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
Q

3 available agents of low molecular weight heparin

A

Dalteparin, enoxaparin, tinzaparin

26
Q

Warfarin

A

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
Q

Warfarin causes an initial fall in

A

Protein C–hypercoagulable state

Must heparinize initially

28
Q

Downfalls of warfarin

A

Multiple drug-drug interactions, very narrow therapeutic index, and requires lab monitoring every 4-6 weeks

29
Q

Direct acting oral anticoagulants

A

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
Q

Recommendation to reverse Warfarin induced bleeding

A

Four factor prothrombin complex concentrates

31
Q

Antidote to heparin

A

Protamine sulfate

32
Q

Heparin induced thrombocytopenia

A

Antibody mediated prothrombotic reaction
Much lower risk with LMWH as opposed to UFH
D/C heparin and give alternative anticoagulant

33
Q

Antiplatelet agents

A

prevention or treatment of stroke, add on therapy to anticoagulants, prevent CV death, MI or stroke following acute coronary syndrome

34
Q

Aspirin

A

Prevents prostaglandin synthesis in platelets by irreversible inhibiting COX which blocks conversion to TXA2
Has effects for lifespan of platelet (7-10 days)

35
Q

Clopidogrel

A

Inhibits ADP, which is a promoter of platelet receptor binding

36
Q

Most appropriate therapy for DVT or PE

A

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
Q

Most appropriate therapy for prophylaxis of DVT or PE

A

For patients undergoing orthopedic surgery

LMWH, fondaparinus, Warfarin, apixaban, rivaroxaban, aspirin

38
Q

Prevention of ischemic stroke and TIA

A

Aspirin is first line

Clopidogrel is second line

39
Q

Stroke prevention in non valvular atrial fibrillation

A

Warfarin or direct thrombin inhibitor if high risk

40
Q

Prophylaxis against systemic embolism in patients with prosthetic heart valves

A

Long term anticoagulation with warfarin alone or in combo with aspirin

41
Q

Anemia values

A

RBC < 13 in men and <12 in women

42
Q

Acute post-hemorrhagic anemia/chronic blood loss

A

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
Q

Sickle cell anemia

A

Abnormal Hgb leads to chronic hemolytic anemia
Susceptible to infection
Vaccinations + folic acid supplementation important

44
Q

Hydroxyurea

A

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
Q

Pain management of sickle cell crisis

A

Hydration, aggressive pain relief with analgesics and opiates (NSAIDs, acetaminophen, morphine, hydromorphone)

46
Q

Diagnostic lab findings in iron deficiency anemia

A

Decreased serum iron, decreased ferritin, increased TIBC

47
Q

Tx of iron deficiency anemia

A

Dietary supplementation or iron preparation

48
Q

Anemia of chronic renal failure

A

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
Q

Anemia of chronic disease

A

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
Q

Thalassemia

A

Hereditary disorder of Hgb synthesis
Decreased production of either alpha or beta globins
Treat severe thalassemia with regular transfusion and folate supplementation

51
Q

tx of vitamin B12 deficiency in pernicious anemia

A

Parenteral administration of B12 every month for the rest of the life

52
Q

Folate deficiency tx

A

Oral replacement therapy until corrected

53
Q

Aplastic anemia tx

A

RBC transfusions and platelets given for bleeding and antibiotics for infection
Severe forms may require stem cell transplant and immunosuppressive therapy