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Step 1 Drugs > Heme/Onc > Flashcards

Heme/Onc Flashcards

1
Q

Heparin

A

MOA: cofactor for the activation of antithrombin, decreased thrombin and decreased factor Xa

Clinical: immediate anticoagulant for PE, acute coronary syndrome, MI, DVT-prophylaxis in knee and hip surgery and non ambulatory patients
Used during pregnancy

Follow PTT

Toxicity: bleeding, thrombocytopenia (IgG antibodies againts heparin boud to platelet factor 4) , osteoporosis, drug-drug interactions
Protamine sulfate for antidote (postively charged binds negatively charged heparin-not effective for LMWH)

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2
Q

enoxaprin

A

LMWH
active antithrombiin III
Act more on factor Xa
Longer half life and better bioavailability
Administered subcutanoeusly and without lab monitoring

Significantly reduces death and recurrent MI when used acutely for MI
better for acute coronary syndrome

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3
Q

Argatroban, bivalirudin, lepirudin

A

Derivatives hirudin an anticoagulant used by leeches
Inhibit thrombin directly (do not require antithormbin III)

Used in patients with heparin induced thrombocytopenia

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4
Q

Warfarin

A

MOA: interfers with normal synthesis and y-carboxylation of glutamic acid of Vitamin K (clotting factors II, VII, IX and X, proteins C and S)
Metabolized by cytochrome P-450 pathway
Monitor PT/ INR

Clinical: chronic anticoagulation (after STEMI, venous thromboembolism prophylaxis, and prevention of stroke in A. fib)
Not used in pregnant women

Toxicity: bleeding, teratogenic (fetal hemorrhagic jaundice, optic neuritis), skin/tissue necrosis, drug-drug interactions

Warfarin overdose: vitamin K antidote
Rapid reversal: fresh frozen plasma

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5
Q

Aixaban, rivaroxaban

A

MOA: direct Xa inhibitors

Clinical: treatment and prophylaxis of DVT and PE (Riva), stroke propylaxis in patients with A. fib

Toxicity: bleeding

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6
Q

Altepase, reteplase, tenectelplase

A

Thrombolytics-alteplase (tPA), reteplase (rPA), tenecteplase (TNK-tPA)

MOA: diretly or indirectly aid conversion of plasminogen to plasmin which cleaves thrombin and fibrin cltos
Increases PT, PTT with no change in platelet count

Clinical: early MI (within 6 hours) early ischemic stroke, direct thrombolysis of severe PE, acute ST eleveation MI decreases mortality

Toxicity: Bleeding, restoration of blood flow after clot lysis can lead to benign arrhythmias

CI: patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension

Treat toxicity with aminocarpoic acid inhibitor of fibrinolysis
Fresh frozen plasma and cryoprecipitate can also correct factor deficiencies

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7
Q

Aspirin

A

Irreversibly inhibits Cyclooxgenase (COX-1 and COX-2) by covalent acetlyation
Platelets cannot synthesize new enzyme
Increases BT, decreases TXA2, prostaglandins
No effect on PT or PTT

Clinical: Antipyretic, analgesic, anti-inflammatory, antiplatelet (decreases aggregation)

Toxicity: gastric ulceration, tinnitus,
Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding
Reye syndrome in children with viral infection

Overdose causes respiratory alkalosis then superimposed metabolic acidosis

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8
Q

Clopidogrel

A

ADP receptor inhibitors
MOA: inhibit platelet aggregation by irreversibly blocking ADP receptors
Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen

Clinical: Acute coronary syndrome, coronary stenting, decrease incidence or recurrence of thormbotic stroke

Toxicity: netuorpenia (ticlopidine-fever and mouth ulcers), TTP/HUS

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9
Q

Cilostazol

A

MOA: phsopdiesterase III inhibitor
Increase cAMP in platelets preventing platelet shape change and granule release
Inhibiting platelet aggregation
Vasodilates

Clinical: intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (with aspirin), angina prophylaxis

Toxicity: nausea, headache, facial flushing, hypotension, abdominal pain

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10
Q

Abcimiximab

A

GP IIb/IIIa inhibitors
MOA: bind to glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation

Clinical: unstable angina, percutaneous transluminal coronary angioplasty

Toxicity: bleeding, thromobcytopenia

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11
Q

Radiation therapy

A

Initiates cell death by
1. DNA strand breakage
2. Formation of free radicals
Most pronounced in rapidly dividing cells
Side effects: damage to epithileal surfaces (bowel and skin)

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12
Q

Methotrexate

A

MOA: folic acid analog that inhibits dihydrofolate reductase (irreversible)
Decraeses dTMP leading to decreased DNA and decreased protein synthesis
S phase specific
Resultant Increase Dihydroflolate polyglutamate

Clinical: leukemias, lymphomas, choriocarcinoma, sarcomas
abortion, ectopic pregnancy, rheumatoid arthritis, psoriasis, IBD, hydatiform mole

Toxicity: myelosuppresion-reversible with leucorvin
leucorvin does not require DHF reductase to convert to THF
Macorvesicular fatty change in liver (Incrased ALT and AST)
Mucositis, stomatitis-painful ulcers
Teratogenic
B cell lymphoma, opportunistic infections
Pulmonary fibrosis

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13
Q

5-fluorouracil

A

MOA: pyrimidine analog bioactivated to 5F-dUMP which covalently complexes folic acid
Inhibits thymidylate synthase leading to decreased dTMP and decreased DNA protein and protein synthesis

Clinical: colon cancer, pancreatic cancer, basal cell carcinoma

Toxicity: myelosuppression, photosensitivity

Overdose rescue with uridine

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14
Q

Cytarabine

A

MOA: pyrimidine analog leading to inhibition of DNA polymerase

Clinical: leukemias, lymphomas

Toxicity: leukopenia, thrombocytopenia, megaloblastic anemia (panCYTOpenia)

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15
Q

Azathiprine, 6-mercaptopurine, 6-thioguanine

A

MOA: purine analogs decreasing de nova pruien synthesis
activated by HGPRT

Clinical: preventing organ rejection, Rheumatoid arthritis, SLE (Azothiroprine), leukemia and IBD (6-MP, 6-TG)

Toxicity: bone marrow, GI, liver

Axothioprine and 6-MP metabolized by xanthine oxidase which increases toxicity with allopurinol

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16
Q

Dactinomycin (actinomycin D)

A

MOA: intercalates in DNA

Clinical: wilms tumor, Ewing sarcoma, rhabdomyosarcoma
Childhood tumors

Toxicity: myelosuppression

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17
Q

Doxorubicin (Adriamycin), daunorubicin

A

MOA: generate free radicals
Intercalate in DNA leading to breaks in DNA decreasing replication

Clinical: solid tumors, leukemias, lymphomas

Toxicity: cardiotoxicity (dilated cardiomyopathy), myelosuppressin, alopecia
Toxic to tissues following extravasation

Dexrazoxane (iron chelator), prevents cardiotoxicity

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18
Q

Bleomycin

A

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

Clinical: testicular cancer, Hodgkin lymphoma

Toxicity: pulmonary fibrosis, skin changes, mucositis, minimal myelosuppression

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19
Q

Cyclophosphamide, ifosfamide

A

MOA: covalently X link DNA at guanine N-7
Require activation by liver

Clinical:solid tumors, leukemia, lymphomas, and some brain cancers
POLYARTERITIS NODOSA
WEGENERS, MICROSCOPIC POLYANGIITIS

Toxicity: myelosuppression, hemorrhagic cystitis,

Partially prevented with MESNA (bind acrolein)

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20
Q

Nitrosoureas (carmustine, lomustine, semustine, streptozocin)

A

MOA: cross BBB
Cross link DNA

Clinical: brain tumors

Toxicity: convulsins, dizziness, ataxia

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21
Q

Busulfan

A

MOA: cross links DNA

Clinical: CML
Ablate bone marrow before transplantation

Toxicity: myelosuppression, pulmonary fibrosis, hyperpigmentation

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22
Q

Vincristine, vinblastine

A

MOA: bind B-tubulin inhibiting its polymerizatin into microtubles preventing mitotic spindle formation
M-phase arrest

Clinical: solid tumors, leukemias and lymphomas

Toxicity: Vincristine-neurotoxicity (areflexia, peripheral neuritis), paralytic ileus
Vinblastine-bone marrow suppression

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23
Q

Paclitaxel

A

MOA: Hyperstablize polymerized microtubules in M phase so mitotic spindle cannot break down (anaphase can’t occur)

Clinical: ovarian and breast carcinomas

Toxicity: myelosuppression, alopecia, hypersensitivity

24
Q

Cisplatin, carboplatin

A

MOA: cross link DNA by forming ROS

Clinical: testicular, bladder, ovary and lung carciomas

Toxicity: nephrotxocity and acoustic nerve damage

Prevent nephrotoxicity with amifostine (free radical scavenger) and chloride diuresis (Cisplatin is nonreactive when there is an increase in Cl concentration)

25
Q

Etoposide

A

MOA: inhibits topoisomerase leading to increase in DNA degradation
Clinical: solid tumors (testicular and small cell lung cancer), leukemias, lymphomas
Genital warts-podophyllin

Toxicity: myelosuppression, GI irritation, alopecia

26
Q

Irinotecan, topotecan

A

MOA: inhibit topisomerase I and prevent DNA unwinding and replication

Clinical: colon cancer (irinotecan), ovarian and small cell lung cancer (topotecan)

Toxicity: myelosuppression, diarrhea

27
Q

Hydroxyurea

A

MOA: inhibits ribonucleotide reductase leading to decreased DNA synthesis (S phase specific)
Clinical: melanoma, CML, sickle cell disease (increases HbF)

Toxicity: bone marrow suppression, GI upset

28
Q

Gardos blockers

A

Used in sickle cell

Calcium dependent K+ channel blockers
Gardos channels block transport of potassium and water through RBC membrane
Blocks efflux preventing dehydration of erythrocytes and polymerization of Hbs

29
Q

Prednisone, prednisolone

A

MOA: may trigger apoptosis, may work on nondividing cells

Clinical: Most commonly used glucocorticoids in cancer chemotherapy
CLL, non-hodgkin lymphomas, immunosuppressant, autoimmune diseases

Toxicity: Cushing like smptoms, weight gain, central obesity, muscle breakdown, cataracts, acne, osteoporosis (inhibits intestinal action of Vit. D), hypertension, peptic ulcers,hyperglycemia, psychosis

30
Q

Tamoxifen, raloxifene

A

MOA: selective receptor modulators-receptor antagonists in breast and agonists in bone
block the binding of estrogen to ER

Clinical: breast cancer treatment (tamoxifen), and prevention, Ralaxoifeen useful in preventing osteoporosis

Toxicity: tamoxifen-partial agonist in endometrium, which increases the risk of endometrial cancer, hot flashes
Raloxifene-no increase risk of endometrial cancer

Agonist for cardiovascular system and blood lipoproteins

31
Q

Trastuzumab

A

Herceptin
MOA: monocolonal Ab againts HER-2 a tyrosine kinase
Kills breast cancer cells that overexpres HER-2 through inhibition of HER2 initiated cellular signaling and Ab-dependent cytotoxicity

Clinical: HER2+ breast cancer and gastric cancer

Toxicity: cardiotoxicity

32
Q

Imatinib

A

Gleevec
MOA: tyrosine kinase inhibitor of bcr-abl and c-Kit (GI stromal tumors)

Clinical: CML, GI stromal tumors

Toxicity: fluid retention

33
Q

Rituximab

A

MOA: monoclonal Ab against CD20 which is found on B cell neoplasms

Clinical: non-hodgkin lymphoma, rheumatoid arthritis (with MTX), ITP

Toxicity: increase risk of progressive mutlifocal leukocencephalopathy

34
Q

Verurafenib

A

MOA: small molecule inhibitor of forms of B-Raf kinase with V600E mutation
Clinical: metastatic melanoma

35
Q

Bevacizumab

A

MOA: monoclonal Ab against VEGF inhibiting angiogenesis

Clinical: solid tumors (colorectal cancer, renal cell carcinoma)

Toxicity: hemorrhage, and impaired wound healing

36
Q

dalteparin

A

LMWH
active antithrombiin III
Act more on factor Xa
Longer half life and better bioavailability
Administered subcutanoeusly and without lab monitoring

Significantly reduces death and recurrent MI when used acutely for MI
better for acute coronary syndrome

37
Q

ticlopidine

A

ADP receptor inhibitors
MOA: inhibit platelet aggregation by irreversibly blocking ADP receptors
Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen

Clinical: Acute coronary syndrome, coronary stenting, decrease incidence or recurrence of thormbotic stroke

Toxicity: netuorpenia (ticlopidine-fever and mouth ulcers), TTP/HUS

38
Q

prasugrel

A

ADP receptor inhibitors
MOA: inhibit platelet aggregation by irreversibly blocking ADP receptors
Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen

Clinical: Acute coronary syndrome, coronary stenting, decrease incidence or recurrence of thormbotic stroke

Toxicity: netuorpenia (ticlopidine-fever and mouth ulcers), TTP/HUS

39
Q

ticagrelor

A

ADP receptor inhibitors
MOA: inhibit platelet aggregation by irreversibly blocking ADP receptors
Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen

Clinical: Acute coronary syndrome, coronary stenting, decrease incidence or recurrence of thormbotic stroke

Toxicity: netuorpenia (ticlopidine-fever and mouth ulcers), TTP/HUS

40
Q

dipyridamole

A

MOA: phsopdiesterase III inhibitor
Increase cAMP in platelets preventing platelet shape change and granule release
Inhibiting platelet aggregation
Vasodilates

Clinical: intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (with aspirin), angina prophylaxis

Toxicity: nausea, headache, facial flushing, hypotension, abdominal pain

41
Q

eptifibatide

A

GP IIb/IIIa inhibitors
MOA: bind to glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation

Clinical: unstable angina, percutaneous transluminal coronary angioplasty

Toxicity: bleeding, thromobcytopenia

42
Q

tiorfiban

A

GP IIb/IIIa inhibitors
MOA: bind to glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation

Clinical: unstable angina, percutaneous transluminal coronary angioplasty

Toxicity: bleeding, thromobcytopenia

43
Q

teniposide,

A

MOA: inhibits topoisomerase leading to increase in DNA degradation
Clinical: solid tumors (testicular and small cell lung cancer), leukemias, lymphomas
Genital warts-podophyllin

Toxicity: myelosuppression, GI irritation, alopecia

44
Q

podophyllin

A

MOA: inhibits topoisomerase leading to increase in DNA degradation
Clinical: solid tumors (testicular and small cell lung cancer), leukemias, lymphomas
Genital warts-podophyllin

Toxicity: myelosuppression, GI irritation, alopecia

45
Q

Ristocetin

A

Activates vWF to bind to GpIb

Useful for diagnosis: normal platelet aggregation is not seen in von Willebrand disease

46
Q

Desmopressin

A

Stimulates vWF release from endothelium

Used in vWF deficiency, diabetes insipidus and bed wetting

47
Q

Cladribine

A

MOA: purine analog (adenosine) incorporated into DNA leading to DNA strand breaks

Clinical: hairy cell leukemia

Resistant to degradation by adenosine deaminase therefore able to reach high Intracellular concentrations

48
Q

Fludarabine

A

MOA: purine analog

Used for CLL

Toxicity: Myelosuppression especially of CD4 and CD8 cells
Athralgias

49
Q

Eculizumab

A

Prevents conversion of C5 to C5a decreasing the risk of thrombosis

Clinical: paroxysmal nocturnal hemoglobnuria

AE: increased risk of fatal meningococcal infections
High cost

50
Q

Ruxolitinib

A

JAK2 inhibitor

Used for primary Myelofibrosis

51
Q

Fondaparinux

A

Synthetic factor Xa inhibitor

Anticoagulant

52
Q

Blood tranfusion therapy: packed RBCs and Platelets

A

RBCs: Increase Hb and O2 carrying capacity
Clinical: acute blood loss, severe anemia

Platelets: Increase platelet count
Clinical: stop significant bleeding (thrombocytopenia, qualitative platelet defects)

53
Q

Fresh frozen plasma

A

Increase coagulation factor levels

Clinical: DIC, cirrhosis, warfarin overdose, exchange transfusion in TTP/HUS

54
Q

Cryoprecipitate

A

Contains fibrinogen, factor VIII, factor XIII, vWF, and fibronectin

Clinical: treat coagulation factor deficiencies involving fibrinogen and factor VIII

55
Q

Blood transfusion risks

A

infection transmission (low)
transfusion reactions
iron overload (increased hemosiderin-yellow, brown pigment)
Hypocalcemia (citrate is calcium chelator)
Hyperkalemia (RBCs may lyse in old blood units)

56
Q

Tranexamic acid

A

Antifibrinolytic agent for heavy menstruation, prevent excessive blood loss during certain surgeries.

Step 1 Drugs (15 decks)

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