Unit 12: Hematologic Flashcards

1
Q

What are reversible risk factors for DVT and PE?

A

trauma, surgery, pregnancy, estrogen therapy, immobility, fractures, obesity

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2
Q

What are acquired risk factors for DVT and PE?

A

age >40, malignancy, h/o thrombus, HF, CVA, nephrotic syndrome, spinal cord injury, varicose veins

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3
Q

What are inherited factors for DVT and PE?

A

activated protein C resistance, antithrombin III deficiency, protein C deficiency, factor V Lieden

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4
Q

What is Virchow’s triad and how is it significant?

A

Triad is venous stasis (sluggish blood flow), vascular endothelial wall injury, and hyper coagulability (propensity for increased blood clotting). It helps to categorize most common causes and risk factors for venous thromboembolism.

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5
Q

What are cardioembolic causes of of CVA?

A

Afib, left atrial appendage, rheumatic heart disease, HF w/ LV thrombus, PFO, Myxoma, IE, DCM, Prosthetic valves

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6
Q

what are two major categories of CVA?

A

ischemic 85% and hemorrhagic 15%

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7
Q

what are antithrombin III, Activated protein C and activated protein S?

A

Natural anticoagulants–deficiencies in these can induce prothrombotic state corresponding to 5-10 fold increase in VTE risk.

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8
Q

How are “massive” and “submissive” PEs defined?

A

Massive is >50% of pulmonary vasculature, submassive is <50%

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9
Q

What d-dimer level indicates probably thrombosis?

A

> 500

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10
Q

What drug class is Pradaxa? How is it eliminated?

A

Direct Thrombin Inhibitor. 80% really eliminated. NOT CYP450, so few interactions. QUINIDINE is one, however

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11
Q

What drug class is Xarelto (rivaroxiban) and Eliquis (apixiban)? How are they metabolized?

A

Direct factor Xa inhibitor. CYP3A4.

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12
Q

What is the starting dose of unfractionated heparin? What is the target aPTT?

A

80U/kg as IV bolus then 18U/kg/hr as continuous infusion. 1.5-2.5x control

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13
Q

What anticoagulants produce effect through extrinsic pathway? Intrinsic?

A

Oral anticoagulants extrinsic, heparin intrinsic.

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14
Q

When does the initial prolongation of bleeding time occur w/ warfarin therapy? When does it evert full effect?

A

1-3 days.

8-14 days, when factor II is depleted

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15
Q

How does warfarin work?

A

Inhibits activation of clotting factors in the liver that depend on vitamin K for synthesis-II, VII, IX, and X.

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16
Q

What is the half life of warfarin?

A

36-42 hours

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17
Q

What is the time needed for peak plasma concentration of dabigitran (pradaxa)?

A

1.5-3 hours

18
Q

How long after dc’ing ASA are platelets still impaired?

A

7-10 days

19
Q

How are plavix and asa different?

A

asa affects COX, Plavix does not.

20
Q

What is the only PPI safe to take with Plavix?

A

Protonix

21
Q

What is first and second line therapy for DVT or PE?

A

Bolus of IV UFH with subsequent infusion/subcutaneous LMWHs/subcutaneous fondaparinux.

22
Q

What is first and second line therapy for prophylaxis of DVT and PE in ortho patients?

A

First line, LMWHs or warfarin, depending on institution. Second line, UFH started preop and SCDs.

23
Q

What is first and second line therapy for secondary stroke prevention (noncardioembolic ischemic stroke)?

A

First line, asa (or Plavix). Second line, Plavix or Aggrenox

24
Q

What is first and second line therapy for cardioembolic stroke prevention (AF)?

A

First line, warfarin (and now paradox). Second line, asa

25
Q

What is first line therapy for prevention of systemic embolism w/ patients with artificial valves?

A

First line, warfarin. Second, asa

26
Q

Where does RBC production start?

A

Starts with erythropoietin which is produced by kidneys

27
Q

What do reticulocytes in peripheral blood indicate?

A

RBC production is being stimulated

28
Q

How are anemias classified?

A

increased destruction as in blood loss, hemolysis, sickle cell or decreased production as in ion deficiency, thalassemia, anemia of chronic disease and aplastic anemia

29
Q

What are treatments for sickle cell?

A

hydroxurea and folic acid

30
Q

What is the earliest and most sensitive indication of iron deficiency?

A

ferritin level <0-12g/L

31
Q

What is the normal dose of iron supplementation in anemia?

A

2-3mg/kg/d in TID dosing

32
Q

what is expected increase in hub with iron supplementation?

A

Increase of 0.7-1.0 g/wk-continue 3-6 months

33
Q

What meds interact the most with iron?

A

tetracyclines and fluorquinolones

34
Q

What is usual dose of Epoetin?

A

50-100u/kg sc or iv 3x wkly

35
Q

What causes anemia of chronic disease?

A

chronic infection, subacute bacterial endocarditis, inflammation, TB, malignancies

36
Q

What affects can iron deficiency have on pediatric patients?

A

impaired mental/psychomotor development

37
Q

In treating anemia of chronic disease, what would indicate a good response?

A

increase of more than 0.5g/dL after 2 weeks

38
Q

What causes aplastic anemia?

A

NSAIDS, sulfas, quinidine, lithium, antiprotazoals

39
Q

What causes vitamin B12 deficiency?

A

inadequate intake, lack of intrinsic factor, H. Pylori, or malignancy.

40
Q

What B12 level is indicative of deficiency?

A

<200

41
Q

What folate level is indicative of deficiency?

A

<4ng/ml