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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
What does OD on aspirin cause
OD causes respiratory alkalosis and metabolic acidosis
26
ADP receptor inhibitors?
Clopidogrel, ticlopidine, prasugrel, ticagrelor
27
MOA, ADP receptor inhibitors?
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.
28
Toxicity, ADP receptor inhibitors (ticlopidine)
Toxicity: neutropenia
29
Cilostazol is what type of drug?
Phosphodiesterase inhibitors
30
Ticlopidine=?
ADP receptor inhibitor
31
Prasugrel=?
ADP receptor inhibitor
32
Clopidogrel=?
ADP receptor inhibitor
33
Ticagrelor=?
ADP receptor inhibitor
34
Dipyridamole=?
Phosphodiesterase III inhibitor
35
Cilostazol, dipyridamole are this type of drug
Phosphodiesterase III inhibitors
36
Abciximab is what type of drug?
GP IIb/IIIa inhibitor
37
Eptifibatide=?
GP IIb/IIIa inhibitor
38
Tirofiban=?
GP IIb/IIIa inhibitor
39
Abciximab, eptifibatide, tirofiban=what type of drugs?
GP IIb/IIIa inhibitors
40
Cilostazol, dipyridamole MOA
Phosphodiesterase III inhibitor, increase cAMP in platelets, thus inhibiting platelet aggregation; vasodilators.
41
Clinical use, cilostazol, dipyridamole?
Use: Intermittent claudification, coronary vasodilation, prevention of stroke or TIAs (combined with aspirin), angina prophylaxis
42
Toxicity, cilostazol, dipyridamole?
Tox: nausea, headache, facial flushing, hypotension, abdominal pain.
43
MOA, abciximab, eptifibatide, tirofiban
MOA: bind to glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation. Abciximab made from monoclonal Ab Fab fragments.
44
Clinical use, abciximab, eptifibatide, tirofiban?
Use: acute coronary syndromes, percutaneous transluminal coronary angioplasty.
45
Toxicity, abciximab, eptifibatide, tirofiban?
Toxicity: bleeding, thrombocytopenia
46
Antimetabolites act at what phase in the cell cycle?
Act on S phase, antimetabolites
47
Etopiside acts on which phases on cell cycle?
Act on S phase, G2 phase
48
Bleomycin acts on which phase of the cell cycle?
G2 phase
49
Vinca alkaloids and taxols work at which phase of the cell cycle?
M phase
50
Methotrexate, MOA
MOA:Folic acid analog that inhibits dihydrofolate reductase, v dTMP, v DNA, and v protein synthesis
51
Methotrexate, clinical use
Cancers: leukemias, lymphomas, choriocarcinoma, sarcomas Non-neoplastic: abortion, ectopic pregnancy, rheumatoid arthritis, psoriasis
52
MTX, toxicity
Toxicity: myelosuppression reversible with leucovorin (folinic acid) rescue) -Macrovesicular Fatty change in Liver - Mucositis - Teratogen
53
5-fluorouracil MOA
Pyrimidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid. This complex inhibits thymidylate synthase--> vdTMP-->v DNA and v protein synthesis
54
5-fluorouracil uses
Uses: Colon cancer, basal cell carcinoma
55
5-fluorouracil toxicity
Myelosuppresion which isn't reversible via leucovorin. - Photosensitivity
56
Antidote for 5-FU OD?
Antidote=thymidine
57
MOA, cytarabine (arabinogfuranosyl cytidine)
MOA: pyrimidine analog-->inhibition of DNA polymerase
58
Clinical use, cytarabine
Clinical use: leukemias, lymphomas
59
Tox, cytarabine
Toxicity: leukopenia, thrombocytopenia, megaloblastic anemia
60
MOA, azathioprine, 6-mercaptopurine (6-MP), and 6-thioguanine (6-TG)
MOA: purine (thiol) analogs-->v de novo purine synthesis. Acitvated by HGPRT.
61
Clinical use, azathioprine, 6-mercaptopurine (6-MP) and 6-thioguanine (6-TG)
Use: Leukemias
62
Azathioprine, 6-mercaptopurine, and 6-thioguanine toxicity
Tox: bone marrow, GI, liver
63
Antitumor antibiotics
What do dactinomycin (actinomycin D), doxorubicin, daunorubicin, and bleomycin have in common?
64
Dactinomycin MOA
Antitumor abx that intercalates in DNA
65
Dactinomycin clinical use
Use: wilm's tumor, Ewing's Sarcoma, Rhabdomyosarcoma, & used for childhood tumors (children ACT out)
66
Dactinomycin, toxicity
Tox: myelosuppression
67
Doxorubicin, daunorubicin MOA
MOA: generate free radicals. Noncovalently intercalate in DNA-->breaks in DNA-->decrease replication
68
Doxorubicin, daunorubicin use
Use: solid tumors, leukemias, lymphomas
69
Doxorubicin, daunorubicin tox
Tox: cardiotoxicity (dilated cardiomyopathy), Myelosuppression, Alopecia, & toxic to tissues following extravasation
70
Doxorubicin, daunorubicin antidote
Dexrazoxane (iron chelating agent), used to prevent cardiotoxicity
71
Bleomycin MOA
MOA: induces free radical formation, which causes breaks in DNA strands
72
Bleomycin uses
use: testicular cancer, lymphoma
73
Bleomycin tox
Tox: pulmonary fibrosis, skin changes. Minimal myelosuppression.
74
Alkylating agents
Cyclophosphamide & Ifosfamide, Nitrosureas (carmustine, lomustine, semustine, streptozocin), Busulfan
75
Cyclophosphamide, ifosfamide MOA
MOA: covalently X-link (interstrnad) DNA @ guanine N-7. Require bioactivation by liver.
76
Uses, cyclophosphamide, ifosfamide
Uses: solid tumors, leukemia, lymphomas, and some brain cancers.
77
Tox, cyclophosphamide, ifosfamide
Tox: Myelosuppression & Hemorrhagic cystitis
78
Mesna (thiol group binds toxic metabolite)
Substance that can be used to prevent hemorrhagic cystitis caused by cyclophosphamide, ifosfamide
79
Nitrousoureas
Carmustine, lomustine, semustine, streptozocin are?
80
MOA, nitrousureas
MOA: require bioactivation, cross BBB-->CNS
81
Uses, nitrousureas
Uses: brain tumors (including glioblastoma multiforme)
82
Toxicity, nitrousureas?
Tox: CNS toxicity (dizziness, ataxia)
83
MOA, busulfan
MOA: alkylates DNA
84
Uses, busulfan
Uses: CML, also used to ablate pt's bone marrow before bone marrow transplantation.
85
Toxicity, busulfan:
Tox: pulmonary fibrosis, hyperpigmentation
86
Microtubule inhibitors
Vincristine, vinblastine, Paclitaxel & other taxols
87
MOA: vincristine, vinblastine
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
Tox, vincristine
Tox: neurotoxicity (areflexia, peripheral neuritis), paralytic ileus
89
Tox, vinblastine
Tox: bone marrow suppress (Vinblastine BLASTS Bone marrow)
90
MOA, paclitaxel, other taxols
MOA: hyperstabilize polymerized microtubules in M phase so that mitotic spindle cannot break down (anaphase cannot occur). "it is TAXing to stay polymerized"
91
Toxicity, paclitaxel and other taxols
Tox: myelosuppression and hypersensitivity
92
MOA, cisplatin and carboplatin
MOA: cross-link DNA
93
Tox, cisplatin and carboplatin
Tox: nephrotoxicity and acoustic nerve damage.
94
Amifostine (free radical scavenger) and chloride diuresis
How to prevent nephrotoxicity with cisplatin and carboplatin?
95
MOA, etopiside, teniposide
MOA: inhibit topoisomerase II-->increase DNA degradation
96
Tox, etopiside, teniposide
Tox: myelosuppression, GI irritation, alopecia
97
MOA, hydroxyurea
MOA: inhibits ribonucleotide reductase-->v DNA Synthesis (S phase specific)
98
Tox, hydroxyurea
TOx: bone marrow suppression, GI upset
99
MOA, prednisone, prednisolone
MOA: may trigger apoptosis, may even work on non-dividing cells
100
Toxicity, prednisone, prednisolone
Tox: Cushing-like sx, immunosuppression, cataracts, acne, osteoporosis, htn, peptic ulcers, hyperglycemia, psychosis
101
MOA: tamoxifen, raloxifene
MOA: SERMs, receptor antagonists in breast and agonists in bone. Block the binding of estrogen to estrogen receptor-positive cells.
102
Toxicity, tamoxifen
Tox: partial agonist in endometrium, which increases the risk of endometrial cancer; hot flashes
103
Tox, raloxifene
Tox: no increase in endometrial CA because it's an endometrial antagonist
104
Trastuzumab (Herceptin) MOA
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
Toxicity, trastuzumab
Tox: cardiotoxicity
106
MOA, Imatinib (gleevec)
MOA: Philadelphia chromosome bcr-abl tyrosine kinase inhibitor
107
Uses, imatinib
Use: CML, GI stromal tumors
108
Tox, imatinib
Fluid retention=tox
109
Rituximab MOA
MOA: monoclonal Ab vs. CD20, which is found on most B cell neoplasms
110
Vemurafenib MOA
MOA: small molecule inhibitor of forms of the B-Rag kinase with the V600E mutation.
111
Vemurafenib use
Use: metastatic melanoma
112
Bevacizumab MOA
MOA: monoclonal ab vs VEGF. Inhibits angiogenesis.

3rd Year (Step 2) (44 decks)

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