Hematology And Oncology Pharm

Front 1

MOA of Heparin

Back 1

Activates Antithrombin which decreases thrombin and factor Xa

Front 2

Clinical use of Heperin?

Monitor using what?

Back 2

Can be used for just about any acute issue (MI, DVT, PE, acute coronary syndrome)

Very short half life (IV). Must be monitored with PTT!

Front 3

Treatment for Heperin overdose?

Back 3

Protamine sulfate (positevly charged molecule which binds to the negatively charged heparin)

Front 4

SE of Heparin

Back 4

Bleeding
Thrombocytopenia (HIT)
Osteoporosis

Front 5

What is Heparin induced thrombocytopenia?

Back 5

Develop IgG antibodies against platelet factor 4 (activates platelets).

IgG + Hep + PF4 activate many platelets leading to thrombosis but you use them up leading to thrombocytopenia

Front 6

What is the IgG made against in Heparin induced thrombocytopenia?

Back 6

IgG against platelet factor 4

Front 7

What is enoxaparin and dalteparin?

Back 7

Low molecular weight heparin?

Front 8

What is the clinical use of low molecular weight heparin (Enoxaparin and Dalteparin)

Back 8

Mainly work on Factor Xa.

Longer half life and can be used orally. Do not require intense laboratory monitor.

Not reversible though.

Front 9

Lepirudin, bivalirudin, desaruin and argatroban

MOA?

Back 9

Inhibit thrombin (come from leeches)

Used as a alternative to Heparin

Front 10

These drugs are used as a replacement for heparin especially in HIT patients

Back 10

Lepirudin, Bivalirudin, Desarudin, Argatroban

Front 11

Warfarin aka Coumadin

MOA? What is the normal role of Vitamin K?

Back 11

Inhibits epoxide reductase which activates VItamin K

The normal role of Vitamin K in the body is to carboxylate factors C, S, 2,7, 9, 10

Front 12

What factors are carboxylated/activated by Vitamin K?

Back 12

1972 + C + S

(10, 9, 7, 2)

Front 13

How do you monitor Warfarin?

What is the worldwide recognized name?

Back 13

PT (it should increase) aka for EXTRINSIC pathway

INR

Front 14

Clinical use of Warfarin

Back 14

Used for many long term things:

prevent stroke in A-fib pt., venous thromboembolosim prophylaxis

Front 15

Which can you use in pregnancy warfarn or Heparin?

Back 15

HEPARIN!!

Warfarin crosses the placenta and causes a mess!!

Front 16

Warfarin has many DDI b/c it is metabolized in the ________________ (what organ)?

Back 16

Liver's P450 enzyme.

IMPORTANT!

Front 17

SE of Warfarin

Back 17

Bleeding
Teratogenic
DDI

Front 18

Treatment for warfarin overdose?

Back 18

Vitamin K and fresh frozen plasma (b/c Vitamin K doesn't work right away)

Front 19

69 year old female has A-fib but we can't cardiovert her right away b/c we are scared to blow the clot to her brain. Thus she is started on warfarin therapy. Heparin is also started with it. WHY?

Back 19

Warfarin initially inhibits C+s first. Thus you will form CLOTS! Thus heparin given until Warfarin can work fully

Front 20

Name some thrombylytics

Back 20

Alteplase (tPA)

reteplase (rPA)

Tenecteplase (TNK-tPA)

Front 21

alteplase, reteplase, tenecteplase

MOA

Back 21

Aid in conversion of Plasminogen to plasmin (CLUT BUSTER!)

Both will Increase PTT and PT

Front 22

Clinical use of thrombolytics

Back 22

Early MI, early stroke, early PE

TIME IS VERY IMPORTANT!

Front 23

What is the bad part about thrombolytics?

Back 23

Time restraint (must use it intially in disease).

Else you risk the patients bleeding out.

Risk outweigh the benefits a lot of the times

Front 24

What are the SE of Thrombolytics?

Back 24

BLEEDING!
CI in active bleeding, or ppl with history of bleeding or recent surgeries or severe HTN

Front 25

Aminocaproic acid

Back 25

Given to patients who you expect will bleed a lot in surgery

It can treat thrombolytics

These STOP bleeding

Front 26

ADP recetor inhibitors

(Clopidogrel, ticlopidine, prasugrel, ticagrelor)

MOA?

Back 26

Block ADP receptor thus prevent aggregation

Front 27

Clinical use of clopidogrel, ticlopidine, prasugrel, ticagrelor

Back 27

Used to prevent clots in patients who have had MI or stroke or any other vessel disorders in which you don't want clots

Front 28

SE of Ticlopidine

Back 28

Neutropenia

Front 29

What kind of drugs are Cilostazol and dipyridamole

Back 29

Phosphodiesterase III inhibitor

Will increase cAMP in platelets thus inhibiting platelet aggregation. Also a vasodilator

Front 30

Clinical use of Cilostazol and dipyridamole

Back 30

Will open up vessels and prevent clotting. (thus has many uses)

Main uses involve: intermitten claudication

Front 31

SE of Cilostazol and dipyridamole

Back 31

Nausea, HA, flushing, hypotension, abdominal pain

(mainly associated with the vasodilatoin)

Front 32

Abciximab, eptifibatide, tirofiban

MOA?

Back 32

GP IIb/IIIa inhibitors

Prevent aggregation

Front 33

Clinical use

Back 33

Decrease clotting thus many uses (just like the other ones)

Main uses: percutaenous transluminal coronary angioplasty (eg. STENT)

Front 34

Toxicity of GP IIb/IIIa inhibitors

Back 34

Bleeding and thrombocytopenia

Front 35

ASPIRIN

Back 35

STUDY THAT ON YOUR OWN.

Front 36

Back 36

Overview

Front 37

Back 37

Overview

Front 38

SE of Cancer drugs

Back 38

GI, hair, blood cells most common toxicity issues.

Bone marrow suppression is key Toxicity with lots of these drugs (thus easier to remember which DON’T target BM)

Front 39

Methotrexate

MOA

Back 39

Folic acid analog

Inhibits dihydrofolate reductase

(converts inactive DHF to active THF which is needed in aiding Thymidylate synthase to convert dUMP to dTMP); thus decrease DNA synthesis

Front 40

Methotrexate

Clinical use

Back 40

Leukemias, lymphomas, choriocarcinoma, sarcomas (nothing specific)

ectopic pregnancy, RA, psoriasis

Front 41

methotrexate

SE

Back 41

BM toxicity (dose limiting)

GI ulcers, Teratogenic*

Macrovesicular fatty change in liver

Front 42

What can you use to treat overdose of Methotrexate?

Back 42

Leucovorin

Front 43

5-flurouracil

MOA

Back 43

Pyrimidine analog

Inhibits Thymidylate synthase (dUMP --> dTMP)

Thus decrease DNA synthesis

Front 44

5-fluorouracil (5-FU)

Clinical use

Back 44

Colon Ca
Basal cell carcinoma (topical)

Front 45

SE of 5-FU

Back 45

BM suppression (dose limiting)

Photosensitivity

Front 46

What can you treat overdose of 5-FU with?

Back 46

Thymidine

Front 47

Cytarabine

MOA

Back 47

Pyrimidine analog

Inhibits DNA polymerase

Front 48

Cytarabine

Clinical use

Back 48

Leukemias and lymphomas

Front 49

Cytarabine

SE

Back 49

BMD - dose limiting

Cerebellar toxicity (ATAXIA)*

Front 50

Azathioprine
6-mercaptopurine (6-MP)
6-thioguanine (6-TG)

MOA

Back 50

Purine analogs which decrease de novo purine synthesis

Activated by HGPRT

Front 51

What enzyme metabolizes Azathioprine, 6MP, 6TG?

Back 51

Xanthine oxidase

Thus be careful when giving allopurinol!

Front 52

Clinical use of azathioprine, 6-mercaptopurine, 6-thioguanine

Back 52

Leukemias

Front 53

Azathioprine, 6-mercaptopurine, 6-thioguanine

SE

Back 53

BM
Hepatotoxicty

Increased toxicity with allopurinol

Front 54

Dactinomycin

MOA

Back 54

Binds and intercalates into DNA (stops replication and transcription)

Front 55

Dactinomycin

Clinical use

Back 55

KIDS TUMORS!

(Wilm's tumor, Ewing's sarcoma, rhabdomyosarcoma)

Front 56

Dactinomyocin

SE

Back 56

BM

Front 57

Doxorubicin and daunorubicin

MOA

Back 57

Intercalates into DNA
Generate free radicals
Inhibits topoisomerase II

(know 3 ways)

Front 58

Doxorubicin and daunorubicin

Clinical use

Back 58

SOlid tumors, leukemias, lymphomas

Front 59

Doxarubicin, daunorubicin

SE

Back 59

CARDIOTOXICITY*
(dilated cardiomyopathy) due to free radicals

BM

Front 60

What drug is given with Doxorubicin and daunorubicin to prevent the cardiotoxicty?

Back 60

Dexrazoxane (iron chelating agent)

Used to prevent cardiotoxicity

Front 61

Bleomycin

MOA

Back 61

Binds to DNA
Forms radical causing DNA damage

Front 62

Clinical use of Bleomycin

Back 62

Testicular cancer
Hodgkin's lymphoma

Front 63

Bleomycin

SE

Back 63

Pulmonary fibrosis*
Significant cutaneous toxicity*

MINIMAL BM (one of the few to have such low effect thus used a lot)

Front 64

Cyclophosphamide,
ifosfamide

MOA

Back 64

Crosslink DNA at guanine N-7

Require activation by LIVER*

Front 65

Cycophosphamide SE

Back 65

BM

Hemorrhagic cystitis*

Front 66

How can you prevent the hemorrhagic cystitis?

Back 66

Mesna and NAC

Front 67

Nitrosoureas (carmustine, lomustine, semustine)

MOA

Back 67

Crosslink DNA

Can enter the BRAIN*******

Front 68

Clinical use of Nitrosoureas (eg. Carmustine, lomustine)

Back 68

Brain tumors**

Front 69

Nitrosureas

SE

Back 69

CNS toxicity (ataxia, dizziness)

BM

Hits many many organs thus use limited

Front 70

Busulfan

MOA

Back 70

Alkylates DNA

Front 71

Busulfan

Clinical use

Back 71

CML**

Used to ablate BM before transplantation

Front 72

Busulfan

SE

Back 72

Pulmonary fibrosis

hyperpigmentation

BM

Front 73

Vincristine, Vinblastine

MOA

Back 73

Bind to tubulin in M phase. Block polymerization thus the miotic spindles can't form

Front 74

Vincristine and vinblastine

Clinical use

Back 74

SOlid tumors, leukemias, and lymphomas

Front 75

Vincristine and Vinblastine

SE

Back 75

Vincristin -- CNS (peripheral neuritis, autonomic, cranial nerves)

Vinblastin - BM

Front 76

Paclitaxel (+other taxols)

MOA

Back 76

Hyperstabalize the polymerized microtubules phase that the the spindle can't break down (can't move onto anaphase)

Front 77

Paclitaxel

Clinical use

Back 77

Ovarian and breast carcinomas

Front 78

Paclitaxel

SE

Back 78

BM

Front 79

Cisplastin and carboplatin

MOA and clinical use

Back 79

Cross link DNA

Testicular, bladder, ovary carcinomas

Front 80

Cisplastin and carboplatin

SE*

Back 80

Nephrotoxicity and acoustic nerve damage*

Front 81

How can you prevent the nephrotoxicity with Cisplatin and carboplatin?

Back 81

Amifostine (free radical scavenger)

Drink plenty of water and stay hydrated

Front 82

Etoposide and teniposide

MOA and clinical use

Back 82

Inhibit topoisomerase II (increase DNA degradation)

Testicular and SCC of lungs

Front 83

Teoposide and teniposide

SE

Back 83

BM

Front 84

Hydroxyurea

MOA

Back 84

Inhibits ribonucleatide reductase (enzyme which converts ribonucleotides to deoxynucleotides which are required for DNA synthesis)

Front 85

Hydroxyurea

Clinical use and SE

Back 85

Melanoma, CML, sickle cell dz (increases HbF)

SE: BM

Front 86

Tamoxifene and Raloxifene

MOA

Back 86

Both work as AGONIST IN BONE and ANTAGONIST in BREAST

Tamoxifene: agonist in endometrium

Front 87

Tamoxifene and Raloxifene

Clinical use

Back 87

Breast cancer treatment and prevention

And osteoporosis

Front 88

Which increases the risk of endometrial cancer and has hot flashes as a SE?

Back 88

Tamoxifene b/c it works on the endometrium

Front 89

Trastuzumab (Herceptin)

Moa + Clinical use

Back 89

AB against HER-2 (tyrosine kinase)

Helps treat HER-2 positive breast cancer

Front 90

Trastuzumab

SE

Back 90

Cardiotoxicity

Front 91

Imatinib

MOA + Clinical use

Back 91

Philadelphia chromosome bcr-abl tyrosine kinase inhibitor

Tx:
CML*

Front 92

Imatinib

SE

Back 92

Fluid retention

Front 93

Rituximab

MOA and clinical use

Back 93

Monoclonal AB against CD20, which is found on most B-cell neoplasms

Non-Hodgkin's lymphoma, RA

Front 94

Vemurafenib

MOA + Clinical use

Back 94

Small molecular inhibitor of forms of the B-Raf kinase with the V600E mutation

Tx:
Metatstatic melanoma

Front 95

Bevacizumab

Clinical use + MOA

Back 95

Monloclonal AB against VGEF. Inhibits angiogenesis

Tx:
Any SOLID tumors