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STEP 1 (2) > Heme Pharm > Flashcards

Heme Pharm Flashcards

1
Q

How does heparin work?

A

activator of antithrombin, decreasing levels of thrombin and factor Xa (short half-life)

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2
Q

What are the main uses of heparin?

A
  • immediate anticoag for PE, acute coronary syndrome, MI, DVT
  • used during pregnancy

monitor PTT

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3
Q

What are the AEs of heparin?

A

bleeding

thrombocytopenia (HIT)

osteoporosis

DDIs

-monitor PTT

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4
Q

What is the antidote to heparin overdose?

A

protamine sulfate (binds to negatively charged heparin)

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5
Q

What are the advantages of LMWH (like enoxaparin, dalteparin) and fondaparinux?

A

they act more on factor Xa

better bioavailability

2-4x longer half-life

can be administered SubQ and without monitoring

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6
Q

What is heparin-induced thrombocytopenia?

A

development of IgG Abs against heparin-bound platelet factor 4, and the complex activates platelets causing thrombosis and then thrombocytopenia

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7
Q

What are the direct thrombin (factor II) inhibitors?

A
  • argatroban and dabigatran
  • bivalirudin

good alternatives fo anticoag in those with HIT

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8
Q

How does warfarin work?

A

it interferes with y-carboxylation of vitamin-K dependent clotting factors II, VII, IX, X, and proteins C and S

  • affects PT
  • long half-life
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9
Q

The metabolism of warfarin is affected by what?

A

polymorphisms in the gene for vitamin K epoxide reductase complex VKORC1)

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10
Q

What are the uses of warfarin?

A
  • chronic anticoag (e.g. venous TE prophylaxis, and prevention of stroke in a. fib)
  • not used in pregnancy
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11
Q

AEs of warfarin?

A
  • bleeding
  • teratogenic

skin/tissue necrosis

-transient hypercoagulability upon administration because of short half-life of proteins C and S

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12
Q

What is the antidote for warfarin OD?

A

vitamin K, or Fresh frozen plasma for rapid reversal

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13
Q

Describe heparin bridging

A

heparin is frequently used with starting warfarin because heparin’s activation of antithrombin enables anticoag during the initial, transient hypercoag state caused by warfarin

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14
Q

What is the structure of heparin?

A

large, anionic, acidic polymer

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15
Q

How is heparin given?

A

IV/SC

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16
Q

What is the onset of action and DOA of heparin?

A

onset of action- rapid (seconds)

DOA- acute (hours)

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17
Q

What is the structure of warfarin?

A

small, amphipathic molecule

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18
Q

How is warfarin given?

A

PO

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19
Q

What are the direct factor Xa inhibitors?

A

ApiXaban, RivaroXaban

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20
Q

What are the uses of direct factor Xa inhibitors?

A
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21
Q

What are the main plasmin activators?

A

alteplase, reteplase, tenecteplase

streptokinase

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22
Q

What are the AEs of plasmin activators?

A

-bleeding (contraindicated in pts. with active bleeding, hx of intracranial bleeding, recent surgery, or severe HTN)

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23
Q

How can bleeding caused by plasmin activators (or other things) be tx?

A

aminocaproic acid

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24
Q

How does aspirin work?

A

it irreversibly inhibits cyclooxygenase 1/2 by covalent acetylation until the platelet is degraded

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25
Q

How does aspirin affect BT, PT, and PTT?

A

BT- increased

PT/PTT- no effect

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26
Q

What are the AEs of aspirin?

A

gastric ulceration

tinnitus (the hearing of sound when no external sound is present- often ringing)

renal failure

hyperventilation and respiratory alkalosis transitioning to mixed metabolic acidosis-respiratory acidosis

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27
Q

What are the ADP receptor inhibitors?

A

clopidogrel,

prasugrel,

ticlopidine

ticagrelor (reversible)

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28
Q

What are the uses of ADP receptor inhibitors?

A

acute coronary syndrome, coronary stenting

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29
Q

What are the AEs of ADP receptor inhibitors?

A

neutropenia

TTP rarely

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30
Q

What do cilostazol and dipyridamole do?

A

phosphodiesterase III inhibitors that cause increased cAMP in platelets, resultng in inhibition of platelet aggregation

also act as vasodilators

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31
Q

What are the direct GpIIb/IIIa inhibitors?

A

-abciximab

tirofiban

-eptigibatide

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32
Q

What are the clinical uses of GpIIb/IIIa inhibitors?

A

unstable angina, percutaneous transluminal coronary angioplasty

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33
Q

What phase of the cell cycle do microtubules inhibitors (paclitaxel) and vinca alkaloids (vinblastine; vincristine) work?

A

Mitosis

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34
Q

What phase of the cell cycle do alkylating agents and nitrosoureas (carmustine, cisplatin, lomustine) work?

A

G1

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35
Q

What phase of the cell cycle do antimetabolites (e.g. 5-FU, methotrexate, 6-MP) work?

A

S

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36
Q

What phase of the cell cycle do etoposide and teniposide work?

37
Q

What phase of the cell cycle does bleomycin work?

38
Q

How do azathioprine, 6-MP, and 6-thioguanine work?

A

these are false-purine analogs activated by HGPRT that decrease de novo purine synthesis (azathioprine is metabolized to 6-MP)

39
Q

What are the uses of azathioprine, 6-MP, and 6-thioguanine?

A

preventing organ rejection

rheumatoid arthritis

IBD

SLE

used to wean pts off steroids in chronic disease and to treat steroid-refractory chronic disease

40
Q

What are the AEs of azathioprine, 6-MP, and 6-thioguanine??

A

myelosuppression

elevated LFTs

GI toxicity

azathioprine and 6-MP are metabolized by xanthine xidase, thus both have increased toxicity with allopurinol or febuxostat

41
Q

How does Cladribine (2-CDA) work?

A

a false purine analog that also inhibits DNA polymerase and causes strand breaks

42
Q

What is the use of 2-CDA?

A

hairy cell leukemia

43
Q

What are the AEs of 2-CDA?

A

myelosuppression

nephrotixicity, neurotoxicity

44
Q

How does Cyatarabine work?

A

it is a false pyrimidine analog that inhibits DNA polymerase for tx of leukemias (AML) and lymphomas

45
Q

What are the AEs of cytarabine?

A

-leukopenia, thrombocytopenia, megaloblastic anemia

46
Q

How does 5-FU work?

A

it is a pyrimidine analog bioactivated to 5F-dUMP which covalently complexes with folic acid to inhibit thymidylate synthase which converts dUMP to dTP

47
Q

What are the uses of 5-FU?

A

colon cancer

pancreatic cancer

basal cell carcinoma

48
Q

How does methotrexate work?

A

it is a folic acid analog that competitively inhibits dihydrofolate reductase which is needed for conversion of DHF to THF in DNA synthesis

49
Q

What are the main uses of methotrexate?

A

cancers: leukemia, lymphomas, choriocarcinoma, sarcoma

ectopic pregnancy elimination/medical abortion

rheumatoid arthrtiis

psoriasis

IBD

vasculitis

50
Q

What are the AEs of methotrexate?

A
  • myelosuppression (reversible with leuocovorin)
  • hepatotoxicity

mucositis (e.g. mouth ulcers)/ skin lesions

pulmonary fibrosis

51
Q

How does bleomycin work?

A

it induces free radical formation to cause DNA stran breaks for tx of testicular cancer and Hodgkin lymphoma

52
Q

What are the AEs of bleomycin?

A

pulmonary fibrosis

skin hyperpigmentation

mucositis

53
Q

How does dactinomycin work?

A

it intercalates with DNA for tx of Wilm’s tumor, Ewing sarcoma, and rhabdomyosarcomas (all pediatric tumors)

54
Q

How do doxorubicin and daunorubicin work?

A

they generate free radicals and intercalate with DNA to form strand breaks

55
Q

What are the AEs of doxo- and daunorubicin?

A

-cardiotoxicity (dilated cardiomyopathy)

myelosuppression

alopecia

56
Q

What can be used to prevent the cardiotoxicity of doxo- and daunorubicin?

A

dexrazoxane

57
Q

What are the main alkylating agents?

A
  • busulfan
  • cyclophosphamide, ifosfamide
  • nitrosoureas (carmustine, lomustine, semustine, streptozocin)
58
Q

Busulfan works by cross-linking DNA for tx of CML and to ablate a pt’s bone marrow before bone marrow transplant. What are the AEs?

A
  • severe myelosuppression- almost always
  • pulmonary fibrosis

hyperpigmentation

59
Q

How do cyclophosphamide and ifosfamide work?

A

they are alkylating agents that cross-link DAN at guanine N-7 after being activated in the liver

60
Q

What are the AEs of cyclophosphamide?

A
  • myelosuppression
  • hemorrhagic cystitis (prevent with mesna)
61
Q

How do nitrosoureas like carmustine and lomustine work?

A

they are alkylators that require bioactivation and cross the BBB for tx of brain tumors

these are the most likely to cause CNS toxicity

62
Q

How do -taxels work?

A

they hyperstabilize polymerized microtubules in M phase so that mitotic spindle cannot break down and anaphase cannot occur

63
Q

What are the main uses of -taxel drugs?

A

ovarian and breast carcinomas

64
Q

How do vincristine and vinblastine work?

A

vinca alkaloids that bind B-tubulin and inhibit its polymerization into microtubules and prevents mitotic spindle formation

65
Q

What are the AEs of vincristine?

A

neurotoxicity (areflexia, peripheral neuritis)

paralytic ileus

66
Q

What are the AEs of vinblastine?

A

bone marrow suppression

67
Q

How do cisplatin and carboplatin work?

A

they cross-link DNA for tx of testicular, bladder, ovary, and lung carcinoma

68
Q

What are the AEs of cisplatin and carboplatin?

A

-nephrotoxicity (prevent with amifostine) and ototoxicity

69
Q

How do etoposide and teniposide work?

A

they inhibit topoisomerase II

70
Q

What are the AEs of etoposide and teniposide?

A

myelosuppression

GI disturbances

alopecia

71
Q

How do irinotecan and topotecan work?

A

topo I inhibitor to prevent DNA unwinding for tx of colon (irinotecan) cancer and ovarian and small cell lung cancer (topotecan)

72
Q

How does hydroxyurea work?

A

it inhibits ribonucelotide reductase to inhibit DNA synthesis (S phase)

73
Q

What are the uses of hydroxyurea?

A
  • melanoma
  • CML
  • sickle cell disease (increased HbF)
74
Q

How do prednisone and prednisolone work?

A

many mechanisms including altering gene transcription to induce immunosuppression

75
Q

What are the AEs of steroids?

A
  • cushing-like rxn
  • weight gain and central obesity
  • muscle breakdown
  • acne
  • cataracts
  • osteoporosis
  • hyperglycemia
76
Q

How does Bevacizumab work?

A

it is a VEGF MAb that inhibits angiogenesis for tx of colorectal cancer and renal cell carcinoma

77
Q

How does Erlotinib work?

A

EGFR tyrosine kianse inhibitor for tx of non-small cell lung cancer (can result in rash)

78
Q

How does Imatinib work? Toxicities?

A

tyrosine kinase inhibitor of BCR-ABL (Philadelphis fusion gene in CML) and c-kit in GIST tumors

may cause fluid retention

79
Q

What is Rituximab?

A

MAb against CD20, found in most B-cell neoplasms such as Non-hodgkin lymphoma

also used to tx CLL, IBD, and rheumatoid arthritis

80
Q

What is a major AE of rituximab?

A

risk of progressive multifocal leukoencephalopathy

81
Q

How do tamoxifen and raloxifene work?

A

they are selective estrogen receptor modulators (SERM)- receptor antagonists in breast and agonists in bone blocking the binding of estrogen to ER+ cells

82
Q

What are the main uses of tamoxifen and raloxifene?

A

breast cancer tx and prevention and raloxifene for osteoporosis prevention

83
Q

What are the AEs of tamoxifen?

A

agonist of endometrium

hot flashes

84
Q

What are the AEs of raloxifene?

A

no risk of endometrial carcinoma because it is an endometrial antagonist

85
Q

How does Trastuzumab (herceptin) work?

A

it is a MAb to HER-2, a tyrosine kinase receptor for tx of HER-2+ breast cancer and metastatic gastric cancer

86
Q

What is the major AE of trastuzumab?

A

Cardiotoxicity

87
Q

What is Vemurafenib?

A

small molecular inhibitor of BRAF+ melanoma

STEP 1 (2) (16 decks)

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