DVT: Test 3 Flashcards

1
Q

What is Virchow’s Triad

A

stasis - decreased BF
endothelial injury - damage to inside of blood vessel
hypercoagulability - blood clots are likely

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2
Q

what are VTE risk factors

A
previous VTE
family history
hospitalization
decreased BF
injury to a vien 
increased estrogen
chronic medical conditions
age
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3
Q

symptoms of DVT

A

leg swelling, pain, or warmth (unilateral)

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4
Q

signs of DVT

A

patients superficial veins may be dilated and a palpable cord may be felt in the affected leg; may experience pain in back of knee when the examiner dorsiflexes the foot of the affected leg (Homan’s sign)

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5
Q

laboratory tests of DVT

A

serum concentration of D-dimer is nearly always elevated

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6
Q

what diagnostic tests are used for DVT

A

compression ultrasound, venography

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7
Q

symptoms of PE

A

cough, chest pain, chest tightness, shortness of breath, or palpitation, may spit or cough up blood, massive: dizziness, light headedness

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8
Q

signs of PE

A

tachypnea, tachycardia, diaphoretic, neck veins may be distended, PE: may appear cyanotic/hypoxic, hypotensive, cardiogenic shock

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9
Q

laboratory tests for PE

A

serum concentration of D-dimer is nearly always elevated

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10
Q

diagnostic tests for PE

A

computerized tomography (CT) scan, ventilation-perfusion scan, pulmonary angiography

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11
Q

once formed thrombus may

A

remain asymptomatic, resolve through normal physiologic processes, obstruct venous circulation, propagate into more proximal veins, embolize to lungs resulting in PE, multiple of these

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12
Q

pharmacologic options must be based on

A

approved indications, patients level of risk of both thrombosis and bleeding, patient specific risk factors, costs and availability

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13
Q

what are the two general treatment catagories

A

primary prevention, secondary prevention

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14
Q

what is the patient population for primary prevention of DVT

A

patients without diagnosed VTE but at very high risk of developing VTE

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15
Q

what is the patient population for secondary prevention of DVT

A

acute treatment (3-6 m) with anticoags in patients with diagnosed VTE, and for some patients long term treatment (> 3-6 m) with anticoagulants to prevent additional future TE

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16
Q

primary prevention treatment duration

A

short terms varies with indication

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17
Q

secondary prevention treatment duration

A

short-term (3-6 m) to long term (>3-6 m)

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18
Q

medications utilized for primary DVT prevention

A

UFH, LMWH, fondaparinux, apixaban, rivaroxaban, warfarin, betrixaban, dabigatran

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19
Q

medications utilized for secondary DVT prevention

A

UFH, LMWH, fondaparinux (only early on) apixaban, rivaroxaban, warfarin, endoxaban, dabigatran

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20
Q

non-orthopedic surgery patients medications

A

LMWH, UFH, (fondaparinux if heparins are CI)

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21
Q

orthopedic surgery patients medications

A

LMWH, UFH, fondaparinux, apixaban, rivaroxaban, dabigatran, warfarin, ASA

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22
Q

length of therapy for non-orthopedic surgery patients

A

prophylaxis started during hospitalization, either before or shortly after surgery, and continued at least until patient is fully ambulatory

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23
Q

orthopedic surgery patients length of therapy

A

begin therapy either before or shortly after surgery, length depends on type (10-35)

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24
Q

alcohol effect on INR

A

increase with binging
decrease with chronic use
limit 1-2 drinks per day

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25
Q

amiodarone effect on INR

A

slowly increase overtime

25-50% warfarin dose reduction

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26
Q

fluconazole effect on INR

A

increase
hold warfarin 1x for single dose
25-50% decrease in dose

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27
Q

metronidazole effect on INR

A

increase

expect 25-50% decrease in dose

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28
Q

phenytoin effect on INR

A

increase initially and decrease after prolonged exposure

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29
Q

rifampin effect on INR

A

decrease expect 2-5 fold increase in warfarin dose requirements

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30
Q

sulfamethoxazole effect on INR

A

increase expect 25-50% dose reduction

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31
Q

general questions for INR assessement

A
duration of current
current dose
missed doses
signs and symps of bleeding
signs and symps of DVT/PE
drug interations
changes in diet/alc use
general complaints
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32
Q

if INR is less than 2,

A

reload 1x

increase by 5-15%

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33
Q

if INR is 2-3

A

no change

34
Q

if INR is 3.1-3.5,

A

decrease by 0-15%

35
Q

if INR is 3.6-4

A

hold 0-1 dose

decrease by 5-15%

36
Q

if INR is >4

A

hold until therapeutic
minidose Vitamin K
decrease by 10-20%

37
Q

what are the two warfarin reversals

A

Vitamin K and Kcentra

38
Q

INR greater than goal but < 4.5

A

no bleeding: hold

rapid reversal: hold, consider vitamin K

39
Q

if INR 4.5-10

A

no bleeding: hold

rapid reversal: hold, give vitamin K 2.5mg oral or 1mg IV infusion

40
Q

if INR > 10

A

no bleeding: hold
give vitamin k 2.5 mg oral or 1-2 mg IV infusion over 30 min and repeat every 24 h as needed
rapid reversal: hold, give vitamin K 1-2 mg IV infusion over 30 min, repeat every 24 hr as needed

41
Q

any INR, serious or life threatening bleeding

A

hold warfarin, give vitamin k 10mg IV infusion over 30 minutes, give 4 units of FFP, 4-factor PCC2000 units if INR is >1.5 (preferred)

42
Q

which doac does not have to be dose adjusted for hepatic dysfunction

A

dabigatran

43
Q
Pradaxa 
age:
CrCl:
wt:
interactions:
A

> 75: extreme caution
30: none (unless crcl is less than 50 and concamitant pgp inhibitor)
crcl< 30: avoid use
wt: >120kg or BMI of 40
interactions: PGP inducers: decrease conc (avoid use), inhibitors: with CrCl < 50 avoid use

44
Q

rivaroxaban
CrCl:
wt:
interactions:

A

crcl<30 avoid use
wt: 120 kg or BMI>40
PGP/CYP3A4:
strong inducers: reduce levels of drug avoid
strong inhibitors: increase levels of drug avoid
moderate: use caution with normal kidney function

45
Q
apixaban
DVT/PE treatment: 
post-op DVT prophylaxis:
wt:
interactions:
A

SCr>2.5 or Crcl<25: avoid use
crcl<30: avoid use
wt: 120 kg or bmi>40
pgp/cyp:
strong inducers: reduce levels of drug avoid use
strong inhibitors: increase drug levels avoid use

46
Q

Edoxaban
wt:
crcl:
interactions:

A

<60: 30 mg PO daily
15-50: 30 mg PO daily (avoid if crcl < 30)
crcl>95 or <15: avoid use
wt: 120 kg or bmi>40
pgp inducers: decrease drug levels avoid use
pgp inhibitors: increase drug levels, reduce dose by 50%

47
Q

betixaban
crcl
wt
interactions

A

crcl 15-30: reduce dose by 50% avoid use if patient receiving PGP inhibitor
wt: avoid use
pgp inducers: decrease conc avoid use
pgp inhibitors: increase conc Crcl > 30: reduce dose by 50%, crcl < 30 avoid use

48
Q

what monitoring for pradaxa? for factor Xa?

A

ecarin clotting test, thrombin time

antifactor Xa

49
Q

if missed dose of dabigatran? riaroxaban? other Xa?

A

D: do not take if <6 hrs before next dose is due
R: 15 mg BID: double up take both together
Xa: take asap dont double

50
Q

which is prodrug?

A

dabigatran

51
Q

which take with meal?

A

betrixaban, rivaroxaban

52
Q

if parenteral therapy to be avoided

A

rivaroxaban, apixaban

53
Q

once daily oral dosing is preferred

A

rivaroxban, edoxaban

54
Q

coronary artery disease

A

rivaroxaban, apixaban, edoxaban

55
Q

dyspepsia or history of GI bleeding

A

apixaban

56
Q

cost, coverage, licensing

A

varies

57
Q

which was approved for CAD

A

rivaroxaban

58
Q

DOAC reversals

A

HD, charcoal, coagulation factor replacement, agent specific treatments, FFP, prothrombin complex

59
Q

advantages of DOACs

A

lower incident of intracranial hemorrhage, reduced risk of ischemic stroke, lower risk of major bleeding, lower risk of mortality, approved indication for CAD, no INR monitoring, bridging/induction therapy, short half life

60
Q

disadvantages of DOACs

A

mealtime requirement may have a negative impact on compliance, no specific monitoring parameters, reversal agents are high costs, higher incidence of GI side effects, increased incidence of certain averse events, lack of monitoring may result in noncompliance, renal monitoring and dose adjustments required, higher out of pocket costs and copays, drug interactions prohibit concurrent use of DOACs

61
Q

changing from warfarin to DOAC

A

dabigatran and apixaban: start when INR < 2
Edoxaban: start when INR < 2.5
Rivaroxaban: start when INR < 3

62
Q

changing from DOAC to warfarin

A

widely varies with each agent

63
Q

last doac before procedure determined by

A

bleeding risk of procedure, elimination half-life of the DOAC

64
Q

lower bleeding risk, stop DOAC

A

> 24 hr before surgery

65
Q

high bleeding risk stop DOAC

A

1-5 days before surgery

66
Q

acute phase:
early maintenance:
extended:

A

5-10 days
5-10 days to 3-6 months
>3-6 months

67
Q

treatment of VTE medications

acute phase:

A

UFH, LMWH, fondaparinux, rivaroxaban, apixaban

68
Q

treatment of VTE medications

early maintenance:

A

warfarin, dabigatran, rivaroxaban, apixaban, edoxaban

69
Q

treatment of VTE medications

extended:

A

rivaroxaban, apixaban, dabigatran, warfarin

70
Q

which is recommended for early maintenance? extended?

A

DOACs

orl anticoag therapy

71
Q

if patient has one of these 3 risk factors for bleeding, they should not receive prophylaxis

A

active gastric ulcer
prior bleeding (last 3 months)
low platelet count

72
Q

if pt has a low risk of thrombosis it is recommended

A

not to use prophylaxis treatment

73
Q

if a patient has bleeding or is at a high risk for bleeding

A

it i recommended to not use prophylaxis treatment

74
Q

what drugs can be used for prophylaxis in nonsurgical patients

A

UFH, LMWH, fondaparinux, betrixaban, rivaroxaban

75
Q

patients with cancer immediate anticoag

A

LMWH, UFH

76
Q

patients with cancer continued anticoag

A

LMWH, edoxaban

77
Q

DVT in pregnancy

A

highest risk 6 weeks postpartum
all screened for signs and symps
treatment if pt has history of VTE

78
Q

which is preferred in pregnancy

A
LMWH, does not cross placenta
NOT warfarin
NOT doacs (no data)
therapy continues until mom is 6 weeks postpartum
79
Q

anticoags in pediatric patients

A

LMWH = preferred
UFH = used if kid has renal failure
warfarin can be used but is difficult to predict

80
Q
in pediatric patients:
provoked:
unprovoked:
recurrent:
treatment lengths
A

P: 3 months
U: 6-12 m
R: indefinite