HEMATOLOGY

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Author:
rere_girl4ever
ID:
303229
Filename:
HEMATOLOGY
Updated:
2015-05-26 03:59:33
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HEMATOLOGY
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HEMATOLOGY
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HEMATOLOGY
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  1. Clopidogrel
    MOA: Inhibit platelet aggregation by irreversibly blocking ADP receptorsprevent expression of glycoproteins IIb/IIIa on platelet surface.

    • USE:
    • 1. Unstable angina (aspirin + clopidogrel)
    • 2. Ischemic stroke
    • 3. Acute coronary syndrome
    • 4. Coronary stenting
    • There is ↓ incidence or recurrence of thrombotic stroke
  2. Prasugrel
    MOA: Inhibit platelet aggregation by irreversibly blocking ADP receptorsprevent expression of glycoproteins IIb/IIIa on platelet surface.

    • USE: Acute coronary syndrome, coronary stenting.
    • There is ↓ incidence or recurrence of thrombotic stroke
  3. Ticagrelor
    MOA: REVERSIBLY Inhibit platelet aggregation by irreversibly blocking ADP receptorsprevent expression of glycoproteins IIb/IIIa on platelet surface.

    • USE: Acute coronary syndrome, coronary stenting.
    • There is ↓ incidence or recurrence of thrombotic stroke
  4. Ticlopidine
    MOA: Inhibit platelet aggregation by irreversibly blocking ADP receptorsprevent expression of glycoproteins IIb/IIIa on platelet surface.

    • USE: Acute coronary syndrome, coronary stenting.
    • There is ↓ incidence or recurrence of thrombotic stroke
    • Toxicity: NEUTROPENIA (↓WBCs, fever, mouth ulcers)
  5. Cilostazol
    MOA: Phosphodiesterase III inhibitor; ↑cAMP in platelets, resulting in inhibition of platelet aggregation; arteriolar vasodilator

    • 1. Intermittent claudication
    • 2. Coronary vasodilation
    • 3. Prevention of stroke or transient ischemic attacks (combined with aspirin)
    • 4. Angina prophylaxis

    • SIDE EFFECTS: Nausea, headache, facial flushing, hypotension, abdominal pain.
  6. Dipyridamole
    MOA: Phosphodiesterase III inhibitor; ↑cAMP in platelets, resulting in inhibition of platelet aggregation; arteriolar vasodilator

    • 1. Intermittent claudication
    • 2. Coronary vasodilation
    • 3. Prevention of stroke or transient ischemic attacks (combined with aspirin)
    • 4. Angina prophylaxis

    • SIDE EFFECTS: Nausea, headache, facial flushing, hypotension, abdominal pain.
  7. Abciximab
    • MOA: Bind to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation.
    • Abciximab is made from monoclonal antibody Fab fragments.

    • USE: 
    • 1. Unstable angina
    • 2. Percutaneous transluminal coronary angioplasty

    SIDE EFFECTS: Bleeding, thrombocytopenia
  8. Eptifibatide
    MOA: Bind to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation.

    • USE: 
    • 1. Unstable angina
    • 2. Percutaneous transluminal coronary angioplasty

    SIDE EFFECTS: Bleeding, thrombocytopenia
  9. Tirofiban
    MOA: Bind to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation.

    • USE: 
    • 1. Unstable angina
    • 2. Percutaneous transluminal coronary angioplasty

    SIDE EFFECTS: Bleeding, thrombocytopenia
  10. Bind to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation.
    • Abciximab
    • Eptifibatide
    • Tirofiban
  11. Phosphodiesterase III inhibitor; ↑cAMP in platelets, resulting in inhibition of platelet aggregation; arteriolar vasodilator
    • Cilostazol
    • Dipyridamole
  12. Inhibit platelet aggregation by irreversibly blocking ADP receptors. Prevent expression of glycoproteins IIb/IIIa on platelet surface.
    • Clopidogrel
    • Prasugrel
    • Ticagrelor (reversible)
    • Ticlopidine
  13. Azathioprine
    • Purine (thiol) analog → ↓de novo purine synthesis.
    • Activated by HGPRT.

    Azathioprine is metabolized into 6 -MP.

    • USE:
    • 1. Preventing organ rejection
    • 2. Rheumatoid arthritis
    • 3. IBD especially Chrons
    • 4. SLE
    • 5. Used to wean patients off steroids in chronic disease and to treat steroid-refractory chronic disease.

    • SIDE EFFECTS:
    • 1. Myelosuppression
    • 2. GI
    • 3. Liver (abdominal pain, jaundice).

    Azathioprine and 6-MP are metabolized by xanthine oxidase; thus both have ↑toxicity with allopurinol or febuxostat.
  14. 6-thioguanine
    • Purine (thiol) analog → ↓de novo purine synthesis.
    • Activated by HGPRT.
    • USE:
    • 1. Preventing organ rejection
    • 2. Rheumatoid arthritis
    • 3. IBD
    • 4. SLE
    • 5. Used to wean patients off steroids in chronic disease and to treat steroid-refractory chronic disease.

    • SIDE EFFECTS:
    • 1. Myelosuppression
    • 2. GI
    • 3. Liver (abdominal pain, jaundice).
  15. Cladribine (2-CDA)
    Purine analog Ž

    • MOA:
    • 1. Inhibition of DNA polymerase
    • 2. DNA strand breaks
    • 3. Resistant to degradation by adenosine deaminase

    USE: Hairy cell leukemia

    • TOXICITY:
    • Myelo
    • Nephro
    • Neuro
  16. Cytarabine (arabinofuranosyl cytidine)
    Pyrimidine analog

    MOAInhibition of DNA polymerase

    USE: Leukemias (AML), lymphomas.

    SIDE EFECTS: Leukopenia, thrombocytopenia, megaloblastic anemia.

    CYTarabine causes panCYTopenia.
  17. Arabinofuranosyl cytidine
    • CYTARABINE
    • Pyrimidine analog

    MOAInhibition of DNA polymerase

    USE: Leukemias (AML), lymphomas.

    SIDE EFECTS: Leukopenia, thrombocytopenia, megaloblastic anemia.

    CYTarabine causes panCYTopenia.
  18. 5-fluorouracil (5-FU)
    • Pyrimidine analog
    • Bioactivated to 5F-dUMP, which covalently complexes folic acid → complex inhibits thymidylate synthase → ↓ dTMP → ↓DNA synthesis.

    USE: Colon cancer, pancreatic cancer, basal cell carcinoma (topical).

    • SIDE EFFECTS:
    • Myelosuppression, which is not reversible with leucovorin (folinic acid).
    • Photosensitivity

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