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USMLE Step 1 > Heme/Onc Drugs > Flashcards

Heme/Onc Drugs Flashcards

(105 cards)

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1
Q

Heparin: Mechanism

A
  • cofactor for activation of antithrombrin
  • decreased thrombrin
  • decreased factor Xa
  • Short half life
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2
Q

Heparin: Clinical Use

A

Immediate anticoagulation for pulmonary embolism, acute coronary syndrome, MI, DVT

  • Used during pregnancy (does not cross placenta)
  • Follow PTT
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3
Q

Heparin: Toxicity

A

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

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4
Q

Antidote for heparin toxicity (not to be confused with HIT)

A

Protamine sulfate - positively charged molecule that binds negatively charged heparin

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5
Q

Low molecular heparin (e.g. enoxaparin, dalteparin)

A

act more on factor Xa, have better bioavailability and 2-4 times longer half life

Can be administered subcutaneously and without laboratory monitoring
- Not easily reversible

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6
Q

Lepirudin, Bivalirudin

A

derivatives of hirudin (anti-coagulant used by leeches)

  • inhibit thrombrin
  • used as an alternative to heparin for anti-coagulating patients with HIT
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7
Q

Heparin-induced thrombocytopenia

A

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

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8
Q

Warfarin: Mechanism

A

interferes with normal synthesis and gamma carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X and proteins C and S.

  • BLOCKS Vitamin K
  • Metabolized by the cytochrome P-450 pathway
  • has effect on EXTRINSIC pathway and increase in PT
  • Long half-life
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9
Q

Warfarin: Clinical Use

A

Chronic anticoagulation (after STEMI, venous thromboembolism prophylaxis, and prevention of stroke in atrial fibrillation).

Follow PT/ INR values

** Don’t use in pregnncy, because unlike heparin, warfarin can cross placents

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10
Q

Warfarin: Toxicity

A

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

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11
Q

Treatment to reverse warfarin overdose

A
  • Give vitamin K

- For rapid reversal of severe warfarin overdose, give fresh frozen plasma

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12
Q

Heparin

A
  • large anionic, acidic polymer
  • given parentally (IV, SC)
  • acts on blood
  • rapid onset
  • activates thrombrin, by decreasing action of IIa (thrombrin) and factor Xa
  • lasts for hours
  • inhibits coagulation in vitri
  • overdose treated with protamine sulfate
  • monitor PTT
  • doesn’t cross placenta
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13
Q

Warfarin

A
  • small lipid-soluble molecule
  • given orally
  • acts on liver
  • slow onset, limited by half lives of normal clotting factors
  • impairs synthesis of vitamin K-dependent clotting factors (II, VII, IX, X, proteins C and S)
  • Vitamin K antagonist
  • Lasts for DAYS
  • overdose treated with IV Vitamin K or fresh frozen plasma
  • Monitor extrinsic pathway (PTT/INR)
  • Teratogenic
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14
Q

Thrombolytics

A

Altepase (tPa), reteplase (rPA), tencteplase (TNK-tPA)

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15
Q

Thrombolytic: Mechanism

A

Directly or indirectly aid conversion of plasminogen to plasmi, which cleaves thrombin and fibrin clots.

Increases PT and PTT. NO CHANGE IN PLATELETS

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16
Q

Thrombolytics (“-eplase”): Clinical Use

A

Early MI, early ischemic stroke, direct thrombolysis of severe pulmonary embolism

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17
Q

Thrombolytics (“-eplase”): Toxicity

A

Bleeding.
Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diathesis, or severe hypertension

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18
Q

Tx of thrombolytic (“-eplase”) toxicity:

A

Aminocaproic acid - inhibitor of fibrinolysis

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19
Q

Aspirin: Mechanism

A

IRREVERSIBLY inhibits cyclooxygenase (both COX-1 and COX-2) enzyme by covalent acetylation.
Platelets cannot synthesize new enzyme, so effect lasts until new platelets are produce

  • Increased bleeding time, decreased thromboxane and prostaglandins
  • NO EFFECT on PT and PTT
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20
Q

Aspirin: Clinical Use

A

Antipyretic, analgesic, anti-inflammatory, antiplatelet (decreased aggregation)

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21
Q

Aspirin: Toxicity

A

Gastric ulceration, tinnitus (CN VIII).
Chronic used can lead to acute renal falire, interstitial nephritis, and upper GI bleeding

** Reye’s syndrome in children with with viral effection

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22
Q

Treatment of Apsitin toxicity

A

N-acetylation -

Aspirin toxicity is respiratory alkaltois and metabolic acidosis

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23
Q

ADP receptor inhibitos

A

Clopidogrel, Ticlipidine, Prasugrel, Ticagrelor

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24
Q

ADP Receptor Inhibitor: Mechanism

A

Inhibit platelet AGGREGATION by irreversibly binding ADP receptors. Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen

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25
ADP receptor inhibitor: Clinical Use
Acute coronary syndrome Coronary stenting Decreased incidence or recurrence of thrombotic stroke
26
ADP Receptor Inhibitior: Toxicity
Neutropenia (ticlopidine)
27
Cliostazol, Dipyridamole: Mechanism
Phosphodiesterase III inhibitor; Increased cAMP in platelets, thus inhibiting platelet aggregation Vasodilators
28
Cliostazol, Dipyridamole: Clinical Use
Intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (combined with aspirin), angina prophylaxis
29
Cliostazol, Dipyridamole: Toxicity
Nausea, headache, facial flushing, hypotension, abdominal pain
30
GP IIb/IIIa inhibitors
Abciximab, Eptifibatide, Tirofiban
31
GP IIb/IIIa Inhibitors (Abciximab, Eptifibatide, Tirofiban): Mechanism
Bind to the glycoprotein receptor IIb/IIa on activated platelets, preventing aggregation. Abciximab is made from monoclonal antibody Fab fragments
32
GPIIb/IIIa inhibitors (Abciximab, Eptifibatide, Tirofiban): Clinical USe
Acute coronary syndromes, percutaneous transluminal coronary angioplasty
33
GPIIb/IIIa inhibitors (Abciximab, Eptifibatide, Tirofiban)
Bleeding, thrombocytopenia
34
Methotrexate (MTX): Mechanism
Folic acid analog that inhibits dihydrofolate reductase --> less dTMP --> less DNA and less protein synthesis
35
Methotrexate (MTX): Clinical Use
Cancers: leukemias, lymphomas, choriocarcinoma, sarcomas Non-neoplastic: abortion, ectopic pregnancy, rheumatoid arthritis, psoriasis
36
Methotrexate (MTX): Toxicity
Myelosuppression, which is reversible with leucorvorin (folinic acid) "rescue" Macrovesicular fatty chain in liver - Mucositis - Teratogenic
37
5-Fluorouracil (5-FU): Mechanism
Pyrimadine analog bioactivated to 5F-dUMP which covalently complexes folic acid. This complex inhibits thymidylate synthase --> dTMP --> less DNA and protein synthesis
38
5-Fluorouracil (5-FU): Clinical Use
Colon cancer, basal cell carcinoma (topical)
39
5-Fluorouracil (5-FU): Toxicity
Myelosuppression, which is NOT reversible with leucorvorin Overdose: "rescue" with thymidine Photosensitivity
40
Cytarabine (arabinofuranoysl cytidine): Mechanism
Pyrimidine analog --> inhibition of DNA polymerase
41
Cytarabine: Clinical Use
Leukemias, lymphomas
42
Cytarabine: Toxicity
Leukopenia, thrombocytopenia, megaloblastic anemia
43
Azathoprine ; 6-mercaptopurine; 6-thioguanine : Mechanism
Purine (thiol) analogs --> decreased de novo purine synthesis - Activated by HGPRT
44
Azathoprine; 6-mercaptopurine; 6-thioguanine: Clinical Use
Leukemias
45
Azathoprine; 5-mercaptopurine; 6-thioguanine: Toxicity
Bone marrow, GI, liver Metabolized by xanthine oxidase --> thus increase toxicity with allopurinol
46
Dactinomycin (actinomycin D): Mechanism
Intercalates in DNA
47
Dactinomycin (actinomycin D): Clinical Use
Wilm's tumor, Ewing's sarcoma, rhabdomyosarcoma Used for childhood tumors ("children ACT out")
48
Dactinomycin (actinomycin D): Toxicity
Myelosuppression
49
Doxorubicin (Adriamycin), Daunorubicin: Mechanism
Generate free radicals | Noncovalently interalate in DNA --> breaks in DNA --> decreased replication
50
Doxorubicin (Adriamycin), Daunorubicin: Clinical Use
Solid tumors, leukemias, lymphomas
51
Doxorubicin (Adriamycin), Daunorubicin: Toxicity
Cardiotoxicity (dilated cardiomyopathy), myelosuppression, Alopecia Toxic to tissues following extravasation Dexrazozane (Fe chelating agent), used to prevent cardiotoxicity
52
Bleomycin: Mechanism
Induces free radical formation , which causes breaks in DNA
53
Bleomycin: Clinical Uses
Testicular cancer, Hodgkin's lymphoma
54
Bleomycin: Toxicity
Pulmonary fibrosis, skin changes. Minimal myelosuppression
55
Cyclophosphamide; Ifosfamide: Mechanism
Covalently X-link (interstrand) DNA at guanine N-7. Require bioactivation by liver
56
Cyclophosphamide; Ifosfamide: Clinical Use
Solid tumors, leukemia, lymphomas, and some brain cancers
57
Cyclophosphamide; Ifosfamide: Toxicity
Myelosuppression; | Hemorrhagic cystitis, partially prevented with mesna (thiol group of mesna binds toxic metabolite)
58
Nitrosoureas (carmustine, lomustine, semustine, streptozocin): Mechanism
Alkylating agent Require bioactivation Cross blood-brain barrier --> CNS
59
Nitrosoureas (carmustine, lomustine, semustine, streptozocin): Clinical Use
Brain tumors (including glioblastoma multiforme)
60
Nitrosoureas (carmustine, lomustine, semusine, streptozocin): Toxicity
CNS toxicity (dizziness, ataxia)
61
Bulsulfan: Mechanism
Alkylates DNA
62
Bulsulfan: Clinical Use
CML. Also used to ablate patient's bone marrow before bone marrow before transplantation
63
Bulsulfan: Toxicity
Pulmonary fibrosis, hyperpigmentation
64
Vincristine, Vinblastine: Mechanism
Alkaloids that bind to tubulin in M phase and block polymerization of microtubules so that mitotic spindle cannot form. "Microtubules are the vines of your cells"
65
Vincristine, Vinblastine: Clinical Use
Solid tumors, leukemias, and lymphomas
66
Vincristine, Vinblastine: Toxicity
Vincristine - nephrotoxicity ( areflexia, peripheral neuritis), paralytic ileus Vinblastine - myelosuppression
67
Paclitaxel, other taxols: Mechanism
Hyperstabilize polymerized microtubules in M phase so that mitotic spindle cannot breakdown (anaphase cannot occur)
68
Paclitaxel, other taxols: Clinical Use
Ovarian and breast carcinomas
69
Paclitaxel, other taxols: Toxicity
Myelosuppression and hypersensitivity
70
Cisplatin, carboplatin: Mechanism
Cross-link DNA
71
Cisplatin, carboplatin: Clinical Use
Testicular, bladder, ovary, and lung carcinomas
72
Cisplatin, carboplatin: Toxicity
Nephrotoxicity and acoustic nerve damage. Prevent nephrotoxicity with amifostine (free radical scavenger) and chloride diuresis
73
Etoposide, Tenoposide: Mechanism
Inhibit DNA topoisomerase II --> increased DNA degradation
74
Etoposide: Tenoposide: Clinical Use
Solid tumors, leukemias, lymphomas
75
Etoposide, Tenoposide: Toxicity
Myelosuppression, GI irritation
76
Hydroxyurea: Mechanism
Inhibits ribonucleotide reductase --> less DNA Synthesis (S phase specific)
77
Hydroxyurea: Clinical Use
Melanoma, CML, sickle cell disease (increase HbF)
78
Hydroxyurea: Toxicity
Bone marrow suppression, GI upset
79
Prednisone, Prenisolone: Mechanism
May trigger apoptosis. May even work on non-dividing cells.
80
Prednisone, Prenisolone: Clinical Use
Most commonly used glucocorticoid in cancer chemotherapy. Used in CLL, non-Hodgkin's lymphoma (part of combination chemotherapy regimen). - Also used as an immunosuppressant (e.g. autoimmune disease)
81
Prednisone, Prenisolone: Toxicity
Cushing-like symptoms; immunosuppression, cataracts, acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis
82
Tamoxifen, Raloxifene: Mechanism
SERMs- receptor antagonist in breast and antagonist in bone. Block the binding of estrogen to estrogen-positive cells
83
Tamoxifen, Raloxifene: Clinical Use
Breast cancer treatment and prevention. Also useful to prevent osteoporosis
84
Tamoxifen Toxicity
Partial agonist in endometrium, which increases risk of endometrial cancer , "hot flashes"
85
Raloxifene: Toxicity
No increased risk of endometrial cancer because it is an endometrial antagonist
86
Trastuzumab (Herceptin): Mechanism
Monoclonal antibody against HER-2 (cerbB2), tyrosine kinase. Helps kill breast cancer that overexpress HER-2, possibly through antibody-dependent cytotoxicity
87
Trastuzumab (Herceptin): Clinical Use
HER-2 positive breast cancer
88
Trastuzumab (Herceptin): Toxicity
Cardiotoxicity
89
Imatinib (Gleevac): Mechanism
Philadelpha chromosome bcl-acr tyrosine kinase inhibitor
90
Imatinib (Gleevac): Clinical Use
CML, GI stromal tumors
91
Imatinib (Gleevac): Toxicity
Fluid retention
92
Rituximab: Mechanism
Monoclonal antibody against CD20, which is found in B cell neoplasms
93
Rituximab: Clinical Use
Non-Hodgkin's lymphoma, rheumatoid arthritis (with methotrexate)
94
Vemurafenib: Mechanism
Small molecule inhibitor of forms of B-RAF kinase with V600E mutation
95
Vemurafenib: Clinical Use
Metastatic melanoma
96
Bevacizumab: Mechanism
Monoclonal antibody against VEGF angiogenesis
97
Bevacizumab: Clinical Use
Solid tumors
98
Cisplatin/Carboplatin Toxicity
Acoustic nerve damage (and nephrotoxicity)
99
Vinecristine: toxicity
Peripheral neuropathy
100
Belomycin, Busulfan: Toxicity
Pulmonary fibrosis
101
Doxorubicin: Toxicity
Cardiotoxicity
102
Trastuzumab: Toxicity
Cardiotoxicity
103
Cyclophosphamide
Hemorrhagic cystitis
104
5-FU and 6-MP: Toxicity
Myelosuppression
105
Methotrexate: Toxicity
Myelosuppression

USMLE Step 1 (34 decks)

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