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3rd Year (Step 2) > Immuno-modulators > Flashcards

Immuno-modulators Flashcards

1
Q

Heparin MOA

A

Cofactor for activation of antithrombin. Decreases thrombin and factor Xa.

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2
Q

Clinical use, heparin

A

Immediate anticoagulation for PE, acute coronary syndrome, MI, DVT. Used during pregnancy (doesn’t cross placenta). Follow PTT.

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3
Q

Toxicity, heparin

A

Bleeding, thrombocytopenia (HIT), osteoporosis, drug-drug interactions.

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4
Q

Antidote, heparin?

A

Antidote=protamine sulfate (positively-charged, binds negatively-charged drug)

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5
Q

Enoxaparin, dalteparin

A

Low weight molecular heparins

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6
Q

Low molecular weight heparins (enoxaparin, dalteparin)

A

Heparins that act more on factor Xa, have better bioavailability and longer half life. Can be given subQ and no lab monitoring necessary. Not easily reversible.

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7
Q

Heparin induced thrombocytopenia (HIT)

A

Development of IgG abs against heparin bound to platelet factor 4 (PF4). Antibody-heparin PF4 complex activates platelets–>thrombosis and thrombocytopenia

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8
Q

Lepirudin, bivalirudin

A

Derivatives of hirudin, the anticoagulant used by leeches; inhibit thrombin. Alternative to heparin for anticoagulating patients with HIT.

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9
Q

Warfarin MOA

A

Interferes with normal synthesis and gamma carboxylation of vitamin K dependent clotting factors II, VII, IX and X and proteins C and S. Metabolized by cytochrome P-450 pathway. In lab, has effect on extrinsic pathway and increases PT (The EX-PresidenT went to war(farin)).

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10
Q

Use, warfarin

A

Used in chronic anticoagulation. Not used in pregnant women because can cross the placenta.

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11
Q

PT/INR values, warfarin

A

What labs should be followed during warfarin ttmt?

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12
Q

Toxicity, warfarin

A

Bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions

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13
Q

Reversal of warfarin

A

Reversal: vitamin K
Rapid reversal of severe overdose: fresh frozen plasma

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14
Q

Alteplase

A

A thrombolytic, tPA

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15
Q

Reteplase

A

A thrombolytic, rPA

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16
Q

Tenecteplase

A

Thrombolytic, TNK-tPA

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17
Q

Alteplase, reteplase, tenecteplase

A

Name the thrombolytics

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18
Q

Thrombolytics

A

Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increased PT and PTT, no change in platelet count.

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19
Q

Uses of thrombolytics?

A

Uses: Early MI, early ischemic stroke, direct thrombolysis of severe PE

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20
Q

Toxicity, thrombolytics?

A

Toxicity=bleeding

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21
Q

Ttmt of toxicity, thrombolytics?

A

Ttmt of toxicity=aminocaproic acid (an inhibitor of fibrinolysis)

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22
Q

Aspirin, MOA

A

Irreversibly inhibits COX1 and 2 via covalent acetylation. Platelets can’t make new enzyme, so effect lasts until new platelets are made. Increases bleeding time, decreases TXA2 and prostaglandins. No effect on PT or PTT.

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23
Q

Clinical use, aspirin

A

Use: antipyretic, analgesic, anti-inflammatory, antiplatelet (decreased aggregation).

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24
Q

Toxicity, aspirin

A

Toxicity: gastric ulceration, tinnitus (CN VIII). Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding. Reye’s syndrome in children with viral infection.

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25
Q

What does OD on aspirin cause

A

OD causes respiratory alkalosis and metabolic acidosis

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26
Q

ADP receptor inhibitors?

A

Clopidogrel, ticlopidine, prasugrel, ticagrelor

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27
Q

MOA, ADP receptor inhibitors?

A

Inhibit platelet aggregation by irreversibly blocking ADP receptors (ADP its receptor on surface of platelet causes GP IIb/IIIa insertion on the membrane, receptor for fibrinogen). Inhibits fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen.

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28
Q

Toxicity, ADP receptor inhibitors (ticlopidine)

A

Toxicity: neutropenia

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29
Q

Cilostazol is what type of drug?

A

Phosphodiesterase inhibitors

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30
Q

Ticlopidine=?

A

ADP receptor inhibitor

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31
Q

Prasugrel=?

A

ADP receptor inhibitor

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32
Q

Clopidogrel=?

A

ADP receptor inhibitor

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33
Q

Ticagrelor=?

A

ADP receptor inhibitor

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34
Q

Dipyridamole=?

A

Phosphodiesterase III inhibitor

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35
Q

Cilostazol, dipyridamole are this type of drug

A

Phosphodiesterase III inhibitors

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36
Q

Abciximab is what type of drug?

A

GP IIb/IIIa inhibitor

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37
Q

Eptifibatide=?

A

GP IIb/IIIa inhibitor

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38
Q

Tirofiban=?

A

GP IIb/IIIa inhibitor

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39
Q

Abciximab, eptifibatide, tirofiban=what type of drugs?

A

GP IIb/IIIa inhibitors

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40
Q

Cilostazol, dipyridamole MOA

A

Phosphodiesterase III inhibitor, increase cAMP in platelets, thus inhibiting platelet aggregation; vasodilators.

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41
Q

Clinical use, cilostazol, dipyridamole?

A

Use: Intermittent claudification, coronary vasodilation, prevention of stroke or TIAs (combined with aspirin), angina prophylaxis

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42
Q

Toxicity, cilostazol, dipyridamole?

A

Tox: nausea, headache, facial flushing, hypotension, abdominal pain.

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43
Q

MOA, abciximab, eptifibatide, tirofiban

A

MOA: bind to glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation. Abciximab made from monoclonal Ab Fab fragments.

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44
Q

Clinical use, abciximab, eptifibatide, tirofiban?

A

Use: acute coronary syndromes, percutaneous transluminal coronary angioplasty.

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45
Q

Toxicity, abciximab, eptifibatide, tirofiban?

A

Toxicity: bleeding, thrombocytopenia

46
Q

Antimetabolites act at what phase in the cell cycle?

A

Act on S phase, antimetabolites

47
Q

Etopiside acts on which phases on cell cycle?

A

Act on S phase, G2 phase

48
Q

Bleomycin acts on which phase of the cell cycle?

A

G2 phase

49
Q

Vinca alkaloids and taxols work at which phase of the cell cycle?

A

M phase

50
Q

Methotrexate, MOA

A

MOA:Folic acid analog that inhibits dihydrofolate reductase, v dTMP, v DNA, and v protein synthesis

51
Q

Methotrexate, clinical use

A

Cancers: leukemias, lymphomas, choriocarcinoma, sarcomas
Non-neoplastic: abortion, ectopic pregnancy, rheumatoid arthritis, psoriasis

52
Q

MTX, toxicity

A

Toxicity: myelosuppression reversible with leucovorin (folinic acid) rescue)
-Macrovesicular Fatty change in Liver
- Mucositis
- Teratogen

53
Q

5-fluorouracil MOA

A

Pyrimidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid. This complex inhibits thymidylate synthase–> vdTMP–>v DNA and v protein synthesis

54
Q

5-fluorouracil uses

A

Uses: Colon cancer, basal cell carcinoma

55
Q

5-fluorouracil toxicity

A

Myelosuppresion which isn’t reversible via leucovorin.
- Photosensitivity

56
Q

Antidote for 5-FU OD?

A

Antidote=thymidine

57
Q

MOA, cytarabine (arabinogfuranosyl cytidine)

A

MOA: pyrimidine analog–>inhibition of DNA polymerase

58
Q

Clinical use, cytarabine

A

Clinical use: leukemias, lymphomas

59
Q

Tox, cytarabine

A

Toxicity: leukopenia, thrombocytopenia, megaloblastic anemia

60
Q

MOA, azathioprine, 6-mercaptopurine (6-MP), and 6-thioguanine (6-TG)

A

MOA: purine (thiol) analogs–>v de novo purine synthesis. Acitvated by HGPRT.

61
Q

Clinical use, azathioprine, 6-mercaptopurine (6-MP) and 6-thioguanine (6-TG)

A

Use: Leukemias

62
Q

Azathioprine, 6-mercaptopurine, and 6-thioguanine toxicity

A

Tox: bone marrow, GI, liver

63
Q

Antitumor antibiotics

A

What do dactinomycin (actinomycin D), doxorubicin, daunorubicin, and bleomycin have in common?

64
Q

Dactinomycin MOA

A

Antitumor abx that intercalates in DNA

65
Q

Dactinomycin clinical use

A

Use: wilm’s tumor, Ewing’s Sarcoma, Rhabdomyosarcoma, & used for childhood tumors (children ACT out)

66
Q

Dactinomycin, toxicity

A

Tox: myelosuppression

67
Q

Doxorubicin, daunorubicin MOA

A

MOA: generate free radicals. Noncovalently intercalate in DNA–>breaks in DNA–>decrease replication

68
Q

Doxorubicin, daunorubicin use

A

Use: solid tumors, leukemias, lymphomas

69
Q

Doxorubicin, daunorubicin tox

A

Tox: cardiotoxicity (dilated cardiomyopathy), Myelosuppression, Alopecia, & toxic to tissues following extravasation

70
Q

Doxorubicin, daunorubicin antidote

A

Dexrazoxane (iron chelating agent), used to prevent cardiotoxicity

71
Q

Bleomycin MOA

A

MOA: induces free radical formation, which causes breaks in DNA strands

72
Q

Bleomycin uses

A

use: testicular cancer, lymphoma

73
Q

Bleomycin tox

A

Tox: pulmonary fibrosis, skin changes. Minimal myelosuppression.

74
Q

Alkylating agents

A

Cyclophosphamide & Ifosfamide, Nitrosureas (carmustine, lomustine, semustine, streptozocin), Busulfan

75
Q

Cyclophosphamide, ifosfamide MOA

A

MOA: covalently X-link (interstrnad) DNA @ guanine N-7. Require bioactivation by liver.

76
Q

Uses, cyclophosphamide, ifosfamide

A

Uses: solid tumors, leukemia, lymphomas, and some brain cancers.

77
Q

Tox, cyclophosphamide, ifosfamide

A

Tox: Myelosuppression & Hemorrhagic cystitis

78
Q

Mesna (thiol group binds toxic metabolite)

A

Substance that can be used to prevent hemorrhagic cystitis caused by cyclophosphamide, ifosfamide

79
Q

Nitrousoureas

A

Carmustine, lomustine, semustine, streptozocin are?

80
Q

MOA, nitrousureas

A

MOA: require bioactivation, cross BBB–>CNS

81
Q

Uses, nitrousureas

A

Uses: brain tumors (including glioblastoma multiforme)

82
Q

Toxicity, nitrousureas?

A

Tox: CNS toxicity (dizziness, ataxia)

83
Q

MOA, busulfan

A

MOA: alkylates DNA

84
Q

Uses, busulfan

A

Uses: CML, also used to ablate pt’s bone marrow before bone marrow transplantation.

85
Q

Toxicity, busulfan:

A

Tox: pulmonary fibrosis, hyperpigmentation

86
Q

Microtubule inhibitors

A

Vincristine, vinblastine, Paclitaxel & other taxols

87
Q

MOA: vincristine, vinblastine

A

MOA: alkaloids that bind to tubulin in M phase and block polymerization of microtubules so that mitotic spindle cannot form “Microtbules are the VINes of your cells

88
Q

Tox, vincristine

A

Tox: neurotoxicity (areflexia, peripheral neuritis), paralytic ileus

89
Q

Tox, vinblastine

A

Tox: bone marrow suppress (Vinblastine BLASTS Bone marrow)

90
Q

MOA, paclitaxel, other taxols

A

MOA: hyperstabilize polymerized microtubules in M phase so that mitotic spindle cannot break down (anaphase cannot occur). “it is TAXing to stay polymerized”

91
Q

Toxicity, paclitaxel and other taxols

A

Tox: myelosuppression and hypersensitivity

92
Q

MOA, cisplatin and carboplatin

A

MOA: cross-link DNA

93
Q

Tox, cisplatin and carboplatin

A

Tox: nephrotoxicity and acoustic nerve damage.

94
Q

Amifostine (free radical scavenger) and chloride diuresis

A

How to prevent nephrotoxicity with cisplatin and carboplatin?

95
Q

MOA, etopiside, teniposide

A

MOA: inhibit topoisomerase II–>increase DNA degradation

96
Q

Tox, etopiside, teniposide

A

Tox: myelosuppression, GI irritation, alopecia

97
Q

MOA, hydroxyurea

A

MOA: inhibits ribonucleotide reductase–>v DNA Synthesis (S phase specific)

98
Q

Tox, hydroxyurea

A

TOx: bone marrow suppression, GI upset

99
Q

MOA, prednisone, prednisolone

A

MOA: may trigger apoptosis, may even work on non-dividing cells

100
Q

Toxicity, prednisone, prednisolone

A

Tox: Cushing-like sx, immunosuppression, cataracts, acne, osteoporosis, htn, peptic ulcers, hyperglycemia, psychosis

101
Q

MOA: tamoxifen, raloxifene

A

MOA: SERMs, receptor antagonists in breast and agonists in bone. Block the binding of estrogen to estrogen receptor-positive cells.

102
Q

Toxicity, tamoxifen

A

Tox: partial agonist in endometrium, which increases the risk of endometrial cancer; hot flashes

103
Q

Tox, raloxifene

A

Tox: no increase in endometrial CA because it’s an endometrial antagonist

104
Q

Trastuzumab (Herceptin) MOA

A

MOA: monoclonal Ab vs HER-2 (c-erb B2), a tyrosine kinase. Helps kill breast cancer cells that overexpress HER-2, possibly through antibody-dependent cytotoxicity.

105
Q

Toxicity, trastuzumab

A

Tox: cardiotoxicity

106
Q

MOA, Imatinib (gleevec)

A

MOA: Philadelphia chromosome bcr-abl tyrosine kinase inhibitor

107
Q

Uses, imatinib

A

Use: CML, GI stromal tumors

108
Q

Tox, imatinib

A

Fluid retention=tox

109
Q

Rituximab MOA

A

MOA: monoclonal Ab vs. CD20, which is found on most B cell neoplasms

110
Q

Vemurafenib MOA

A

MOA: small molecule inhibitor of forms of the B-Rag kinase with the V600E mutation.

111
Q

Vemurafenib use

A

Use: metastatic melanoma

112
Q

Bevacizumab MOA

A

MOA: monoclonal ab vs VEGF. Inhibits angiogenesis.

3rd Year (Step 2) (44 decks)

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