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Pharmacology > Unit 12: Hematology > Flashcards

Unit 12: Hematology Flashcards

1
Q

Venous thrombi are formed due to

A

Venous stasis, vascular endothelial wall injury, hypercoagulability

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2
Q

Risk factors for venous thrombus

A

Prolonged immobility, varicose veins, obesity, pregnancy, recent surgery, thrombophilia

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3
Q

Major source of pulmonary embolism

A

DVT in lower extremity

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4
Q

A fibrillation

A

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

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5
Q

Goals of A fib treatment

A

Prevention of TIA with anticoagulants, restore SR, control of ventricular rate

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6
Q

Mechanical prosthetic valves require

A

Lifelong anticoagulation

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7
Q

Final step in clotting cascade

A

Formation of thrombin (IIA)

Converts fibrinogen to fibrin to form a clot

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8
Q

Extrinsic clotting pathway

A

Initiated by components from blood with factor VII as initiating factor

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9
Q

Intrinsic clotting pathway

A

Initiated when blood comes into contact with foreign surface such as a prosthetic device
Factor XII is initiating factor

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10
Q

Both clotting pathways converge at

A

Factor X

Converts prothrombin to thrombin

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11
Q

Antithrombin III

A

Blocks clotting factors IIa, VIIa, IXa, Xa, XIa, XIIa

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12
Q

Protein C, S, Z

A

Prevent excess clot formation by inactivating Va and VIIIa

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13
Q

Venous thrombi form in

A

Areas of sluggish blood flow and contain primarily red cells held together with fibrin

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14
Q

Arterial thrombi form in

A

Areas of high blood flow and composed primarily of platelets bound with fibrin strands

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15
Q

S/S of DVT

A

erythema, pain, swelling, venous distention, warmth
50% have no symptoms
Increased D-Dimer

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16
Q

Gold standard for diagnosing a DVT

A

Contrast enhanced venography

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17
Q

S/S A fib

A

Palpitations, chest pain, SOB, weakness, decreased BP, dizziness, syncope, irregular pulse

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18
Q

ECG for A Fib

A

Irregularly irregular rhythm, absence of P waves, ventricular rate 100-180

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19
Q

Heparin indicated for

A

Treatment and prevention of VTE and acute coronary syndromes and hospitalized patients undergoing cardiac procedures

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20
Q

Warfarin indicated for

A

Prevention of valve thrombosis, prevention of VTE in orthopedic or abdominal surgery and tx/prevention of VTE

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21
Q

CI to anticoagulation

A

Recent hemorrhagic stroke, active major bleeding, recent trauma or surgery, immediate postop after CNS or ocular surgery, aneurysms
Warfarin CI in pregnancy

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22
Q

Unfractionated heparin

A

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

23
Q

Indications for unfractionated heparin

A

Immediate tx of acute DVT, PE or unstable angina

24
Q

Low molecular weight heparin

A

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

25
3 available agents of low molecular weight heparin
Dalteparin, enoxaparin, tinzaparin
26
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
27
Warfarin causes an initial fall in
Protein C--hypercoagulable state | Must heparinize initially
28
Downfalls of warfarin
Multiple drug-drug interactions, very narrow therapeutic index, and requires lab monitoring every 4-6 weeks
29
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
30
Recommendation to reverse Warfarin induced bleeding
Four factor prothrombin complex concentrates
31
Antidote to heparin
Protamine sulfate
32
Heparin induced thrombocytopenia
Antibody mediated prothrombotic reaction Much lower risk with LMWH as opposed to UFH D/C heparin and give alternative anticoagulant
33
Antiplatelet agents
prevention or treatment of stroke, add on therapy to anticoagulants, prevent CV death, MI or stroke following acute coronary syndrome
34
Aspirin
Prevents prostaglandin synthesis in platelets by irreversible inhibiting COX which blocks conversion to TXA2 Has effects for lifespan of platelet (7-10 days)
35
Clopidogrel
Inhibits ADP, which is a promoter of platelet receptor binding
36
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
37
Most appropriate therapy for prophylaxis of DVT or PE
For patients undergoing orthopedic surgery | LMWH, fondaparinus, Warfarin, apixaban, rivaroxaban, aspirin
38
Prevention of ischemic stroke and TIA
Aspirin is first line | Clopidogrel is second line
39
Stroke prevention in non valvular atrial fibrillation
Warfarin or direct thrombin inhibitor if high risk
40
Prophylaxis against systemic embolism in patients with prosthetic heart valves
Long term anticoagulation with warfarin alone or in combo with aspirin
41
Anemia values
RBC < 13 in men and <12 in women
42
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
43
Sickle cell anemia
Abnormal Hgb leads to chronic hemolytic anemia Susceptible to infection Vaccinations + folic acid supplementation important
44
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
45
Pain management of sickle cell crisis
Hydration, aggressive pain relief with analgesics and opiates (NSAIDs, acetaminophen, morphine, hydromorphone)
46
Diagnostic lab findings in iron deficiency anemia
Decreased serum iron, decreased ferritin, increased TIBC
47
Tx of iron deficiency anemia
Dietary supplementation or iron preparation
48
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)
49
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
50
Thalassemia
Hereditary disorder of Hgb synthesis Decreased production of either alpha or beta globins Treat severe thalassemia with regular transfusion and folate supplementation
51
tx of vitamin B12 deficiency in pernicious anemia
Parenteral administration of B12 every month for the rest of the life
52
Folate deficiency tx
Oral replacement therapy until corrected
53
Aplastic anemia tx
RBC transfusions and platelets given for bleeding and antibiotics for infection Severe forms may require stem cell transplant and immunosuppressive therapy

Pharmacology (56 decks)

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