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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
Q

Prednisone

  • phase
  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Prednisolone

  • phase
  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Tamoxifen

  • phase
  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Raloxifene

  • phase
  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Trastuzumab

  • phase
  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Imatinib

  • phase
  • MOA
  • Use
  • Toxicity
A
  • Gleevac
  • not phase specific
  • MOA: philadelphia chromosome bcr-abl tyrosine kinase inhibitor
  • Use:
    • CML
    • GI stromal tumors
  • Toxicity:
    • fluid retention
31
Q

Rituximab

  • phase
  • MOA
  • Use
  • Toxicity
A
  • not phase specific
  • MOA: monoclonal antibody against CD20
    • found on B-cell neoplasm
  • Use:
    • non-hodgkins lymphoma
    • Rheumatoid arthritis with methotrexate
32
Q

Vemurafenib

  • phase
  • MOA
  • Use
  • Toxicity
A
  • not phase specific
  • MOA: small molecule inhibitor of forms of the B-Raf kinase with the V600E mutation
  • Use:
    • metastatic melanoma
33
Q

Bevacizumab

  • phase
  • MOA
  • Use
  • Toxicity
A
  • not phase specific
  • MOA: monoclonal antibody against VEGF
    • inhibits angiogenesis
  • Clinical use:
    • solid tumor
34
Q

Heparin

  • MOA
  • Use
  • Toxicity
A

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
Q

Lepirudin

A
  • Derivative of hirudin (Anticoag in leech)
  • Inhibit thrombin
  • alternative to heparin for patients with HIT
36
Q

Bivalirudin

A
  • Derivative of hirudin (Anticoag in leech)
  • Inhibit thrombin
  • alternative to heparin for patients with HIT
37
Q

Warfarin

  • MOA
  • Use
  • Toxicity
A

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
Q

Ateplase (tPA)

  • MOA
  • PT, PTT, PC effect
  • Use
  • Toxicity
A
  • 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
Q

Reteplase (rPA)

  • MOA
  • PT, PTT, PC effect
  • Use
  • Toxicity
A
  • 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
Q

Tenecteplase (tNK-tPA)

  • MOA
  • PT, PTT, PC effect
  • Use
  • Toxicity
A
  • 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
Q

Aspirin (asa)

  • MOA
  • PT, PTT, bleeding time
  • Use
  • Toxicity
A
  • 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
Q

Clopidogrel

  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Ticlopidine

  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Prasugrel

  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Ticagrelor

  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Cilostazol

  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Dipyridamole

  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Abiciximab

  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Eptifibatide

  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Tirofiban

  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Argatroban

  • MOA
  • Use
A
  • MOA: Direct thrombin inhibitors

- Use: patients with heparin induced thrombocytopenia (HIT)

52
Q

Streptokinase

  • MOA
  • Use
  • Toxicity
A
  • 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
Q

Desmopressin

A
  • synthetic ADH
  • increase vWF release from endothelial cells
  • useful in patients with mild vWF disease
54
Q

Cladribine

  • MOA
  • Use
A
  • MOA: adenosine analog
    • resistant to degradation by adenosine deaminase
    • high intracellular [ ] –> incorporated into DNA –> DNA strand breaks
    • penetrates CNS
  • Use: hairy cell leukemia
55
Q

Enoxaparin

A

LMW heparin

  • MOA: bind antithrombin III
    • prevents 10a from converting prothombin to thrombin
  • Use: MI

Me (13 decks)

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