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PT (Prothrombin Time)
Measures clotting time via the extrinsic pathway.
Normal PT range
~11–13.5 sec.
INR (International Normalized Ratio)
Standardized value calculated from the PT for comparability.
Normal INR value
≈ 1.0.
Target INR for DVT/AF
2.0–3.0 (goal ~2.5).
aPTT (Activated Partial Thromboplastin Time)
Measures clotting time via the intrinsic pathway.
Normal aPTT range
21–35 sec.
Therapeutic aPTT range for heparin
1.5–2.5 × baseline.
Risk for hemorrhage aPTT value
If aPTT >100 sec.
Anti-Factor Xa Level
Alternative to aPTT for monitoring UFH.
Therapeutic Anti-Factor Xa Level
0.3–0.7 units/mL.
UFH (Unfractionated Heparin)
Indirect thrombin inhibitor; binds antithrombin III to inactivate thrombin & factor Xa.
Primary use of UFH
DVT prevention (SQ) and treatment (IV).
Route of administration for UFH
SQ for prophylaxis, IV continuous infusion for treatment.
Onset of action for UFH (IV)
Immediate.
Onset of action for UFH (SQ)
Slower onset.
Dosing strategy for UFH
Weight-based; IV via infusion pump.
Monitoring considerations for UFH
aPTT (primary) or anti-factor Xa level.
Therapeutic anti-Xa monitoring in UFH
0.3–0.7 units/mL.
Lab timing for UFH monitoring
aPTT or anti-Xa checked 6 hours after initiation and after each dose change.
Half-life of UFH
~60 minutes (IV).
Bleeding risk with UFH
HIGH if aPTT > 100 seconds.
HIT (Heparin-Induced Thrombocytopenia) risk with UFH
Higher with both Type 1 and Type 2.
Pregnancy considerations for UFH
Not preferred.
Reversal agent for UFH
Protamine sulfate.
LMWH (Low-Molecular-Weight Heparin)
Indirect thrombin inhibitor with greater anti-Xa activity.
Primary use of LMWH
Treatment of some DVT cases; VTE prophylaxis.
Dosing for LMWH
Weight-based; varies by product and institutional protocol.
Monitoring for LMWH
Not routinely required; monitor renal function.
HIT risk with LMWH
Lower risk than UFH.
Direct Thrombin Inhibitors (DTIs)
Directly inhibits thrombin to prevent conversion of fibrinogen to fibrin.
Examples of DTIs
Bivalirudin, Argatroban, Dabigatran.
Direct Factor Xa Inhibitors
Directly inhibits factor Xa to prevent clot formation.
Examples of Direct Factor Xa Inhibitors
Rivaroxaban, Apixaban, Edoxaban.
Onset of action for DTIs and Factor Xa Inhibitors
Rapid; predictable pharmacokinetics.
Monitoring for DTIs
Not routinely required; renal and hepatic function as indicated.
Reversal agent for Dabigatran
Idarucizumab (Praxbind) for emergencies.
Oral anticoagulant example
Warfarin (Coumadin).
MOA of Warfarin
Vitamin K antagonist that inhibits vitamin K-dependent clotting factors.
Primary use of Warfarin
Long-term anticoagulation for DVT, PE, AF.
Onset of Warfarin
SLOW; full effect takes 3–5 days.
Bridging therapy for Warfarin
Requires bridging with heparin until INR is therapeutic.
Drug/food interactions with Warfarin
Vitamin K can reduce effects; many drugs can enhance or reduce.
Bleeding risk with Warfarin
Narrow therapeutic window increases hemorrhage risk.
Reversal for Warfarin
Vitamin K (phytonadione); Fresh frozen plasma (FFP) for urgent reversal.
Thrombolytic therapy
Fibrinolytic agents that actively lyse and dissolve existing thrombi.
Examples of thrombolytics
Alteplase (Activase), Reteplase.
Indication for thrombolytic therapy
Reserved for life-threatening limb ischemia due to massive thrombosis.
Risks associated with thrombolytic therapy
Significantly higher bleeding risk.
Management for HIT Type 2
STOP all heparin and initiate a non-heparin anticoagulant.
4Ts scoring system
Used for pretest probability assessment of HIT.
Pharmacologic MOA of Heparins
Indirectly inhibits thrombin and factor Xa activity.
Monitoring frequency for Warfarin
Once INR is stable: weekly for 2–4 weeks, then monthly.
Indicators of HIT
Platelet count drop ≥50% from baseline.
Adjustments for renal insufficiency with LMWH
Lower doses may be required.
Patient education for anticoiougulant therapy
Educate on bleeding precautions and medication adherence.
Bleeding assessment points for anticoagulants
Monitor for gums, bruising, hematuria, melena.
Continuous monitoring requirements for UFH
aPTT or anti-Xa monitoring.
Signs of bleeding to check for
Gums, epistaxis, hematuria, bruising, tarry stools.
Importance of INR monitoring with Warfarin
Critical for safe and effective anticoagulation.
HIT Type 1 description
Mild, transient platelet decrease, prevalent in 10-20% of patients.
HIT Type 2 description
Autoimmune, severe platelet decrease, often leads to thromboemboli.
Tertiary assessments for anticoagulants
Ensure adherence to medications; assess renal function.
Signs of thrombocytopenia
Platelet count below the normal range.
Major risk factors for thrombolytic therapy complications
Older age, low body weight, uncontrolled hypertension.
Ongoing assessments during thrombolytic therapy
Monitor vital signs and neurologic status.
Urgent interventions for acute thromboembolism
Immediate clot lysis with thrombolytic agents.
Venous Thrombosis
Formation of a blood clot in a vein.
Deep Vein Thrombosis (DVT)
A specific type of venous thrombosis occurring in the deep veins, typically of the legs.
Thrombophlebitis
Inflammation of a vein associated with a blood clot.
Venous Thromboembolism (VTE)
A condition that includes both DVT and pulmonary embolism.
Phlebothrombosis
The formation of a thrombus in a vein without inflammation.
Virchow's Triad
The three factors that contribute to thrombosis: stasis of blood, vessel wall injury, and altered coagulation.
Stasis of Blood
Slowed blood flow caused by various factors like immobility or varicose veins.
Vessel Wall Injury
Damage to the blood vessel wall due to trauma or invasive procedures.
Altered Coagulation
Changes in blood coagulation factors that can increase the risk of clotting.
Hypercoagulability
An increased tendency of blood to clot, which can be due to genetic or acquired factors.
Clinical Manifestations of DVT
Symptoms include leg circumference difference, erythema, warmth, tenderness, fever, and dilated veins.
Risk Factors for DVT
Includes history of varicose veins, cancer, old age, BMI > 35, and recent major surgery.
Prevention of DVT
Strategies include use of compression stockings, exercise, and anticoagulant medications.
Medical Management of DVT
Includes heparin, oral anticoagulants, and thrombolytic therapy.
Nursing Management for DVT
Involves monitoring labs, administering medications, and promoting ambulation.
Inferior Vena Cava (IVC) Filter
A device placed in the IVC to prevent blood clots from reaching the lungs.
Varicose Veins
Enlarged veins caused by malfunctioning valves leading to blood pooling.
Clinical Manifestations of Varicose Veins
Symptoms include dull aches, muscle cramps, and lower extremity fatigue.
Diagnosis of Varicose Veins
Key diagnostic methods include venous duplex scan and air plethysmography.
Prevention Strategies for Varicose Veins
Includes avoiding tight clothing, frequent position changes, and elevating legs.
Surgical Management for Varicose Veins
Options include ligation & stripping, sclerotherapy, and ablation.
Post-Phlebitic Syndrome
A condition resulting from valve injury leading to chronic venous issues.
Clinical Manifestations of Post-Phlebitic Syndrome
Includes edema, hemosiderosis, and varicosities.
Management of Post-Phlebitic Syndrome
Strategies include leg elevation, compression stockings, and walking.
Vascular Ulcers
Ulcers that occur due to insufficient vascular supply or pressure.
Pathophysiology of Vascular Ulcers
Results primarily from increased venous pressure or ischemia.
Management of Venous Ulcers
Includes wound cleaning, debridement, and possible antibiotic treatment.
Debridement Types for Ulcers
Methods include surgical, wet-to-dry, enzymatic, and autolytic.
Lymphedema
Swelling due to accumulation of lymph fluid from obstruction or damage.
Clinical Manifestations of Lymphedema
Soft tissue swelling that progresses to firm, non-pitting edema.
Stemmer Sign
A test indicating lymphedema; inability to pinch a thin fold of skin.
Management of Lymphedema
Includes compression, exercise, and potential surgical intervention.
Cellulitis
An acute bacterial skin infection characterized by inflammation.