Heme Onc Flashcards

1
Q

Heparin

A
  • Activates AT3 which cleaves factors 2 and 10
  • Highle negatively charged and rapid action
  • Used in acute settings
  • Reversal is protamine
  • Use in pregnant women instead of warfarin
  • Follow effect with PTT
  • Can cause HIT with a hapten to platelet facto 4 that cuases activation, thrombosis and thromboytopenia, use lepirudin/valirudin instead
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2
Q

Lepirudin/Bivalirudn

A

-Direct thrombin inhibitors that are used in pts with HIT

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3
Q

Enoxparin, daliparin

A
  • LMWH have longer halflife and can be adminitered subQ

- Easier to control

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4
Q

Warfarin

A
  • Inhibits gamma crboxylation and Ca binding site of vitamin K dependent clotting factors (2,7,9,10, C, S)
  • Used as long teerm antocoagulation
  • Check with PT/INR
  • Vitamin K will decrese effec
  • CYp metabolism
  • Antidote is FFP and vitamin K
  • Take effect in days
  • Teratotgen that can cause hydrops and death, most associated with bleeds and retinopathy in infant
  • Skin Necrosis from differentia C and S half lfe
  • C activated by thrombomodulin and S to cleave factor 5
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5
Q

Urokinase

A

-Prtoease that activates TPA

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6
Q

Ateleplse, reteleplase

A

Thrombolytics that activate tPA

  • Used in acute stroke, embolism, etc
  • Contraindicated in active bleeds/HTN
  • Aminocaproic acid is antidote
  • Plasminogen cleaves thrombin and fibrin leading to elevation in PT and PTT
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7
Q

ASA

A

IRreversible acetylation of COX leads to impaired TXA2 function and decreased aggregation

  • Used prophylaxis in MI and cloting
  • Increase in bleeding time with normal PT and PTT
  • Can cause renal failure (decrease in PGE at afferent arteriole), interstitial nephritis, decreased PGE leads to GI bleeding and ulcers
  • Reye’s with mitochondrial dysfunction
  • Overdose is rapid respiratory alkalosis followed by metabolic acidosis
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8
Q

Clopidrogel, toclodipine,tigrecglacor

A
  • ADP recepor inhibitors that are irreversible
  • Prevent expression of GP2b3a on cell surface and decrease aggreation
  • Increase BT with no change in PT/PTT
  • used post stent commonly
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9
Q

Cilostazol, dipyramidole

A
  • PDE inhibitors lead to decreeased platelet activation and also vasodilation
  • Can be used as angina prophylaxis and TIA
  • Can cause hypotenion, fatigue, abdomiinal and headache
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10
Q

Abciximab, tirofiban, excibitide

A
  • Inhibitors of GP2b3a
  • Prevent aggregation and increase BT wiht no change in PT or PTT
  • Used stenting and MI
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11
Q

Rivaroxiban, apixiban, idoparinox

A

-Direct factor 10 inhibitors that can be taken orally and have minimal S/E

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12
Q

S phase

A
  • ANtimetabolites

- MTX, 5FU, HU, 6MP, Cytarabine

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13
Q

G2

A
  • Etoposides

- Bleomycin

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14
Q

M

A

Taxols and vinca

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15
Q

MTX

A
  • Folate analog that inhibits DHFR
  • Bone marrow supression is reversible with leucoverin
  • Also causes mucocitis
  • Can also be used as an immunosupressant, abortifactant
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16
Q

5-FU

A

Inhibitor of thymitdylate synthase leads to decreased DNA synthesis S phasse
-Myelsupresion without leucoverin

17
Q

Cytarabine

A

Pyrimidine analog that inactivates DNA pol

18
Q

6-MP

A
  • Pyrimidine synthesis inhibitor
  • BM supression, not reversible with leucoverin
  • Activated by HGPRT and metabolized by xanthine oxidase. Use of allopurinol will increase side effects
19
Q

Doxirubicine

A
  • DNA intercalator

- CAuses DCM use dexrzoxane to prevent DCM

20
Q

Bleomycin

A
  • Generates free radicals that destroy DNA

- Causes pulmonary fibrosis and changes in skin

21
Q

Cyclophosphamide

A
  • Cross links DNA

- Caues hemorrhagic cystitis, treat with mesna (thiol group that scavenges metabolite

22
Q

Nitrosamines

A
  • Cross BBB and cross link DNA

- Can be used for GBM

23
Q

Busulfan

A
  • Alkylating agent

- Causes pulmonary fibrosis and skin changess

24
Q

Vincristine and blastine

A
  • Bind to tubulin dimers and prevent MT frmation, used only in M phase
  • Cause neurotoxicity (ileus or peripheral neuropathy)