; 2.5mg BID
dabigatran
-150mg BID; consider 110mg BID if bleeding risk
edoxaban
-60mg OD (after bridging x 5-10d)
-<60kg: 30mg

91
Q

Describe DOAC dosing in obesity.

A

BMI <40 or <120kg: standard dosing
BMI >40, or >120kg: can use, but patient must understand potential unknown risks
-avoid dabigatran & edoxaban
-avoid in acute setting after bariatric surgery

92
Q

What are the common side effects of DOACs?

A

minor bleeding
GI upset and dyspepsia (dabigatran more)
diarrhea or constipation
itch

93
Q

What are the serious side effects of DOACs?

A

bleeding
-mostly better or same as warfarin

94
Q

What are examples of thrombolytics?

A

alteplase and tenecteplase
-strong clot busters

95
Q

Where do thrombolytics fit in for DVT?

A

benefit
-more rapid and complete lysis of DVT, less PTS
risk
-more major bleeding
-other anticoagulation has similar rates of recurrence and overall mortality
only VTE indication: high risk PE

96
Q

What is the duration of treatment for VTE provoked by a transient risk factor?

A

first: 3 months
second: same as for first

97
Q

What is the duration of treatment for VTE associated with ongoing non-cancer related risk factors?

A

indefinite therapy with periodic reviews or as long as risk factor persists

97
Q

What is the duration of treatment for unprovoked VTE?

A

first: minimum 3 months and then reassess
-with low-mod bleed risk: indefinite therapy
-with high bleed risk: 3 months
second: same as for first

98
Q

What is the duration of treatment for cancer-associated VTE?

A

minimum 3 months then reassess

99
Q

Describe the switch from heparin to the DOACs and LMWH.

A

apixaban: stop infusion and start apixaban at the same time
dabigatran: stop infusion and start dabigatran at the same time
edoxaban: stop the infusion and start edoxaban 4h later
rivaroxaban: stop infusion and start rivaroxaban at same time
LMWH: stop infusion and start LMWH at same time

100
Q

Describe the switch from LMWH to DOACs.

A

apixaban: start at same time as next scheduled dose of LMWH is due
dabigatran: start 0-2h before the next dose of LMWH is due
edoxaban: start at same time the next scheduled dose of LMWH is due
rivaroxaban: start 0-2h before next dose of LMWH is due

101
Q

Describe the switch from DOAC to parenteral.

A

apixaban:
-UFH: stop apixaban and start UFH at time next dose of apixaban is due
-LMWH: stop apixaban and give LMWH at time next dose of apixaban is due
dabigatran
-UFH: CrCl>30 wait 12hrs after last dose of dabigatran, CrCl <30 wait 24hrs after last dose of dabigatran
-LMWH: same as UFH
edoxaban:
-UFH: dc edoxaban and start UFH at next scheduled dose of edoxaban
-LMWH: dc edoxaban and start LMWH at next scheduled dose of edoxaban
rivaroxaban:
-UFH: stop rivaroxaban and start UFH at next scheduled dose of rivaroxaban
-LMWH: stop rivaroxaban and give LMWH at next scheduled dose of rivaroxaban

102
Q

Describe the switch from warfarin to DOAC.

A

to rivaroxaban:
-stop warfarin, wait until INR <2.5
to dabigatran/edoxaban/apixaban:
-stop warfarin, wait until INR <2.0

103
Q

Describe the switch from DOAC to warfarin.

A

from rivaroxaban/apixaban:
-use both concurrently, test INR on day 3, then each day prior to dose, once INR >2.0 can dc DOAC
from dabigatran/edoxaban:
-if CrCl >50ml/min, start warfarin 3d before dc
-if CrCl 30-50ml/min, start warfarin 2d before dc

104
Q

What is the most important patient safety strategy in patients admitted to the hospital?

A

thromboprophylaxis
-PE is the leading cause of preventable in hospital death
-risk depends on medical vs surgical admission

105
Q

What are the reasons for no VTE prophylaxis?

A

on therapeutic anticoagulation
fully mobile and expected length of stay less than 48hrs
palliative/compassionate terminal care/end of life care
no acute medical conditions and awaiting placement in LTC
psychiatric admission with no known VTE risk factors

106
Q

What are the agents used for VTE prophylaxis in the SHA?

A

tinzaparin
heparin
mechanical

107
Q

What are examples of mechanical devices for VTE prophylaxis?

A

graduated compression stockings
intermittent pneumatic compression device

108
Q

What is the VTE risk for air travel?

A

0.5% for flights <12hrs
1.5-10% for flights >24hrs
risk is elevated for up to 2-8wks post-travel
almost all who have a VTE during travel had many risk factors for VTE

109
Q

What are the recommendations for those who have VTE risk factors when travel is >6hrs?

A

compression stockings
frequent ambulation
flexion of ankles and knees
hydration

110
Q

Is pharmacologic prophylaxis needed for air travel?

A

pharmacologic prophylaxis NOT needed
highest risk individuals may receive LMWH
other antiplatelets or anticoagulants have no proven value

111
Q

Which anticoagulants cannot be used in pregnancy?

A

warfarin (teratogenic)
DOACs have not been studied

112
Q

What are the treatment choices for VTE during pregnancy and post-partum?

A

UFH
LMWH
danaparoid/fondaparinux?
multi-dose heparin preparations have benzyl alcohol as a preservative; must select preservative free options

113
Q

List some tips regarding VTE treatment in pregnancy and post-partum.

A

initiate treatment as soon as pregnancy occurs
if already on anti-coagulation, switch to safer alt
monitoring same as regular anti-coagulation
doses usually increase throughout pregnancy

114
Q

What are the three types of dosing protocols for VTE and pregnancy/post-partum?

A

prophylactic dosing (low, fixed)
intermediate dosing (adjust upwards based on weight)
therapeutic dosing (full dose, weight adjusted)
which dosing to use depends on clot risk

115
Q

Which agent should be used at 36-37 weeks of gestation?

A

switch to UFH

116
Q

How long after delivery should anticoagulation be initiated?

A

4-6hrs

117
Q

How long should anticoagulation continue for after delivery?

A

at least 6 weeks post-partum

118
Q

What are the complications from VTE treatment during pregnancy and post-partum?

A

bleeds
HIT
-lower incidence in pregnancy
-platelets decrease in pregnancy
bone loss

119
Q

What is the takeaway regarding malignancy and thrombosis?

A

malignancy poses pro-thrombotic factors as well as bleeding risks

120
Q

What is the treatment for cancer associated thrombosis?

A

LMWH is the DOC historically
evidence for DOAC usage
-not in GI/GU malignancy
duration depends on provoking factors

121
Q

What are some considerations for treatment of cancer associated thrombosis?

A

drug interactions with chemotherapy
renal impairment
thrombocytopenia
dosing in underweight cancer patients?
ICH risk in brain cancers

PHAR253 (16 decks)

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