DVT Flashcards

1
Q

S/sx of PE

A

Dyspea
Pleuritic Pain
Cough

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2
Q

Criteria for hemodynamically unstable PE

A

SBP <90 mm Hg for a period >15 mins
Requires vasopressors or inotropic support
NOT explained by other causes

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3
Q

Criteria for hemodynamically stable PE

A

Does not meet criteria for unstable PE

Unstable PE has a higher chance of death from obstructive shock

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4
Q

Clinical S/sx of DVT

A

Non-specific, pain, edema, swelling

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5
Q

Unprovoked DVT

A

No identifiable cause or provoking event

Higher risk of VTE (venous thromboembolism)

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6
Q

Provoked DVT

A

Caused by a known event

Surgery, major trauma, estrogen therapy, prolonged immobility

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7
Q

RFs for VTE

A
Age >40
Long auto/plane trips
Malignancy
Previous DVT or stroke
CHF 
Lower extremity fxs
Spinal cord trauma
Inherited hypercoagulable factors
Obesity
Immobilization
Major surgery
Serious infection/sepsis
Acute AMI
Burns
Vasculitis
Thrombocytosis
Pregnancy/postpartum
Trauma
Cigarette smoking
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8
Q

Diagnostic approach for DVT

A
D-dimer (sensitivity varies)
DVT-specific:
Compression u/s
Serial testing
PE-specific:
ECG
CT chest
V/Q scanning
Pulmonary angiography
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9
Q

D-dimer details

A

Low positive predictive value
Assays differ in sensitivity and units of measure
>500 mg/mL
Positive tests require further evaluation
Measures the amount of fibrin

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10
Q

What is the other name for minimum duration therapy

A

Long-term therapy

3 mos

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11
Q

What is the other term for extended anticoagulation therapy?

A

Implies indefinite therapy

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12
Q

Duration of therapy for DVT/PE provoked by proximal surgery

A

3 mos

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13
Q

Duration of therapy for DVT/PE provoked by nonsurgical transient risk factor- proximal

A

3 mos

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14
Q

Duration of therapy for unprovoked DVT/PT

A

3 mos

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15
Q

Duration of therapy for VTE association with active cancer (until resolution or CI to therapy)

A

Extended anticoag therapy

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16
Q

Duration of therapy for second unprovoked VTE

A

Extended anticoag therapy

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17
Q

Duration of therapy for first VTE and one interited hypercoagulable RF

A

Extended anticoag therapy

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18
Q

How is decision making made for duration of anticoagulation?

A

Decision requires individualization based on pt preferences and assessment of the pt’s added risk of recurrent VTE and risk of bleeding

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19
Q

Deciding to d/c anticoag therapy factors

A

Risk of bleeding
Pt sex (males 75% increase risk of recurrence)
D-dimer level (measure 1 mo after d/cing therapy)
-Pos D-dimer result 50% risk of recurrence

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20
Q

Non-pharmacologic therapies

A

Leg elevations
Ambulation
Fitted graduated compression stockings (CHEST does not recommend for post-thrombotic syndrome)
IVC- only recommended in situations due to CI anticoagulation
Catheter embolectomy/local thrombolytic therapy
Surgical embolectomy

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21
Q

Outpatient tx

A

Hemodynamically stable
Low risk of bleeding
Renal function stable
Home environment

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22
Q

Inpatient tx

A

Massive DVT
High risk of bleeding
Comorbid conditions/other factors that warrant in-hospital care
Pulmonary embolism

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23
Q

Traditional tx of VTE

A

Initial therapy bridging therapy
Unfractionated heparin OR
LMWH- 5 to 7 days OR until INR is therapy
Warfarin: 3 mos to lifetime

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24
Q

MOA of unfractionated heparin (UFH)

A

Indirectly inactivates thrombin and factor Xa by activating antithrombin

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25
Q

Monitoring for UFH

A

aPTT, anti-factor Xa, platelets

Therapeutic aPTT is typically 2-3x prolongation of aPTT

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26
Q

Side effects of UFH

A

Bleeding
Thrombocytopenia (HIT)
Osteoporosis
Elevation of transaminases

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27
Q

Prophylaxis dosing of UFH

A

Trying to prevent a clot when one already hasn’t happened
5000 units subQ BID-TID daily usually in abdomen
Renal impairment is usually twice a day

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28
Q

Regular tx with UFH

A

Use weight-based nomograms with continuous infusion
Draw an initial PTT then dose based on nomogram
Then, after six hours, draw another one and use the nomogram

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29
Q

Limitations of UFH

A

Poor bioavailability at low doses
Dose-dependent clearance
Variable anticoagulant response
Reduced activity in the vicinity of platelet-rich thrombi

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30
Q

Reversal of UFH

A

D/c (short 1/2 life) and/or protamine sulfate

Protamine sulfate neutralizes the heparin molecule

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31
Q

Dose of protamine sulfate

A

1 mg IV neutralizes 100 units of heparin

UFH short 1/2 life/IV/drip/general only calculate the amount of heparin given in last 2-2.5 hrs

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32
Q

Max dose of protamine sulfate

A

50 mg

Excessive protamine may worsen bleeding

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33
Q

Place of UFH in therapy

A

Overlap therapy bridging 5-7 days until warfarin reaches steady-state and the INR is at least 2.0 for at least 24 hrs.

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34
Q

What drug is considered a LMWH?

A

Enoxaparin (Lovenox)

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35
Q

Pros of LMWH

A

Less chance of thrombocytopenia

No monitoring for coagulation

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36
Q

MOA of enoxaparin (LMWH)

A

Accelerate factor Xa inhibition by antithrombin but are too short to convert thrombin by antithrombin

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37
Q

Monitoring for enoxaparin (LMWH)

A

No coagulation monitoring required, serum creatinine, platelets
May measure anti-Xa levels if needed 3-4 hrs after giving the dose

38
Q

Procedure for checking for HIT

A

Platelet count at baseline, between days 3 and 5 repeat
D/c if platelets <100,000 cell/mm cubed
Direct thrombin inhibitor can be utilized for tx
Cross-reactivity with heparin and other LMWH
After true HIT occurs, we can never use these agents again

39
Q

Side effects of LMWH (enoxaparin)

A

Bleeding

Less concerned with HIT and osteoporosis

40
Q

Prophylaxis dose of LMWH (enoxaparin)

A

40 mg subq daily or 30 mg subq bid (certain surgical procedures- hips and knees)
Renal adjustment: CrCl <30 mL/min = 30 mg subq daily

41
Q

Tx VTE for LMWH (enoxaparin)

A

1 mg/kg subq bid (dosed on ABW) or 1.5 mg/kg subq daily

Renal adjustment: CrCl <30 mL/min = 1 mg/kg subq daily

42
Q

Inpatient DVT dosing

A

1 mg/kg subq bid OR
1.5 mg/kg subq daily
Renal adustment: CrCl <30 mL/min 1 mg/kg subq daily

43
Q

Outpatient DVT dosing

A

1 mg/kg subq bid

Renal adjustment: CrCl <30 mL/min 1 mg/kg subq daily

44
Q

Inpatient PE dosing

A

1 mg/kg subq bid OR
1.5 mg/kg subq daily
Renal adjustment: CrCl <30 mL/min 1 mg/kg subq daily

45
Q

Advantages of LMWH

A
Better bioavailability and longer half-life
Dose-independent clearance
Predictable anticoagulant response
Lower risk of HIT
Lower risk of osteoporosis
46
Q

Reversal of LMWH

A

No true antidote
Protamine can be used off-label
Active bleed may also require FFP

47
Q

LMWH place in therapy

A

Overlap therapy bridging 5-7 days until warfarin reaches steady stead and the INR is at least 2.0 for at least 24 hrs
Preferred over UFH due to ease of administration and may be utilized in outpatient therapy
CHEST guidelines: “Cancer associated therapy”. LMWH over warfarin and the newer anticoagulants

48
Q

Pentasaccharide MOA

A

Binds only to antithrombin, catalyzes factor Xa inhibitors by antithrombin and does not enhance the rate of thrombin inhibition
Does not cause HIT

49
Q

Monitoring of pantasaccharide

A

Platelets, serum creatinine (CIed in renal impairment), no coagulation monitoring needed
Since thrombin is not inhibited, no effect on aPTT

50
Q

SEs of pentasaccharide

A

Bleeding

No cross-reactivity of fondaparinux with HIT antibodies

51
Q

What is another name for pentasaccharide?

A

Fondaparinux (Arixtra)

52
Q

Pentasaccharide prophylaxis

A

Adults greater than or equal to 50 kg: 2.5 mg subq once daily
Renal adjustment: CrCl <30 mL/min is contraindicated

53
Q

Pentasaccharide (fondaparinux) rversal

A

No antidote, FFPs, bleeding emergency

54
Q

Place of pentasaccharide (fondaparinux) in therapy

A

Overlap therapy bridging 5-7 days until warfarin reaches steady state and the INR is at least 2.0 for 24 hrs
Effective tx option for HIT
Utilized in high-risk ortho pts

55
Q

What is an example of a vit K antagonist?

A

warfarin (Coumadin)

56
Q

MOA of warfarin

A

Interferes with synthesis of the vit K-dependent clotting proteins, prothrombin (factor II), factors VII, IX, and X. Along with proteins C and S.

57
Q

Monitoring for warfarin

A

PT, INR

58
Q

What is a nl INR range on warfarin?

A

INR range 2-3 nl (2.5-3.5 mechanical heart valves)

Initial INR reflects depletion of factor VII, depletion of factor II takes several days

59
Q

Why do we use bridging therapy?

A

As depletion of protein C occurs and with a slow onset of anticoag effect, pts develop increased hypercoagulability during the first few days

60
Q

Frequency of INR monitoring in warfarin

A

Initial: INR checked daily for days 1-4, then monitored as needed until INR is greater than or equal to 2 for 24hrs then weekly until stable
Maintenance: Typically every 3-4 wks if stable, with dose changes, new medications added, recheck INR in 7-14 days
Many factors can affect the INR, monitor appropriately

61
Q

SEs of warfarin

A
Bleeding
Mild: epistaxis or hematuria
Severe: retroperitoneal or GI bleeding
Life-threatening: intracranial bleeding
Skin necrosis: rare complication typically seen in 1st 2-5 days
Fetal abnormalities- crosses placenta
Tx of choice of VTE in pregnancy is LMWH
62
Q

Initiation dose of warfarin

A

Adults (18-70 yrs): 5-10 mg once daily for 1-4 days
Geriatrics (>70 yrs): 2.5-5 mg once daily for 1-4 days
His rule: <65: 5 mg, >65: 2.5 mg

63
Q

Maintenance dose for warfarin

A

Adults: 5 mg (range 1-20 mg) once daily, based on INR
Geriatrics: 2.5 mg (range 1-20 mg) once daily, based on INR
Maintenance adjustments are typically based on dosing algorithms

64
Q

Drug interactions with warfarin that cause increased INR

A
Metronidazole
Bactrim/septra
Cipro
Levo
Fluconazole
Amiodarone
65
Q

Drug interactions with warfarin that cause decreased INR

A

Rifampin
Carbamazapine
Phenytoin

66
Q

OTC drugs that increase risk of bleeding with warfarin

A
NSAIDs
ASA
Ginger
Gingko biloba
Garlic
67
Q

Foods that have high interactions with warfarin

A
Broccoli (cooked)
Brussels sprouts
Cabbage (raw)
Canola oil
Endive (raw)
Kale
Lettuce (gourmet)
Liver
Parsley
Silver beet (cooked)
Soybean oil (mayo)
Spinach
68
Q

Foods that have a moderate interaction with warfarin

A
Abalone
Asparagus
Avocado
Beans (snap)
Cabbage (cooked)
Cheese (blue)
Margarine
Olive oil
Peas
Pickle, dill
Red cabbage
69
Q

Pt education for warfarin

A
Drug knowlege
Administration of dose
ID of SEs
Awareness of drug, food, and herbal meds
Importance of monitoring
S/Sx of bleeding
Pregnancy precautions
Verbal instruction must be supplemented with written materials
Want to take it in the afternoon or evening
Do not give refills easily
70
Q

Reversal of warfarin

A

Vit K (oral/injection), prothrombin complex concentrate (PCC), FFPs, and recombinant factor VIIa

71
Q

vit K dose with INR 5-9/no bleeding

A

2.5-5 mg oral x 1 dose

72
Q

vit K dose with INR >10/No bleeding

A

5-10 mg oral x 1 dose

73
Q

vt K dose with INR >10/bleeding

A

5-10 mg IV (slow infusion) or PCC +/- FFP

74
Q

vit K dose with major bleeding

A

10 mg IV (slow infusion) or PCC +/- FFP

75
Q

What are names of NOACs?

A

dabigatran
rivaroxaban
apixaban
edoxaban

76
Q

What is still the standard of care for a mechanical heart valve?

A

VKA

77
Q

Which NOAC(s) requires 5-10 days of parental therapy (not the same as bridging)?

A

Dabigatran

Edoxaban

78
Q

SEs of NOACs

A

Bleeding
Less intracranial bleeding than VKA but more GI bleeding
Dyspepsia in dabigatran

79
Q

DIs in NOACs

A

Low potential, P-glycoprotein based (lovastatin and simvastatin), CYP3A4

80
Q

CIs for NOACs

A

Pregnancy

81
Q

Reversal of NOACs

A

Praxabind (idirucizumab)
3-factor prothrombin complex concentrate (3-F PCC)
4-factor prothrombin complex concentrate (4-F PCC)
FFP
Contain all blood factors found in plasma
Disadvantage: volume/thawing, and infectious dz/transfusion rxn

82
Q

Clinical pearls for NOACs

A

Surgery stop them 1-2 days prior to procedure
Dialysis removes 60% of dabigatran from circulation in pts
Rivaroxaban/apixaban/edoxaban NOT considered dialyzable
Increased incidence of MI associated with dabigatran
Dabigatran has a tartaric acid core/capsule is unable to be opened
Apixaban associated with less GI bleeds than other NOACs

83
Q

CHEST guidelines

A

Risk reduction for recurrent VTE appears to be similar between NOACs and VKA.
Pts with VTE and CA have a lower recurrent rate of VTE with LMWH compared to VKA.
Risk reduction for recurrent VTE with different NOACs has not been compared but appears to be similar to all of the NOACs.
Based on less bleeding and greater convenience, NOACs are preferred to VKA for initial and long-term tx in pt with CI and CA.

84
Q

What drug should you give in CA?

A

LMWH

Recent diagnosis, extensive VTE, metastatic CA, N/V with chemo

85
Q

What drug should you give in pregnancy?

A

LMWH

86
Q

What drug should you give for compliance

A

VKA/NOACs
Frequent monitoring of INR/detect issues with VKA
NOACs dosing less complex
If you miss a NOAC, won’t be covered. If you miss warfarin, you’ll still be partially covered

87
Q

Which drugs are given once daily?

A

Rivaroxaban
Edoxaban
VKA
Edoxaban is CIed in pts with CrCl >95 mL/min

88
Q

Which drugs should be given when parenteral therapy must be avoided?

A

Rivaroxaban

Apixaban

89
Q

Which drugs should be given with renal dz and/or CrCl <30 mL/min?

A

VKA

90
Q

What drugs should be given with liver dz and coagulopathy?

A

LMWH

91
Q

Which drugs should be given with dyspepsia/hx of GI bleed?

A

VKA

Apixaban

92
Q

If you are concerned about a reversal agent, which drugs should you use?

A

VKA
UFH
Dabigatran