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Pharmacology II > Venous Thromboemobolism (anticoagulants/thrombolitics) > Flashcards

Venous Thromboemobolism (anticoagulants/thrombolitics) Flashcards

1
Q

What is the pathological formation of a clot, which may cause occlusion w/in blood vessels of the heart?

A

Thrombosis

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2
Q

What forms as a result of endothelial injury because of arterial wall pathology like atherosclerosis and usually consists of platelets?

A

Arterial thrombus

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3
Q

What can arterial occlusion lead to?

A

MI
Stroke
Peripheral ischemia

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4
Q

What tends to forrm as a result of blood stasis allowing the build up of fibrin and platelets and consists more of fibrin?

A

Venous occlusions

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5
Q

What can venous occlusions lead to?

A

DVT

PE

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6
Q

What occludes blood vessels and adheres to vessel walls?

A

Thrombus

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7
Q

What occludes blood vessels and is an intravascular clot that floats with the blood?

A

Emboli

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8
Q

What encompasses both deep venous thrombosis (DVT) and pulmonary embolism (PE)?

A

Venous thromboemoblism

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9
Q

What do the majority of patients with a proximal DVT have?

A

PE and vice versa

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10
Q

What is a thrombus composed of cellular material (RBCs, WBCs, platelets) bound together by fibrin strands?

A

Deep Vein Thrombosis

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11
Q

What type of DVT has typical location of DVTs is in the veins of the calf (peroneal, anterior and posterior tibial veins). Thrombi arising from these veins are small and rarely cause significant emboli?

A

Distal DVT

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12
Q

What type of DVT is characterized by about 20% propagate or extend above the knee to the larger veins such as the popliteal and pelvic veins?

A

Proximal DVT

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13
Q

What is a thrombus or foreign substance arising from systemic circulation and lodging in pulmonary artery or one of its branches causing complete or partial obstruction of blood flow?

A

Pulmonary embolism

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14
Q

Thrombi usually derive from where?

A

Larger veins above the knees

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15
Q

Where do 95% of PEs derive from and what fraction of patients die within 30 minutes?

A

2/3 of patients die within 30 minutes

95% of PE’s derived from deep vein thrombi

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16
Q

What is the process of intact endothelium protecting against coagulation?

A

Normal Endothelial cells make prostacycline (PGI2) → activates cAMP in platelets → inhibits Ca2+ → inhibits platelet aggregation.
During clot formation the fibrinolytic pathway is locally activated and plasminogen is processed to plasmin. Plasmin dissolves the fibrin network as wounds heals.

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17
Q

What is the pathophysiology for clot formation?

A

Vascular injury exposes the subendothelium and platelets adhere becoming activated
Resting → Adhesion → Activation → Aggregation→ Clot → Fibrinolysis
Fibrin cross-links and stabilizes the clot.

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18
Q

What defense mechanism dissolves the fibrin network as injury heals?

A

Fibrinolysis-plasmin

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19
Q

What is the blood coagulation intrinsic and extrinsic pathway?

A

Extrinsic: TISSUE INJURY expresses TISSUE FACTOR
TISSUE FACTOR complexes with and converts factor VII to VIIa.
VIIa converts factor IX to IXa
Which in turn converts factor X to Xa.
Factor Xa CONVERTS PROTHROMBIN (FACTOR II) TO THROMBIN
THROMBIN removes small peptides from FIBRINOGEN CONVERTING IT TO FIBRIN monomer which POLYMERIZES TO GIVE THE FIRBIN CLOT.

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20
Q

What is virchow’s triad?

A

Venous stasis
Venous endothelial injury
Hypercoagulability

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21
Q

What results from various conditions (surgery, trauma, MI, CHF, varicose veins, etc) and leads to formation of thrombi as a result of high concentrations of clotting factors?

A

Venous stasis

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22
Q

What is mechanical or chemical trauma that as a result of collagen exposure activates coagulation cascade?

A

Venous endothelial injury

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23
Q

What is Activation of coagulation system in excess of the fibrinolytic system. Several inherited or genetic conditions (activated protein C resistance, protein C & S deficiency, anti-phospholipid ab’s, lupus anticoagulant, antithrombin III deficiency, malignancy)?

A

Hypercoagulability

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24
Q

What are the risk factors for VTE?

A 
Age 
PRIOR HISTORY OF VTE (DVT/PE)
Major surgery/Trauma of lower extremity, pelvis, hip, abdomen 
Immobility (bedridden) or paralysis
Malignancy
Pregnancy
Estrogen use
Obesity
Inflammatory bowel disease
Varicose Veins
Chronic venous insufficiency
Chronic lung disease
Heart disease: CHF, Afib,
Myeloproliferative disorders
Antiphospholipid ab’s (lupus anticoagulant, anticardiolipin ab)
Indwelling central venous catheters
Nephrotic syndrome
Hypercoagulable state
Inherited Risk Factors
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25
Q

What is the gold standard, invasive, procedure that has adverse effects of allergic rxn, neprhotoxicity, pain, and is the only test available to detect proximal and distal?

A

Venography

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26
Q

What is a non-invasive measure of blood flow following occlusion that is only sensitive for proximal DVT?

A

Impedance plethysomography (IPG)

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27
Q

What is a non-invasive, test that measures rate of blood flow from the reflection of sound waves off RBCs?

A

Doppler U/S

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28
Q

What combines doppler with real-time B-mode U/S to give better sensitivity and specificity of detecting proximal DVTs?

A

Duplex U/S

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29
Q

What involved A fibrin-derived fragments that are released into circulation when cross-linked fibrin is broken down by the fibrinolytic system?

Hint- high sensitivity but low specificity, useful to rule out but not to rule in if elevated

A

D-Dimer Test

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30
Q

What should you do if non-invasive tests are negative but you are clinically suspicious of a DVT?

A

If non-invasive tests are negative but clinically suspicious of DVT, perform serial testing on days 5-7 and again on days 10-14.

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31
Q

What should you do in you suspect a PE and non-invasive tests are negative?

A

For suspected PE, if non-invasive tests are negative, perform ventilation/perfusion radionuclide scan (V/Q scan)
Detects ventilation/perfusion mismatch
Reported as normal, low, intermediate/indeterminate, or high probability
May need pulmonary angiography if low or intermediate probability and moderate clinical suspicion.

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32
Q

What are the objectives for the treatment of DVT?

A

Prevent development of PE
Prevent postphlebitic syndrome
Reduce mortality
Minimize adverse events and cost

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33
Q

What does the treatment of DVT involve?

A 
General Measures
Elevation of affected extremity
Localized heat/antiembolic exercises (flexion/extension)
Reduced activity/bedrest
Analgesics for pain
Oxygen for pulmonary embolism
Pharmacologic treatment
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34
Q

What medications can be used for DVT?

A

Platelet Aggregation inhibitors
Anticoagulants
Fibrinolytics (Thrombolytics)- clot busters.

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35
Q

What are the platelet aggregation inhibitors?

A 
Aspirin
Dipyridamole 
Clopidogrel (Plavix®)
Glycoprotein IIb/IIIa inhibitors- option for substitution or adding for coronary clotting as well. 
--Abciximab- specific link to PCI
--Tirofiban
--Eptifbatide
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36
Q

Aspirin-MOA

A

Blocks the synthesis of thromboxane A2 from arachidonic acid by inhibiting the enzyme cyclooxygenase. (Irreversible acetylation)
Salicylic acid is a reversible inhibitor of prostacyclin formation

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37
Q

Aspirin- Indications

A

Prevention and treatment of MI and ischemic strokes, and TIAs.
Analgesic
Anti-inflammatory
Anti-pyretic

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38
Q

Aspirin- contraindications

A 
Children under age 12- due to reyes syn
Breast feeding
Hemophilia
PUD
Known hypersensitivity rxns
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39
Q

Aspirin- ADRs

A

Bronchospasms

GI hemorrhage

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40
Q

Dipyridamole (Persantine®)- MOA

A

ER dipyridamole in the combination product with aspirin (Aggrenox®)
MOA: causes inhibition of phosphodiesterase enzyme that hydrolyses cAMP. Increase cAMP levels result in decreased thromboxane A2 synthesis and thus platelet aggregation.
Indications:

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41
Q

Dipyridamole (Persantine®)- Indications

A

Aggrenox® to prevent thrombosis.
Licensed indication for prosthetic mechanical valves, in combo with warfarin
Alternative to exercise in thallium myocardial perfusion imaging.

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42
Q

Dipyridamole (Persantine®)- ADRs

A

Headache- typically self limiting
GI Bleed
Hypotension

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43
Q

Can Dipyridamole (Persantine®) be used as a monotherapy?

A

No

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44
Q

Dipyridamole (Persantine®)- contraindications

A

Contraindications
Caution in patients w/ hypotension
Caution in patients w/serious CAD
Combination w/aspirin was not much more effective than aspirin alone in controlled trials.

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45
Q

Ticlopidine (Ticlid®)- MOA

A

Blocks ADP-induced platelet-fibrinogen and platelet-platelet binding.

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46
Q

Ticlopidine (Ticlid®)- pharmacokinetics

A

ROA: Oral administration
Better absorption when administered w/food
Highly protein bound

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47
Q

Ticlopidine (Ticlid®)- Indications

A

Prevention of repeat stroke or TIA

Coronary Artery Stinting

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48
Q

Ticlopidine (Ticlid®)- contraindications

A

Patients w/severe liver dysfunction
Patients w/blood disorders such as thrombocytopenia, neutropenia
PUD
Internal bleeding

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49
Q

Ticlopidine (Ticlid®)- drug/drug interactions

A

Cimetidine
Digoxin
Theophylline
Red clover (herb)

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50
Q

Ticlopidine (Ticlid®)- ADRs

A

Bleeding
N/V/D
Thrombocytopenia, NEUTROPENIA, pancytopenia—monitor CBC
Nephrotic syndrome, dark colored urine

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51
Q

Clopidogrel- MOA

A

inhibits activation of the glycoprotein IIb\IIIa receptor on the surface of platelets, which is required for aggregation to occur.

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52
Q

Clopidogrel- Indications

A

Secondary prevention of cardiovascular and cerebrovascular events.
In patients allergic to aspirin

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53
Q

Clopidogrel- ADRs

A

Hemorrhage
Abdominal discomfort
N/V

54
Q

What is clopidogrel safer than and often added to to obtain a better platelet inhibition?

A

Clopidogrel is safer than ticlopidine, and often added to aspirin to obtain better platelet inhibition.

55
Q

Glycoprotein IIb/IIIa Inhibitors- Abciximab (reopro)-MOA

A

Prototype
MOA: Abciximab is an antibody fragment directed towards the glycoprotein IIb/IIIa receptor of platelets. Binding & Blocking the receptor prevents platelet aggregation.
ROA: IV

56
Q

Glycoprotein IIb/IIIa Inhibitors- Abciximab (reopro)- indications

A

Prevention of ischemic cardiac complications in patients undergoing percutaneous coronary intervention.
Short-term prevention of MI in patients w/unstable angina.

57
Q

Glycoprotein IIb/IIIa Inhibitors- Abciximab (reopro)- contraindications and ADRs

A 
Contraindications:
Active bleeding
ADRs
Hemorrhage
N/V
HPOTN
58
Q

Tirofiban and eptifbatide

A

Tirofiban & eptifbatide work similarly to abciximab but are peptide fragments. They are potentially antigenic, & should only be used once.

59
Q

What work by inhibiting the action of coagulation factors (thrombin inhibitors) or interfere with the synthesis of the coagulation factors (vitamin K antagonists)?

A

Anticoagulants

60
Q

What are heparin and low molecular weight heparins?

A

Anticoagulants
Heparin
Enoxaparin (Lovenox®) prototype of low molecular weight heparins

61
Q

Heparin & LMWH- MOA

A
  • Heparin binds to antithrombin III and accelerates inactivation of coagulation factors.
  • Antithrombin III inhibits the binding of fibrinogen to thrombin and hence is an anticoagulant.
  • Changes antithrombin from slow acting to rapid acting
  • Heparin binds to thrombin, inhibiting activity
  • Heparin binds and inhibits Factor Xa which converts prothrombin to thrombin.

LMWH complexes with antithrombin III & inactivates Factor Xa but does not bind as well to thrombin.

62
Q

Heparin- Administration

A

IV

Sub Q

63
Q

LMWH- Administration

A

Sub Q

64
Q

Heparin- Indications

A
  • DVT, PE (Treatment and Prophylaxis)
  • Coronary Artery Re-thrombosis after thrombolytic therapy
  • Heparin can be used in pregnancy since it does not cross the placenta, therefore is ideal to use for pregnancy
65
Q

LMWH- Indications

A
  • DVT, PE (Treatment and Prophylaxis)
  • Unstable Angina (LMWH)
  • MI (LMWH)
  • Can be used in pregnancy.
66
Q

LMWH- criteria for tx

A
  • Stable proximal DVT or PE
  • Normal vital signs
  • Low bleeding risk
  • Absence of severe renal insufficiency
  • Availability of a practical system for administering –LMWH and warfarin, with appropriate monitoring
67
Q

Heparin & LMWH- Contraindications

A

Hemophilia
Thrombocytopenia- monitor CBC and platelet counts
PUD

68
Q

Heparin/LMWH- ADRs

A 
Bleeding (< 5%)
Risk Factors
Increased dose
Intermittent vs continuous intravenous administration (Heparin)
Recent surgery or trauma
Renal failure
Age > 70 (older)
Concurrent ASA or NSAID use (something that is thinning your blood)
69
Q

What is used to reverse bleeding if it occurs with heparin/LMWH?

A

If bleeding should occur, reverse with protamine 1mg for every 100U of heparin given in previous 4 hours
LMWH anti-Xa activity partially reversed by protamine

70
Q

Heparin- Adverse effects

A

Heparin-induced Thrombocytopenia (HIT)
HIT associated with arterial or venous thrombosis in 60% of patients
Occurs in 3% of UFH treated patients
Platelet counts fall 5-15 days after treatment
Reductions of > 50% from baseline diagnostic of HIT or platelet counts < 100,000

71
Q

What are the complications of heparin-induced thrombocytopenia?

A
  • deep vein thrombosis
  • pulmonary embolism
  • MI, stroke, TIA
  • end organ damage (adrenal, spleen, gallbladder, renal)
72
Q

What is the HIT treatment?

A

-D/C Unfractionated Heparin usually resolves within 1 week
-Can use DTIs (argotroban or lepirudin- comes from leech spit)
-Lepirudin: LD 0.4 mg/kg IV, then 0.15 mg/kg/hr IV with dose adjusted to aPTT 1.5 – 2.5 x control.
Do not use if CrCl < 60 ml/min
-Argatroban: 2 mcg/kg/min IV, then adjust dose to maintain aPTT 1.5 – 3.0 x control.
-Can increase the INR
-Initiate warfarin once platelets > 100 x 109
-LMWH less likely to cause HIT (< 1%) but high cross-reactivity (~ 90%)

73
Q

Heparin/LMWH- ADRs

A

Osteoporosis
Seen during use in pregancy (long-term use)
Inhibits osteoblast activity (bone formation)
Increases osteoclast activity (bone resorption)
LMWHs < UH

74
Q

Heparin- monitoring

A
  • Baseline aPTT, PT/INR, and CBC
  • aPTT or UFH level q 6h until stable (therapeutic x2) then daily
  • CBC every other day x 14 days until heparin stopped
  • Signs and symptoms of bleeding
75
Q

LMWHs- monitoring

A
  • Baseline aPTT, PT/INR, CBC, and SrCr (added because of contraindication with renal compromised)
  • CBC between days 3 and 5 (to monitor platelet count)
  • Anti factor Xa activity
76
Q

What are the indirect factor Xa Inhibitor?

A

Fondaparinux

77
Q

Fondaparinux

A
  • Prevention of deep vein thrombosis following orthopedic surgery
  • Treatment of DVT/PE
  • Requires cofactor of Anti-thrombin III for activity
  • Contraindicated in patients with CrCl< 30ml/min
  • Subcutaneous injection
78
Q

What are the factor Xa inhibitors?

A

Rivaroxaban

Apixaban

79
Q

Rivaroxaban

A
  • Indicated in prevention of DVT in patients undergoing knee or hip replacement surgery
  • Stroke and systemic embolism prophylaxis in patients with non-valvular a fib
  • Oral
80
Q

Apixaban

A
  • Indicated for DVT prophylaxis in patients post hip and knee replacement
  • Oral
  • Not recommended in CrCl < 15mL/min or severe liver failure (Child-Pugh class C)
81
Q

What are the direct thrombin inhibitors?

A

Dabigatran
Agratroban
Hirudins
Warfrin

82
Q

Dabigatran

A

Direct Thrombin Inhibitors

  • Reduce risk of stroke and systemic embolism in patients with non-valvular atrial fibrilation
  • Direct thrombin inhibitor able to inhibit both free and clot-bound thrombin
  • Oral
  • Dosage adjustment for CrCl< 30mL/min
83
Q

Argatroban

A

Direct Thrombin Inhibitors

  • Binds selectively and reversibly to the catalytic site of thrombin, as a competitive inhibitor.
  • Different from heparin and some other direct thrombin inhibitors in its ability to inhibit clot-bound thrombin.
  • Short T ½ = 40-50 min, reversible binding
  • Use: Heparin-induced thrombocytopenia with and without thrombosis, possible use in ischemic stroke, hemodialysis, percutaneous coronary intervention.
  • No antidote is currently approved.
84
Q

Hirudins-MOA

A

Direct Thrombin Inhibitors

Derived from the leech, the recombinant derivatives, Desirudin and Lepirudin, inactivate thrombin

85
Q

Hirudins- Indications

A
  • In patients who have had heparin induced thrombocytopenia

- Prophylaxis of DVT in patients undergoing hip and knee replacement.

86
Q

Hirudins- contraindications

A

Active Bleeding

Renal or hepatic impairment

87
Q

Hirudins- ADRs

A

Hemorrhage

Hypersensitivity

88
Q

Warfarin- MOA

A 
Direct Thrombin Inhibitors
Vitamin K antagonist 
Block the reduction of vitamin K epoxide the necessary cofactor for the synthesis of clotting factors:
II
VII
IX
X
89
Q

Warfarin- Drug interactions

A

Drug interactions-Lots always look up.

Due to working through the P450 system

90
Q

Warfarin- Pharmacokinetics

A 
Route of administration- Oral
Onset of action
Several hours due to the half life needed for the degradation of the clotting factors, which are:
VII ~ 6 hours
IX  ~ 24 hours
X ~ 40 hours
II ~ 60 hours
91
Q

Warfarin- indications

A
  • Acute MI
  • Prophylaxis & treatment of DVT
  • Prophylaxis & treatment of PE
  • Prophylaxis of embolization in atrial fibrillation
  • Prophylaxis of embolization in rheumatic disease
  • Prophylaxis of embolization in patients w/prosthetic heart valves.
  • Prophylaxis of embolization in patients who have undergone hip or knee replacement.
92
Q

Warfarin- Contraindications

A
  • Cerebral thrombosis
  • Peptic Ulcer
  • Pregnancy- crosses the placenta and is teratogenic, initially sold as rat poison
93
Q

Warfarin- ADRs

A

–Bleeding
Treated w/vitamin K administration takes ~ 24 hours for effect (need to regenerate all of the clotting factors)
Blood, plasma, etc.
–Skin Necrosis- doesn’t happen with every patient but something to monitor.

94
Q

Warfarin- Monitoring

A
  • Baseline PT/INR (tells how quickly blood is clotting and how well its going to work), aPTT, CBC, LFTs
  • Yearly CBC
  • Urinalysis and fecal occult test as needed
  • PT/INR should be monitored every 2 to 3 days initially until INR in therapeutic range x 2 then spread out (done at a coumadin clinic)
  • PT/INR as required (no greater than 4 weeks)
  • Signs and symptoms of bleeding
95
Q

Warfarin- Patient counseling

A
  • Strict compliance
  • Side effects—Bleeding
  • Dietary instruction- vitamin K
  • INR monitoring- important
  • Physical Activity limitations
  • Pregnancy Avoidance
  • Drug Interactions- might mean you adjust the drug you are giving or warfarin. Works as an ibhibitor and inducer, also as being induced and being inhibited.
96
Q

What are the thrombolytic (fibrinolytic) agents?

A

Alteplase (Activase®)
Streptokinase (Streptase®)
Anistreplase (Eminase®)
Urokinase

97
Q

Thrombolytic (fibrinolytic) agents- General actions

A
  • Turn plasminogen to plasmin, which cleaves fibrin, thus lysing thrombi
  • Clots are more resistant to lysis as they age
  • Increased local thrombin may occur as the clot dissolves-many times co-administered w/antiplatelet or anticoagulant.
98
Q

Thrombolytic (fibrinolytic) agents- administrations

A

MI—intracoronary if possible

IV—otherwise

99
Q

Thrombolytic (fibrinolytic) agents- Therapeutic uses

A
  • Acute MI
  • Massive/Submassive PE with hemodynamic compromise
  • Massive PE without hemodynamic compromise and low-risk of bleeding
  • Submassive PE in patients intolerable of CV compromise
  • Heparin treatment failures
  • Extensive proximal DVT- these are the ones we worry about progressing to PE.
100
Q

Thrombolytic (fibrinolytic) agents- ADRs

A

Hemorrhage

Reperfusion arrhythmias- concern primarily when used for coronary problems. Not as concerning if treating PE.

101
Q

Thrombolytic (fibrinolytic) agents- Contraindications

A
  • Recent surgery/trauma within 7 - 10 days (you have a clot you want to keep and these wont let you)
  • CVA within 2 months
  • Recent needle puncture of noncompressible vessels (epidural puncture)
  • Active bleeding
  • Uncontrolled HTN
  • Malignancy (patients that will clot a lot so this is not an option anymore)
  • Pregnancy
  • CPR (before or during admission, this is brutal don’t administer something to make them bleed out)
102
Q

What are the tissue-type plasminogen activators (t-PAs)?

A

Alteplase (Activase)

Streptokinase

103
Q

Alteplase (Activase)- MOA

A

T-PAs
A serine protease obtained from recombinant DNA.
MOA: enzyme that catalyzes the conversion of tissue plasminogen to plasmin in the presence of fibrin. Fibrin specificity produces local fibrinolysis in the area of a recent clot w/limited systemic proteolysis.

104
Q

Alteplase (Activase)- indications

A

Acute MI
PE
Acute ischemic stroke
Do not give this in hemorrhagic stroke

105
Q

Alteplase (Activase)- pharmacokinetics

A

IV administration

Short half life

106
Q

Alteplase (Activase)- ADRs

A
  • Bleeding
  • Arrhythmias-monitor ECG for arrhythmias associated w/reperfusion.
  • N/V
  • Cardiac arrest, stroke, thromboembolism
107
Q

Streptokinase- MOA

A

Derived from culture broths of Group C β-hemolytic streptococci.
MOA:
Forms a 1:1 complex w/plasminogen to convert to the active enzyme plasmin.
Hydolysis fibrin plugs
Catalyzes the degradation of fibrinogen 7 clotting factors V & VII.

108
Q

Streptokinase- Indications

A
  • Life-threatening DVT
  • PE
  • Arterial thromboembolism
  • Acute MI
109
Q

Streptokinase- ADRs

A

N/V
Bleeding
Antigenic
Allergic reactions—Rash, fever, Anaphylactic reactions
Therapeutic failure as a result of endogenous antibodies

110
Q

What is the treatment of DVT?

A

-Treatment of Acute DVT of the Leg
-If objectively confirmed, initiate short-term tx with
SC low-molecular-weight heparin (LMWH) or
IV unfractionated heparin (UFH) or
SC fondaparinux
(all Grade 1A)
-If high clinical suspicion of DVT, initiate treatment while waiting for diagnostic study results (Grade 1C)
-In acute DVT, tx with LMWH, UFH, or fondaparinux for at least 5 days and until the INR is ≥ 2.0 for 24 hours (Grade 1C).
-In patients with severe renal failure (CrCl <
30 ml/min), suggest UFH over LMWH(Grade 2C)
-Warfarin should be initiated together with antithrombotic agent (the same day) (Grade 1A).

111
Q

What is thrombolysis for DVT?

A
  • In selected patients with extensive acute proximal DVT (i.e. iliofemoral DVT, symptoms < 14 d, good functional status, life expectancy of ≥ 1 yr) who have a low risk of bleeding, suggest that catheter-directed thrombolysis (CDT) may be used to reduce acute symptoms and post-thrombotic morbidity if appropriate expertise and resources are available (Grade 2B).
  • After successful CDT, suggest correction of underlying DVT using balloon angioplasty and stents (Grade 2C).
  • In selected patients with extensive proximal DVT (symptoms< 14 d, good functional status, life expectancy of ≥ 1 yr) who have a low risk of bleeding, suggest systemic thrombolytic therapy may be used to reduce acute symptoms and post thrombotic morbidity if CDT not available (Grade 2C).
112
Q

What is the treatment for DVT?

A

Recommend early ambulation in preference to initial bed rest when this is feasible (Grade 1A).

113
Q

What is acute treatment for PE?

A

-For objectively confirmed PE, recommend short-term treatment with:
SC LMWH
IV UFH
SC fondaparinux
(all Grade 1A).
-In patients with non-massive PE recommend LMWH over UFH (Grade 1A).
Massive PE recommend UFH over LMWH (Grade 2C).
-Patients with acute PE should also be routinely assessed for treatment with thrombolytic therapy (if massive PE mainly)
-For patients in whom there is a high clinical suspicion of PE, recommend treatment with anticoagulants while awaiting the outcome of diagnostic tests (Grade 1C).
-Initial treatment should be continued for at least 5 days and until the INR is ≥ 2.0 for at least 24 h (Grade 1C).
-Warfarin should be initiated together with antithrombotic agent (the same day) (Grade 1A).

114
Q

What is thrombolytics in PE?

A
  • In selected high-risk patients without hypotension who are judged to have a low risk of bleeding, suggest administration of thrombolytic therapy
  • The decision to use thrombolytic therapy depends on the clinician’s assessment of PE severity, prognosis, and risk of bleeding.
  • For the majority of patients with PE, recommend against using thrombolytic therapy
115
Q

What is long term treatment of DVT/PE for patients with DVT/PE secondary to a transient reversible risk factor?

A

For patients with DVT/PE secondary to a transient (reversible) risk factor, recommend treatment with warfarin for 3 months (Grade 1A).

116
Q

What is long term treatment of DVT/PE for patients with unprovoked DVT/PE?

A
  • For patients with unprovoked DVT/PE, recommend treatment with warfarin for at least 3 months (Grade 1A).
  • After 3 months of anticoagulant therapy, all patients with unprovoked DVT/PE should be evaluated for the risk/benefit ratio of long-term therapy (Grade 1C).
  • For patients with a first unprovoked VTE that is a proximal DVT or PE, and in whom risk factors for bleeding are absent and for whom good anticoagulant monitoring is achievable, long-term treatment is recommended (Grade 1A).
  • For patients with a first isolated distal DVT that is unprovoked, it is suggested that 3 months of anticoagulant therapy is sufficient rather than indefinite therapy (Grade 2B).
  • For patients with a second episode of unprovoked VTE, long-term treatment is recommended (Grade1A).
117
Q

What is the intensity of anticoagulant treatment for long term treatment of DVT/PE?

A
  • In patients with DVT/PE, recommend that the dose of warfarin be adjusted to maintain a target INR of 2.5 (range, 2.0 to 3.0) for all treatment durations (Grade 1A).
  • For patients with unprovoked DVT/PE who have a strong preference for less frequent INR testing to monitor their therapy, after the first 3 months of conventional-intensity anticoagulation (INR range, 2.0 to 3.0), recommend low-intensity therapy (range, 1.5 to 1.9) with less frequent INR monitoring over stopping treatment (Grade 1A).
118
Q

What is done for DVT/PE prevention?

A

-Without prophylaxis DVT risk is 10 – 40% in medical or general surgical patients and 40 – 60% in orthopedic surgery patients
-25 – 33% of these involve proximal veins (these are the bad ones that we end up with PE)
10% of hospital deaths are attributed to PE
-PE is the most preventable cause of hospital death
The Agency for Healthcare Research and Quality ranked 79 patient safety interventions
-#1: “…appropriate use of prophylaxis to prevent VTE in patients at risk.”
-Bleeding risk with prophylaxis very low

119
Q

What are low risk prevention patients?

A

general surgery patients who are undergoing minor procedures and have no additional VTE risk factors (Caprini score 0-1)

120
Q

What are moderate risk prevention patients?

A

patients who are undergoing a major procedure for benign disease (Caprini score 2)

121
Q

What are higher-risk prevention patients?

A

patients who are undergoing a major procedure for cancer (Caprini score 3-4)

122
Q

What are very-high risk prevention patients?

A

patients with multiple risk factors for VTE (Caprini score >5)

123
Q

What are the prevention recommendations for low-risk?

A

Early Ambulation (Grade 1A)

124
Q

What are the prevention recommendations for moderate-risk?

A

ES, IPC, Low dose UFH, LMWH (Grade 1A)

125
Q

What are the prevention recommendations for high-risk?

A

IPC, Low dose UFH, LMWH alone or with ES or IPC (Grade 1A)

126
Q

What are the prevention recommendations for very high-risk?

A

LMWH, low dose UFH, Factor Xa Inh combined with IPC/ES (Grade 1C)

127
Q

What are the DVT/PE preventions for total hip replacement?

A

LMWH, Warfarin (INR 2.5, range 2-3), Factor Xa inh (Grade1A)

128
Q

What are the DVT/PE preventions for total knee replacement?

A

LMWH, Warfarin, Factor Xa inh(Grade 1A); +/- IPC (Grade 1B)

129
Q

What are the DVT/PE preventions for hip fracture surgery?

A

Factor Xa inh (Grade 1A), LMWH (Grade 1B), Warfarin (Grade 1B), LDUH (Grade 1B)

130
Q

What are the DVT/PE preventions for trauma?

A

LMWH (Grade 1A); IPC or ES if LMWH C/I (Grade 1B)*

131
Q

What are the DVT/PE preventions for general med?

A

General Med-something else going on besides whats goin on (CHF, COPD) or bedrest and > 1 RFs (CA, previous VTE, sepsis, IBD, acute neurologic disease)
LDUH, LMWH, or fondaparinux (Grade 1A)

132
Q

What are the DVT/PE preventions for above contraindications?

A

then ES or IPC (Grade 1A) go back to compression devices listed

Pharmacology II (23 decks)

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