DVT: Test 3 Flashcards

(80 cards)

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
amiodarone effect on INR
slowly increase overtime | 25-50% warfarin dose reduction
26
fluconazole effect on INR
increase hold warfarin 1x for single dose 25-50% decrease in dose
27
metronidazole effect on INR
increase | expect 25-50% decrease in dose
28
phenytoin effect on INR
increase initially and decrease after prolonged exposure
29
rifampin effect on INR
decrease expect 2-5 fold increase in warfarin dose requirements
30
sulfamethoxazole effect on INR
increase expect 25-50% dose reduction
31
general questions for INR assessement
``` 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 ```
32
if INR is less than 2,
reload 1x | increase by 5-15%
33
if INR is 2-3
no change
34
if INR is 3.1-3.5,
decrease by 0-15%
35
if INR is 3.6-4
hold 0-1 dose | decrease by 5-15%
36
if INR is >4
hold until therapeutic minidose Vitamin K decrease by 10-20%
37
what are the two warfarin reversals
Vitamin K and Kcentra
38
INR greater than goal but < 4.5
no bleeding: hold | rapid reversal: hold, consider vitamin K
39
if INR 4.5-10
no bleeding: hold | rapid reversal: hold, give vitamin K 2.5mg oral or 1mg IV infusion
40
if INR > 10
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
any INR, serious or life threatening bleeding
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
which doac does not have to be dose adjusted for hepatic dysfunction
dabigatran
43
``` Pradaxa age: CrCl: wt: interactions: ```
> 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
rivaroxaban CrCl: wt: interactions:
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
``` apixaban DVT/PE treatment: post-op DVT prophylaxis: wt: interactions: ```
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
Edoxaban wt: crcl: interactions:
<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
betixaban crcl wt interactions
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
what monitoring for pradaxa? for factor Xa?
ecarin clotting test, thrombin time | antifactor Xa
49
if missed dose of dabigatran? riaroxaban? other Xa?
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
which is prodrug?
dabigatran
51
which take with meal?
betrixaban, rivaroxaban
52
if parenteral therapy to be avoided
rivaroxaban, apixaban
53
once daily oral dosing is preferred
rivaroxban, edoxaban
54
coronary artery disease
rivaroxaban, apixaban, edoxaban
55
dyspepsia or history of GI bleeding
apixaban
56
cost, coverage, licensing
varies
57
which was approved for CAD
rivaroxaban
58
DOAC reversals
HD, charcoal, coagulation factor replacement, agent specific treatments, FFP, prothrombin complex
59
advantages of DOACs
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
disadvantages of DOACs
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
changing from warfarin to DOAC
dabigatran and apixaban: start when INR < 2 Edoxaban: start when INR < 2.5 Rivaroxaban: start when INR < 3
62
changing from DOAC to warfarin
widely varies with each agent
63
last doac before procedure determined by
bleeding risk of procedure, elimination half-life of the DOAC
64
lower bleeding risk, stop DOAC
> 24 hr before surgery
65
high bleeding risk stop DOAC
1-5 days before surgery
66
acute phase: early maintenance: extended:
5-10 days 5-10 days to 3-6 months >3-6 months
67
treatment of VTE medications | acute phase:
UFH, LMWH, fondaparinux, rivaroxaban, apixaban
68
treatment of VTE medications | early maintenance:
warfarin, dabigatran, rivaroxaban, apixaban, edoxaban
69
treatment of VTE medications | extended:
rivaroxaban, apixaban, dabigatran, warfarin
70
which is recommended for early maintenance? extended?
DOACs | orl anticoag therapy
71
if patient has one of these 3 risk factors for bleeding, they should not receive prophylaxis
active gastric ulcer prior bleeding (last 3 months) low platelet count
72
if pt has a low risk of thrombosis it is recommended
not to use prophylaxis treatment
73
if a patient has bleeding or is at a high risk for bleeding
it i recommended to not use prophylaxis treatment
74
what drugs can be used for prophylaxis in nonsurgical patients
UFH, LMWH, fondaparinux, betrixaban, rivaroxaban
75
patients with cancer immediate anticoag
LMWH, UFH
76
patients with cancer continued anticoag
LMWH, edoxaban
77
DVT in pregnancy
highest risk 6 weeks postpartum all screened for signs and symps treatment if pt has history of VTE
78
which is preferred in pregnancy
``` LMWH, does not cross placenta NOT warfarin NOT doacs (no data) therapy continues until mom is 6 weeks postpartum ```
79
anticoags in pediatric patients
LMWH = preferred UFH = used if kid has renal failure warfarin can be used but is difficult to predict
80
``` in pediatric patients: provoked: unprovoked: recurrent: treatment lengths ```
P: 3 months U: 6-12 m R: indefinite