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Heme- Onc Flashcards

1
Q

Methotrexate (MTX)

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Antimetabolite (inhibit nucleotide synthesis)
- S phase
- MOA: folic acid analog
- inhibits dihydrofolate reductase *
- no dTMP –> no DNA + no protein synthesis
- Use:
- cancer: leukemia, lymphoma, choriocarcinoma,
sarcoma
- non- neoplastic: abortion, ectopic pregnancy, RA,
psoriasis
- Toxicity:
- Myelosuppression (reversible with leucovorin = folinic
acid)
- Macrovesicular fatty change in liver
- Mucositis
- Teratogenic
- stomatitis = painful mouth ulcers

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2
Q

5- fluorouracil (5-FU)

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A 
Antimetabolite (inhibit nucleotide synthesis)
- S phase
- MOA: pyrimidine analog
     - bioactivated to 5F-dUMP --> covalently complex folic   
     acid
     - Inhibits thymidylate synthase *
     - no dTMP --> no DNA + no protein synthesis 
- Use: 
     - colon cancer
     - basal cell carcinoma (topical)
- Toxicity:
     - Myelosuppression (NOT reversible with leucovorin)
     - Photosensitivity 
     - Overdose rescue = thymidine
- Catabolism
     - Dihydropyridine Dehydrogenase 
     - deceased DPD = severe toxicity
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3
Q

Cytarabine (arabinofuranosyl cytidine)

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Antimetabolite (inhibit nucleotide synthesis)

  • S phase
  • MOA: pyridmidine analog
    • inhibits DNA polymerase *
  • Use:
    • leukemia
    • lymphoma
  • Toxicity
    • Leukopenia
    • Thrombocytopenia
    • Megaloblastic anemia
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4
Q

Azathioprine- 6- mercaptopurine (6-MP)

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Antimetabolite (inhibit nucleotide synthesis)

  • S phase
  • MOA: purine analog
    • decrease de novo purine synthesis
    • activated by HGPRT
  • Use:
    • leukemia
    • lymphoma
  • Toxicity:
    • bone marrow
    • GI
    • liver
  • Metabolized: xanthine oxidase
    • increase toxicity with allopurinol
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5
Q

6- Thioguanine (6-TG)

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Antimetabolite (inhibit nucleotide synthesis)

  • S phase
  • MOA: purine analog
    • decrease de novo purine synthesis
    • activated by HGPRT
  • Use:
    • leukemia
    • lymphoma
  • Toxicity:
    • bone marrow
    • GI
    • liver
  • Metabolized: xanthine oxidase
    • increase toxicity with allopurinol
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6
Q

Dactinomycin (actinomycin D)

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Antitumor antibiotics (disrupts DNA)

  • Not cell cycle specific
  • MOA: intercalates in DNA
  • Use:
    • Wilm’s Tumor
    • Ewing’s sarcoma
    • Rhabdomyosarcoma
    • childhood tumors
  • Toxicity
    • myelosuppression
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7
Q

Doxorubicin (adriamycin)

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A 
Antitumor antibiotics (disrupts DNA)
- Not cell cycle specific 
- MOA: generate free radicals
    - Noncovalently intercalate in DNA --> breaks DNA --> 
     decrease DNA replication 
- Use
     - Solid tumors
     - leukemias
     - lymphomas
- Toxicity
     - Dilated Cardiotoxicity (due to free radicals) 
          - Dexrazoxane: iron chelator prevents cardiotoxicity 
     - CHF
     - myelosuppression
     - alopecia
     - toxicity to tissues following extravastion
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8
Q

Daunorubicin

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Antitumor antibiotics (disrupts DNA)
- Not cell cycle specific
- MOA: generate free radicals
- Noncovalently intercalate in DNA –> breaks DNA –>
decrease DNA replication
- Use
- Solid tumors
- leukemias
- lymphomas
- Toxicity
- Dilated Cardiotoxicity (due to free radicals)
- Dexrazoxane: iron chelator prevents cardiotoxicity
- myelosuppression
- alopecia
- toxicity to tissues following extravastion

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9
Q

Bleomycin

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Antitumor antimetabolite (disrupts DNA)

  • G2 phase
  • MOA: induce free radical formation
    • DNA strand breaks
  • Use:
    • Testicular cancer
    • Hodgkin’s lymphoma
  • Toxicity
    • Pulmonary fibrosis *
    • skin changes
    • minimal myelosuppression
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10
Q

Cyclophosphamide

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Alkylating agent (cross link DNA at guanine)
- Not cell cycle specific
- MOA: covalently x- link DNA at guanine N-7
- requires bioactivation by liver
- Use:
- solid tumors
- leukemia
- lymphoma
- brain cancers
- autoimmune disease: minimal change, RA, Wegener’s,
granulomatosis, multiple sclerosis
- Toxicity:
- myelosuppression
- hemorrhagic cystitis: dysuria, hematuria, hemorrhage of
lower urinary tract, due to excretion of toxic metabolite
- Mesna: partially prevents (thiol group binds toxic
metabolite)
- Transitional cell carcinoma
- SIADH

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11
Q

Ifosfamide

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Alkylating agent (cross link DNA at guanine)
- Not cell cycle specific
- MOA: covalently x- link DNA at guanine N-7
- requires bioactivation by liver
- Use:
- solid tumors
- leukemia
- lymphoma
- brain cancers
- autoimmune disease: minimal change, RA, Wegener’s,
granulomatosis, multiple sclerosis
- Toxicity:
- myelosuppression
- hemorrhagic cystitis: dysuria, hematuria, hemorrhage of
lower urinary tract
- Mesna: partially prevents (thiol group binds toxic
metabolite)
- Transitional cell carcinoma

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12
Q

Carmustine

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Alkylating agent (cross link DNA at guanine)

  • Nitrosourea
  • Not cell cycle specific
  • MOA: cross blood brain barrier —> CNS ***
    • require bioactivation
  • Use:
    • brain tumors (including gliobastoma multiforme)
  • Toxicity:
    • CNS toxicity= dizziness, ataxia
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13
Q

Lomustine

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Alkylating agent (cross link DNA at guanine)

  • Nitrosourea
  • Not cell cycle specific
  • MOA: cross blood brain barrier —> CNS ***
    • require bioactivation
  • Use:
    • brain tumors (including gliobastoma multiforme)
  • Toxicity:
    • CNS toxicity= dizziness, ataxia
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14
Q

Semustine

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Alkylating agent (cross link DNA at guanine)

  • Nitrosourea
  • Not cell cycle specific
  • MOA: cross blood brain barrier —> CNS ***
    • require bioactivation
  • Use:
    • brain tumors (including gliobastoma multiforme)
  • Toxicity:
    • CNS toxicity= dizziness, ataxia
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15
Q

Streptozocin

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Alkylating agent (cross link DNA at guanine)

  • Nitrosourea
  • Not cell cycle specific
  • MOA: cross blood brain barrier —> CNS ***
    • require bioactivation
  • Use:
    • brain tumors (including gliobastoma multiforme)
  • Toxicity:
    • CNS toxicity= dizziness, ataxia
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16
Q

Busulfan

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A 
Alkylating agent ( cross link DNA at guanine)
- Nitrosurea
- Not cell cycle specific
- MOA: alkylates DNA
- Use:
     - CML
     - ablate bone marrow before bone marrow   
     transplantation
- Toxicity
     - pulmonary fibrosis
     - hyperpigmentation 
     - adrenal insufficiency
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17
Q

Vincristine

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Microtubule inhibitors (inhibit cell division)
- M phase specific
- MOA: destabilizer
- alkaloid
- bind tubulin in M phase and block polymerization of
microtubules –> mitotic spindle cannot form
- Use:
- solid tumors
- leukemias
- lymphomas
- Toxicity:
- neurotoxicity = areflexia, peripheral neuritis
- paralytic ileus

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18
Q

Vinblastine

  • class
  • phase
  • MOA
  • Use
  • Toxicity
A 
Microtubule inhibitors (inhibit cell division)
- M phase specific
- MOA: destabilizer
     - alkaloid
     - bind tubulin in M phase and block polymerization of   
     microtubules --> mitotic spindle cannot form 
- Use:
     - solid tumors
     - leukemias
     - lymphomas 
- Toxicity:
     - bone marrow suppression
     - potent vesicant
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19
Q

Paclitaxel

  • other “taxols”
  • class
  • phase
  • MOA
  • Use
  • Toxicity
A

Microtubule inhibitors (inhibit cell division)

  • M phase specific
  • MAO: stabilizer
    • hyperstabilize polymerized microtubules in M phase
    • mitotic spindle cannot break down (no anaphase)
  • Use:
    • ovarian cancel
    • breast cancer
  • Toxicity
    • myelosuppression
    • hypersensitivity
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20
Q

Cisplatin

  • phase
  • MOA
  • Use
  • Toxicity
A
  • Not cell cycle specific
  • MOA: cross- link DNA (intrastrand + inter strand)
  • Use:
    • testicular
    • bladder
    • ovary
    • lung
  • Toxicity
    • nephrotoxicity
      • Amifostone: free radical scavenger, prevent
        nephrotoxicity
    • acoustic nerve damage
    • chloride diuresis
  • need pre-hydration
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21
Q

Carboplatin

  • phase
  • MOA
  • Use
  • Toxicity
A
  • Not cell cycle specific
  • MOA: cross- link DNA (intrastrand + inter strand)
  • Use:
    • testicular
    • bladder
    • ovary
    • lung
  • Toxicity
    • nephrotoxicity
      • Amifostone: free radical scavenger, prevent
        nephrotoxicity
    • acoustic nerve damage
    • chloride diuresis
    • less nephrotoxic –> no prehydration
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22
Q

Etoposide

  • phase
  • MOA
  • Use
  • Toxicity
A
  • S-G2 phase specific
  • MOA: inhibit topoisomerase II
    • increase DNA degradation
  • Use
    • solid tumors
    • leukemias
    • lymphomas
  • Toxicity
    • myelosuppression
    • GI irritation
    • alopecia
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23
Q

Teniposide

  • phase
  • MOA
  • Use
  • Toxicity
A
  • S-G2 phase specific
  • MOA: inhibit topoisomerase II
    • increase DNA degradation
  • Use
    • solid tumors
    • leukemias
    • lymphomas
  • Toxicity
    • myelosuppression
    • GI irritation
    • alopecia
24
Q

Hydroxyurea

  • phase
  • MOA
  • Use
  • Toxicity
A
  • S- phase specific
  • MOA: inhibit ribonucleotide reductase*
    • decease DNA synthesis
  • Use:
    • melanoma
    • CML
    • sickle cell disease = increase HbF
  • Toxicity:
    • bone marrow suppression
    • GI upset
25
Prednisone - phase - MOA - Use - Toxicity
- Not phase specific - MOA: may trigger apoptosis - may work on nondividing cells - Use: - most commonly used glucocorticoids in cancer chemo - CLL - non-hodgkins lymphoma - immosuppressant (autoimmune disease) - Toxicity: - Cushing like syndrome - immunosuppression - acne - osteoporosis - HTN - peptic ulcers - hyperglycemia - psychosis
26
Prednisolone - phase - MOA - Use - Toxicity
- Not phase specific - MOA: may trigger apoptosis - may work on nondividing cells - Use: - most commonly used glucocorticoids in cancer chemo - CLL - non-hodgkins lymphoma - immosuppressant (autoimmune disease) - Toxicity: - Cushing like syndrome - immunosuppresion - acne - osteoporosis - HTN - peptic ulcers - hyperglycemia - psychosis
27
Tamoxifen - phase - MOA - Use - Toxicity
- Not phase specific - MOA: SERM -estrogen receptor antagonists in breast -estrogen receptor agonist in bone - Use: - breast cancer treatment + prevention - osteoporosis prevention - Toxicity - partial agonist in endometrium --> increase risk of endometrial cancer - hot flashes
28
Raloxifene - phase - MOA - Use - Toxicity
- Not phase specific - MOA: SERM - estrogen receptor antagonists in breast - estrogen receptor agonist in bone - estrogen receptor antagonists in endometrium - Use: - breast cancer treatment + prevention - osteoporosis prevention - Toxicity - no increase risk of endometrial cancer
29
Trastuzumab - phase - MOA - Use - Toxicity
- Herceptin - not phase specific - MOA: monoclonal antibody against HER-2, tyrosine kinase - helps kill breast cancer cells that over express HER-2 - antibody- dependent cytotoxicity may be mechanism - Use: HER-2 positive breast cancer - Toxicity: - cardiotoxicity
30
Imatinib - phase - MOA - Use - Toxicity
- Gleevac - not phase specific - MOA: philadelphia chromosome bcr-abl tyrosine kinase inhibitor - Use: - CML - GI stromal tumors - Toxicity: - fluid retention
31
Rituximab - phase - MOA - Use - Toxicity
- not phase specific - MOA: monoclonal antibody against CD20 - found on B-cell neoplasm - Use: - non-hodgkins lymphoma - Rheumatoid arthritis with methotrexate
32
Vemurafenib - phase - MOA - Use - Toxicity
- not phase specific - MOA: small molecule inhibitor of forms of the B-Raf kinase with the V600E mutation - Use: - metastatic melanoma
33
Bevacizumab - phase - MOA - Use - Toxicity
- not phase specific - MOA: monoclonal antibody against VEGF - inhibits angiogenesis - Clinical use: - solid tumor
34
Heparin - MOA - Use - Toxicity
PTT Rapid onset - MOA: activates antithrombin - decrease factor 2, 10 - Use: - immediate anticoagulant for: - PE, acute coronary syndrome, MI, DVT - pregnancy (does not cross placenta) - unfractionated and LMW heparin --> prevention of DVT in non-ambulatory patients or patients undergoing elective surgery (Esp of knee and hip) --> IV so in hospital - only unfractionated** heparin can bind both antithrombin + thrombin - Toxicity - bleeding - thrombocytopenia (HIT) - osteoporosis - drug-drug interactions - Heparin induced thrombocytopenia - develop IgG antibodies against heparin bound to platelet factor 4 (PF4) --> activates platelets --> thrombosis --> thrombocytopenia - Protamine Sulfate = antidote for overdose - (+) charged molecules that bind negatively charged heparin - Enoxaparin, Dalteparin - LMW heparin: act more on factor 10, better bioavailability, 2-4 times longer half life, administered subQ and w/o lab monitoring, not easily reversed
35
Lepirudin
- Derivative of hirudin (Anticoag in leech) - Inhibit thrombin - alternative to heparin for patients with HIT
36
Bivalirudin
- Derivative of hirudin (Anticoag in leech) - Inhibit thrombin - alternative to heparin for patients with HIT
37
Warfarin - MOA - Use - Toxicity
PT/ INR Slower onset - MOA: inhibits epoxide reductase - no activation of vitamin K - Vit K gamma- carboxylates factors 2, 7, 9, 10, protein C, protein S - Use: - chronic anticoagulant - after, STEMI, venous thromboembolism prophylaxis, prevention of stroke and a-fib - after mechanical valve replacement - do NOT use in pregnancy (Cross placenta) - Toxicity - bleeding - teratogenic - drug- drug interactions - metabolized by CYP450 - Skin/ tissue necrosis - Needs to be given with another anticoag initially - Protein C + S: shorter 1/2 life, removed quicker with start of warfarin - factors 2, 7, 9, 10: longer 1/2 life, remain for first few days of treatment --> knocks out natural anti-coags while pro-coags remain therefore procoagulant for first few days - Vitamin K = antidote for overdose - fresh frozen plasma = rapid reversal
38
Ateplase (tPA) - MOA - PT, PTT, PC effect - Use - Toxicity
- Thrombolytic - MOA: directly or indirectly aid in conversion of plasminogen --> plasmin - cleaves thrombin + fibrin clots - increase PT, PTT - no change in platelet count - Use: - early MI (within 6 hours of onset) - early ischemic stroke - direct thrombolysis of severe PE - Toxicity: - bleeding - dont use in patients with active bleed, history of intracranial bleed, recent surgery, known bleeding diatheses, severe HTN - reperfusion arrhythmias on arterial re-opening - aminocaproic acid = antidote for overdose - inhibits fibrinolysis
39
Reteplase (rPA) - MOA - PT, PTT, PC effect - Use - Toxicity
- Thrombolytic - MOA: directly or indirectly aid in conversion of plasminogen --> plasmin - cleaves thrombin + fibrin clots - increase PT, PTT - no change in platelet count - Use: - early MI (within 6 hours of onset) - early ischemic stroke - direct thrombolysis of severe PE - Toxicity: - bleeding - dont use in patients with active bleed, history of intracranial bleed, recent surgery, known bleeding diatheses, severe HTN - reperfusion arrhythmias on arterial re-opening - aminocaproic acid = antidote for overdose - inhibits fibrinolysis
40
Tenecteplase (tNK-tPA) - MOA - PT, PTT, PC effect - Use - Toxicity
- Thrombolytic - MOA: directly or indirectly aid in conversion of plasminogen --> plasmin - cleaves thrombin + fibrin clots - increase PT, PTT - no change in platelet count - Use: - early MI (with 6 hours of onset) - early ischemic stroke - direct thrombolysis of severe PE - Toxicity: - bleeding - dont use in patients with active bleed, history of intracranial bleed, recent surgery, known bleeding diatheses, severe HTN - reperfusion arrhythmias on arterial re-opening - aminocaproic acid = antidote for overdose - inhibits fibrinolysis
41
Aspirin (asa) - MOA - PT, PTT, bleeding time - Use - Toxicity
- MOA: irreversibly inhibits COX-1 + COX-2 - covalent acetylation - platelet cannot synthesize new enzymes so effect last until new platelets made - Decreases thromboxane A2 (platelet aggregation) + prostaglandin - no change in PT, PTT - increased bleeding time - Use - antipyretic (PGE) - analgesic - anti-inflammatory - decrease platelet aggregation - Toxicity - gastric ulceration - tinnitus (CN8) - chronic use: acute renal failure, interstitial nephritis, upper GI bleed - Reye's syndrome: dont give to kids with viral infection - Overdose - respiratory alkalosis + metabolic acidosis
42
Clopidogrel - MOA - Use - Toxicity
- ADP receptor inhibitor - MOA: inhibit platelet aggregation - irreversible block ADP receptors - inhibit fibrinogen binding by preventing GPIIb/IIIa from binding fibrinogen - Use: - acute coronary syndrome, coronary stenting - decrease incidence of recurrence of thrombosis - ischemic stroke prevention - peripheral vascular disease - 1st line, often used with aspirin
43
Ticlopidine - MOA - Use - Toxicity
- ADP receptor inhibitor - MOA: inhibit platelet aggregation - irreversible block ADP receptors - inhibit fibrinogen binding by preventing GPIIb/IIIa from binding fibrinogen - Use: - acute coronary syndrome, coronary stenting - decrease incidence of recurrence of thrombosis - ischemic stroke prevention - peripheral vascular disease - Toxicity - neutropenia = fever + mouth ulcers - Use if allergic to aspirin or clopidogrel
44
Prasugrel - MOA - Use - Toxicity
- ADP receptor inhibitor - MOA: inhibit platelet aggregation - irreversible block ADP receptors - inhibit fibrinogen binding by preventing GPIIb/IIIa from binding fibrinogen - Use: - acute coronary syndrome, coronary stenting - decrease incidence of recurrence of thrombosis
45
Ticagrelor - MOA - Use - Toxicity
- ADP receptor inhibitor - MOA: inhibit platelet aggregation - irreversible block ADP receptors - inhibit fibrinogen binding by preventing GPIIb/IIIa from binding fibrinogen - Use: - acute coronary syndrome, coronary stenting - decrease incidence of recurrence of thrombosis
46
Cilostazol - MOA - Use - Toxicity
- MOA: phosphodiesterase III inhibitor - increase caMP in platelets - inhibit platelet aggregation - vasodilate - Use - intermittent claudication (peripheral artery disease) - coronary vasodilation - prevention of strokes or TIA (with aspirin) - angina prophylaxis - Toxicity - Nausea - headache - facial flush - abdominal pain
47
Dipyridamole - MOA - Use - Toxicity
- MOA: phosphodiesterase III inhibitor - increase caMP in platelets - inhibit platelet aggregation - vasodilate - Use - intermittent claudication (peripheral artery disease) - coronary vasodilation - prevention of strokes or TIA (with aspirin) - angina prophylaxis - Toxicity - Nausea - headache - facial flush - abdominal pain
48
Abiciximab - MOA - Use - Toxicity
- GP IIb/ IIIa inhibitor - MOA: bind GPIIb/IIIa on activated platelets - prevent platelet aggregation - Use: - acute coronary syndrome - percutaneous transluminal coronary angioplasty - Toxicity: - bleeding - thombocytopenia
49
Eptifibatide - MOA - Use - Toxicity
- GP IIb/ IIIa inhibitor - MOA: bind GPIIb/IIIa on activated platelets - prevent platelet aggregation - Use: - acute coronary syndrome - percutaneous transluminal coronary angioplasty - Toxicity: - bleeding - thombocytopenia
50
Tirofiban - MOA - Use - Toxicity
- GP IIb/ IIIa inhibitor - MOA: bind GPIIb/IIIa on activated platelets - prevent platelet aggregation - Use: - acute coronary syndrome - percutaneous transluminal coronary angioplasty - Toxicity: - bleeding - thombocytopenia
51
Argatroban - MOA - Use
- MOA: Direct thrombin inhibitors | - Use: patients with heparin induced thrombocytopenia (HIT)
52
Streptokinase - MOA - Use - Toxicity
- Thrombolytic - - Protein synthesized by beta hemolytic streptococci - MOA: forms complex with plasminogen that cleaves plasminogen to plasmin --> cleaves fibrin --> dissolve clots - - also destroys fibrinogen and clotting factors 5 + 7 - Use: treat within 6 hours of acute MI - Toxicity: hemorrhage of any organs - -( cerebral hemorrhage: decrease level of consciousness, asymmetric pupils, irregular bleed)
53
Desmopressin
- synthetic ADH - increase vWF release from endothelial cells - useful in patients with mild vWF disease
54
Cladribine - MOA - Use
- MOA: adenosine analog - - resistant to degradation by adenosine deaminase - - high intracellular [ ] --> incorporated into DNA --> DNA strand breaks - - penetrates CNS - Use: hairy cell leukemia
55
Enoxaparin
LMW heparin - MOA: bind antithrombin III - - prevents 10a from converting prothombin to thrombin - Use: MI

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