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Hematology, oncology > Drugs > Flashcards

Drugs Flashcards

1
Q

Xa reversal agent

A

Andexxa (recombinant Xa, very expensive)

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2
Q

Dabigatran reversal agent

A

Idarucizumab

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3
Q

Xa inhibitors

A

rivaroxaban, apixaban, betrixaban and edoxaban

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4
Q

warfarin onset

A

48 to 72 hours

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5
Q

how does heparin work

A

by activating antithrombin III, which blocks thrombin from clotting blood.

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6
Q

use of LMWH

A

does not require monitoring of the APTT coagulation parameter and has fewer side effects.

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7
Q

why are NOACs better than warfarn

A

relatively short half life + rapid onset

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8
Q

inherited thrombophilias

A 
Lupus anticoagulant 
Prothrombin gene mutation
Protein S
Factor V Leiden
Antithrombin 3 deficiency
Protein C
APS
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9
Q

Lovenox class

A

LMWH

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10
Q

LMWH drugs

A

dalteparin, fondaparinux, enoxaparin

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11
Q

fondaparinux trade name

A

Arixtra

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12
Q

direct thrombin inhibitors

A

argatroban, dabigatran

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13
Q

acquired VTE conditions

A

antiphospholipid syndrome, paroxysmal nocturnal hemoglobinuria (PNH), disseminated intravascular coagulation (DIC)

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14
Q

NOAC encompasses

A

Direct thrombin inhibitors + Xa inhibitors

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15
Q

cryoprecipitate

A
  • FFP that is centrifuged, then you collect precipitate.
  • fibrinogen (factor I), factor VIII, factor XIII, von Willebrand factor (VWF), and fibronectin derived from one unit of Fresh Frozen Plasma (FFP).
  • Cryoprecipitate (cryo) contains a concentrated subset of FFP components including fibrinogen, factor VIII coagulant, vonWillebrand factor, and factor XIII. Cryo IS NOT just a concentrate of FFP. In fact, a unit of cryo contains only 40-50% of the coag factors found in a unit of FFP, but those factors are more concentrated in the cryo.
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16
Q

cryoprecipitate uses

A

hypofibrinogenemia, vonWillebrand disease, and in situations calling for a “fibrin glue.”

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17
Q

FFP clinical use

A

MULTIPLE factor deficiencies and active BLEEDING.

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18
Q

How does irradiation work for blood transfusions?

A

Irradiation is needed to destroy all living leukocytes (white blood cells), particularly lymphocytes that could cause transfusion associated graft versus host disease (TAGVD).

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19
Q

leukocyte reduction

A

Red blood cell and platelet units may be filtered to remove most of the leukocytes (white blood cells). This may reduce the risk for febrile transfusion reactions, may help prevent alloimmunizaton to MHC (HLA) donor antigens, and help reduce the risk for cytomegalovirus (CMV) infection.

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20
Q

washed RBCs

A

A unit of packed red blood cells (PRBCs) is washed to reduce plasma proteins. This reduces the risk for allergic transfusion reactions. Washing reduces immunoglobulins, such as anti-IgA that could cause anaphylactic transfusion reactions in persons with selective IgA deficiency.

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21
Q

Use of flow cytometry

A

evaluate for clonal populations of cells

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22
Q

What is a mixing study?

A

Test performed on blood plasma of patients or test subjects to distinguish factor deficiencies from factor inhibitors, such as lupus anticoagulant, or specific factor inhibitors, such as antibodies directed against factor VIII. The purpose is to determine the cause of prolongation of PT, Partial Thromboplastin Time, or sometimes of thrombin time (TT).

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23
Q

how a mixing study works

A

If the problem is a simple factor deficiency, mixing the patient plasma 1:1 with plasma that contains 100% of the normal factor level results in a level ≥50% in the mixture (say the patient has an activity of 0%; the average of 100% + 0% = 50%).[3] The PT or PTT will be normal (the mixing study shows correction). Correction with mixing indicates factor deficiency; failure to correct indicates an inhibitor.

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24
Q

colony stimulating factor medications + caveat

A
  • GCSF
  • Neupogen, Granix and Zarxio and trade names for G-CSF
  • Can’t get neulasta inpatient, only granix
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25
Q

jadenu

A

deferasirox (treatment for iron overload)

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26
Q

function of PD-1

A

This receptor is generally responsible for preventing the immune system from attacking the body’s own tissues; it is a so-called immune checkpoint.

27
Q

pembrolizumab mechanism

A

Blocks PD-1 located on lymphocytes. This receptor is generally responsible for preventing the immune system from attacking the body’s own tissues; it is a so-called immune checkpoint.

28
Q

pembrolizumab trade name

A

keytruda

29
Q

anastrozole trade name

A

arimidex

30
Q

prolia generic name + use

A
  • denosumab

- It can treat osteoporosis and hypercalcemia.

31
Q

source of stem cells for nonmalignant HCT and why

A

Bone marrow - Contains a lower dose of T cells and confers a lower risk of graft-versus-host disease (GVHD).

32
Q

cyclophosphamide trade name

A

cytoxin

33
Q

cyclophosphamide chemo mechanism

A

crosslinking leading to apoptosis

34
Q

adeno tumor markers

A

1) PD-L1
2) ROS-1
3) EGFR
4) ALK
5) BRAF
6) KRAS

35
Q

TXA mechanism

A

antifibrinolytic

36
Q

TXA use

A

heavy vaginal bleeding

vWF

37
Q

blast crises in CML defined as any of the following…

A

≥20 percent peripheral blood or bone marrow blasts [3]
●Large foci or clusters of blasts on the bone marrow biopsy [4]
●Presence of extramedullary blastic infiltrates (eg, myeloid sarcoma also known as granulocytic sarcoma or chloroma)

38
Q

AI’s

A

There are 3:
exemestine
anastrozole
lestrozole

39
Q

tumors that metastasize to bone

A

prostate, breasts, lungs, thyroid, and kidneys

40
Q

xgeva generic name

A

denosumab

41
Q

capecitabine mechanism

A

metabolised to 5-FU which in turn is a thymidylate synthase inhibitor

42
Q

HER2 directed drugs

A

trastuzumab, pertuzumabm lapatinib

43
Q

perjeta generic name

A

pertuzumab

44
Q

paclitaxel mechanism

A

microtubule inhibition

45
Q

medication approved for breast cancer BRCA patients

A

olaparib

46
Q

preferred endocrine therapy for postmenopausal women

A

aromatase inhibitor (AI) rather than tamoxifen.

47
Q

NOAC with lowest GI bleed risk

A

eliquis

48
Q

when NOAC’s can be restarted following bleed

A

2 weeks following resolution of bleed

49
Q

sorafenib

A

protein kinase inhibitor

50
Q

TKI’s approved for CML

A

imatinib, dasatinib, and nilotinib

51
Q

vitamin k dependent clotting factors

A

II, VII, IX, and X.

52
Q

Primary cisplatin contraindication

A

CKD

53
Q

DOAC contraindications

A

1) elevated INR because of liver disease
2) severe renal impairment (CrCl <30)
3) BMI >40

54
Q

risk of XRT to chest

A

CAD and LV dysfunction

55
Q

difference in coverage between zosyn and cefepime

A

lose anaerobe coverage

56
Q

pradaxa generic name

A

dabigatran

57
Q

pradaxa problem

A 
pH sensitive (problem with PPI's), which causes decreased GI absorption.
Try to avoid using it.
58
Q

interactions with NOACs

A

cyp450

59
Q

intracranial hemorrhage and AC

A

NOACs as a class better than warfarin, but apixaban

60
Q

GI bleed and AC

A

apixaban has less GI bleed risk, but other NOACs have the same or possibly slightly higher risk of GI bleed

61
Q

AC and fall risk

A

It’s overblown, there’ve been studies looking in it, and there’s no significantly increased risk. Intracranial bleeds are rare and intracranial bleeds related to falls are even more rare.

62
Q

definition of anemia in men and women

A

below 12 Hgb in women, 13.5 in men

63
Q

therapeutic Xa level on heparin ggt

A

UH: 0.3-0.7 IU/mL

Hematology, oncology (218 decks)

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