Unit 12: Hematology Flashcards
Venous thrombi are formed due to
Venous stasis, vascular endothelial wall injury, hypercoagulability
Risk factors for venous thrombus
Prolonged immobility, varicose veins, obesity, pregnancy, recent surgery, thrombophilia
Major source of pulmonary embolism
DVT in lower extremity
A fibrillation
Loss of coordination of electrical and mechanical activity in atria; thrombi can form in left atrial appendage due to impaired ventricle filling and incomplete emptying of atria
Goals of A fib treatment
Prevention of TIA with anticoagulants, restore SR, control of ventricular rate
Mechanical prosthetic valves require
Lifelong anticoagulation
Final step in clotting cascade
Formation of thrombin (IIA)
Converts fibrinogen to fibrin to form a clot
Extrinsic clotting pathway
Initiated by components from blood with factor VII as initiating factor
Intrinsic clotting pathway
Initiated when blood comes into contact with foreign surface such as a prosthetic device
Factor XII is initiating factor
Both clotting pathways converge at
Factor X
Converts prothrombin to thrombin
Antithrombin III
Blocks clotting factors IIa, VIIa, IXa, Xa, XIa, XIIa
Protein C, S, Z
Prevent excess clot formation by inactivating Va and VIIIa
Venous thrombi form in
Areas of sluggish blood flow and contain primarily red cells held together with fibrin
Arterial thrombi form in
Areas of high blood flow and composed primarily of platelets bound with fibrin strands
S/S of DVT
erythema, pain, swelling, venous distention, warmth
50% have no symptoms
Increased D-Dimer
Gold standard for diagnosing a DVT
Contrast enhanced venography
S/S A fib
Palpitations, chest pain, SOB, weakness, decreased BP, dizziness, syncope, irregular pulse
ECG for A Fib
Irregularly irregular rhythm, absence of P waves, ventricular rate 100-180
Heparin indicated for
Treatment and prevention of VTE and acute coronary syndromes and hospitalized patients undergoing cardiac procedures
Warfarin indicated for
Prevention of valve thrombosis, prevention of VTE in orthopedic or abdominal surgery and tx/prevention of VTE
CI to anticoagulation
Recent hemorrhagic stroke, active major bleeding, recent trauma or surgery, immediate postop after CNS or ocular surgery, aneurysms
Warfarin CI in pregnancy
Unfractionated heparin
Inhibits reactions that lead to clotting but does not alter concentration of normal clotting factors
Binds to antithrombin III and increases inactivation rate of intrinsic clotting cascade pathway and thrombin
Must be given parenterally
Immediate onset
Monitor PTT
Indications for unfractionated heparin
Immediate tx of acute DVT, PE or unstable angina
Low molecular weight heparin
Produce major effect via thrombin and clotting factor X
Used for prophylaxis of VTE due to surgery or decreased mobility
Longer half life than UFH
Greater bioavailability
Less intense lab monitoring and more predictable anticoagulant effect
3 available agents of low molecular weight heparin
Dalteparin, enoxaparin, tinzaparin
Warfarin
Inhibits activation of clotting factors in liver that depend on vitamin K–2, 7, 9, 10 and protein C, Z, S
Does not effect function of existing clotting factors and has no effect on existing thrombus
Long onset of effect–8-14 days until full effect
Monitor INR
Warfarin causes an initial fall in
Protein C–hypercoagulable state
Must heparinize initially
Downfalls of warfarin
Multiple drug-drug interactions, very narrow therapeutic index, and requires lab monitoring every 4-6 weeks
Direct acting oral anticoagulants
Dabigatran, Rivaroxaban, apixaban, edoxaban
Faster onset of action than warfarin and has fixed dosing, no dietary interaction and no intense lab monitoring required
More expensive, no antidote and faster offset
Recommendation to reverse Warfarin induced bleeding
Four factor prothrombin complex concentrates
Antidote to heparin
Protamine sulfate
Heparin induced thrombocytopenia
Antibody mediated prothrombotic reaction
Much lower risk with LMWH as opposed to UFH
D/C heparin and give alternative anticoagulant
Antiplatelet agents
prevention or treatment of stroke, add on therapy to anticoagulants, prevent CV death, MI or stroke following acute coronary syndrome
Aspirin
Prevents prostaglandin synthesis in platelets by irreversible inhibiting COX which blocks conversion to TXA2
Has effects for lifespan of platelet (7-10 days)
Clopidogrel
Inhibits ADP, which is a promoter of platelet receptor binding
Most appropriate therapy for DVT or PE
All patients should receive bolus IV UFH followed by continuous IV infusion of UFH; SC LMWH and oral rivaroxaban or apixaban as initial therapy
Injectable UFH/LMWH followed by warfarin or direct thrombin inhibitor for at least 3 months
Most appropriate therapy for prophylaxis of DVT or PE
For patients undergoing orthopedic surgery
LMWH, fondaparinus, Warfarin, apixaban, rivaroxaban, aspirin
Prevention of ischemic stroke and TIA
Aspirin is first line
Clopidogrel is second line
Stroke prevention in non valvular atrial fibrillation
Warfarin or direct thrombin inhibitor if high risk
Prophylaxis against systemic embolism in patients with prosthetic heart valves
Long term anticoagulation with warfarin alone or in combo with aspirin
Anemia values
RBC < 13 in men and <12 in women
Acute post-hemorrhagic anemia/chronic blood loss
Initial increase in RBC, HgB and Htc followed by dilution
Immediate therapy: hemostasis, restoration of blood volume and treatment of shock with blood transfusion
Sickle cell anemia
Abnormal Hgb leads to chronic hemolytic anemia
Susceptible to infection
Vaccinations + folic acid supplementation important
Hydroxyurea
Can be used for prophylaxis of sickle cell crises
Increases Hgb F, increases water content of RBC, increases deformability of sickled cells and altering RBC adhesions
Pain management of sickle cell crisis
Hydration, aggressive pain relief with analgesics and opiates (NSAIDs, acetaminophen, morphine, hydromorphone)
Diagnostic lab findings in iron deficiency anemia
Decreased serum iron, decreased ferritin, increased TIBC
Tx of iron deficiency anemia
Dietary supplementation or iron preparation
Anemia of chronic renal failure
Decreased EPO production by kidney due to low GFR
Iron supplementation given first
Then treat reversible causes of decreased renal function
Then give recombinant EPO (Epoetin, epogen, procrit)
Anemia of chronic disease
Associated with infection, organ failure, trauma, inflammation, neoplasia
Decreased serum iron, transferrin and TIBC
MCV normal
Tx aimed at eliminating exacerbating factors
Increased doses of epoiten administered subcu
Thalassemia
Hereditary disorder of Hgb synthesis
Decreased production of either alpha or beta globins
Treat severe thalassemia with regular transfusion and folate supplementation
tx of vitamin B12 deficiency in pernicious anemia
Parenteral administration of B12 every month for the rest of the life
Folate deficiency tx
Oral replacement therapy until corrected
Aplastic anemia tx
RBC transfusions and platelets given for bleeding and antibiotics for infection
Severe forms may require stem cell transplant and immunosuppressive therapy
