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Hematology > Heme Pharm > Flashcards

Heme Pharm Flashcards

1
Q

Aspirin: MOA, Use, Contraindications, and AE

A

MOA: Irreversible COX-1 inhibitor- prevents TXA2 synthesis, which prevents platelet aggregation

Use: Prevention or atherothrombosis and DVT; also some prophylaxis against colorectal cancer

Contraindications: Other NSAID use; true hypersensitivity; active pathologic bleeding/high risk of bleed

AE: GI side effects; risk of hemorrhagic stroke in men

*Mostly metabolized in liver, with high first-pass metabolism

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2
Q

Clopidogrel: MOA, Use, Contraindications, and AE

A

MOA: ADP inhibitor. Irreversibly binds P2Y12 receptors, preventing ADP-driven platelet activation. PRODRUG and requires activation in liver by CYP2C19.

Use: Use in ACS with or w/o PCI. Often used with aspirin as part of a dual-therapy regimen after ACS event OR in place of aspirin for those who are allergic to aspirin.

Contraindications: BOX WARNING for poor metabolizers. LOTS of drug-drug interactions.

AE: DRUG INTERACTIONS! / genetic variability of CYP2C19. Loss of function = less drug effect.

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3
Q

Prasugrel: MOA, Use, Contraindications, and AE

A

MOA: ADP inhibitor. Irreversibly binds P2Y12 receptors, preventing ADP-driven platelet activation. Prodrug that is activated by ESTERASES (not cyp enzymes).

Use: ONLY USE in patients with STENT/PCI! Use as part of ACS regimen.

Contraindications: Patient CANNOT be a CABG candidate! DO NOT give to patients without stent. Do NOT give to patients with hx of stroke, TIA, or >75YO.

AE: Increased risk of bleeding, especially in CABG-related bleeds

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4
Q

Ticagrelor: MOA, Use, Contraindications, and AE

A

MOA: ADP inhibitor. Reversibly binds P2Y12 and acts as an allosteric inhibitor, preventing ADP-driven platelet activation. NOT a prodrug. Also blocks ENT1 - affecting adenosine re-uptake, creating anti-platelet, anti-inflammatory, and vasodilatory effects.

Use: Reduce mortality and CV events when used as ACS regimen.

Contraindications: Do not use in patients taking aspirin doses >100mg

AE: Sensation of dyspnea due to binding of P2Y12 on neuronal cells (clopidogrel does this too, but Tricagrelor is dosed more frequently and binds newly-synthesized receptors on neurons = constant bombardment on neural receptors)

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5
Q

Cangrelor: MOA, Use, Contraindications, and AE

A

MOA: ADP analog - competitively inhibits ADP from activating platelets

Use: Only use during PCI procedure; IV only; Not commonly used

Contraindications: Use with caution in patients with renal dysfunction

AE: Similar dyspnea to ticagrelor; can reduce renal fxn in patients with renal function

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6
Q

Cilostazol: MOA, Use, Contraindications, and AE

A

MOA: Phosphodiesterase-III inhibitor: leads to increased levels of cAMP, reducing platelet function and promoting vasodilation (vessel walls cannot contract)

Use: Peripheral arterial disease; helps with intermittent claudication and increased walking/exercise tolerance

Contraindications: BOX WARNING: do not use in patients with any severity of heart failure (guilt by association with another drug)

AE: None mentioned in lecture.

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7
Q

Dipyridamole: MOA, Use, Contraindications, and AE

A

MOA: Phosphodiesterase-V inhibitor: blocks re-uptake of adenosine and degradation of cAMP, reducing platelet function and promoting vasodilation (vessel walls cannot contract)

Use: Can use with aspirin after heart surgery, stroke/TIA (not as effective as clopiogrel). Also used in cardiac imaging/nuclear imaging (think contrast/DYE = DYE-pyridamole)

Contraindications: None listed in lecture

AE: GI, headache, flushing, dizziness, hypotension

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8
Q

Vorapaxar: MOA, Use, Contraindications, and AE

A

MOA: Inhibits thrombin receptors (PAR-1) on platelets = prevents platelet activation

Use: Added to aspirin and clopidogrel for secondary prevention of atherothrombotic events (only in stable patients)

Contraindications: Do not use in patients with hx of stroke, TIA, ICH, or bleeding problems. Do not use in small (<60kg) or elderly patients.

AE: THROMBOCYTOPENIA. Considerable increase in BLEEDING; DRUG INTERACTIONS due to metabolism via CYP3a (if other drugs metabolized by CYP3a are taken at same time, will take longer to eliminate drug)

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9
Q

Abciximab: MOA, Use, Contraindications, and AE

A

MOA: GPIIb/IIIa inhibitor: inhibits fibrinogen from forming cross links (final step of primary hemostasis). Short half life but stays bound for several days.

Use: Use during PCI procedure. IV or intracoronary administration. Must monitor platelet count while using. CAN be given to patient in ESRD, but that’s the only reason to use this GPIIb/IIIa inhibitor.

Contraindications: Do not use with active bleeding, high BP, history of strokes, recent trauma, or warfarin patients with elevated INR

AE: Very high bleed risk; thrombocytopenia risk

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10
Q

Tirofiban: MOA, Use, Contraindications, and AE

A

MOA: GPIIb/IIIa inhibitor: reversibly inhibits fibrinogen from forming cross links (final step of primary hemostasis)

Use: Use during PCI procedure. IV or intracoronary administration. Must monitor platelet count while using.

Contraindications: CANNOT use in ESRD.

AE: High bleed risk; thrombocytopenia risk

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11
Q

Eptifibatide: MOA, Use, Contraindications, and AE

A

MOA: GPIIb/IIIa inhibitor: inhibits fibrinogen from forming cross links (final step of primary hemostasis)

Use: Use during PCI procedure. IV or intracoronary administration. Must monitor platelet count while using.

Contraindications: CANNOT use in ESRD.

AE: High bleed risk; thrombocytopenia risk

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12
Q

CT Regimens: CHOP, R-CHOP

A

cyclophosphamide, doxorubicin, vincristine, prednisone (R=rituximab)

AE: Extreme fatigue, weight loss, malaise

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13
Q

HEPARIN

A pt receiving heparin therapy asks you how the “blood thinner” works. Your best response would be:

a. “Heparin makes the blood less thick”
b. “Heparin does not thin the blood, but prevents clots from forming as easily in the blood vessels.”
c. “Heparin decreases the number of platelets so that blood clots more slowly.”
d. “Heparin dissolves the clot.”

A

b. “Heparin does not thin the blood, but prevents clots from forming as easily in the blood vessels.”

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14
Q

HEPARIN

method of administration of heparin?

A 
IV
subcutaneous (low doses)
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15
Q

HEPARIN

two types of heparin

A

unfractionated heparin

low molecular weight heparin (LMWH)

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16
Q

parenteral definition

A

“introduced otherwise than by way of the intestines”

Merriam Webster

17
Q

Parenteral Anticoagulants

list three common clinical uses for these

A
  • Venous Thombosis treatment and prophylaxis
  • Pulmonary Embolism (PE) treatment and prophylaxis
  • Acute Coronary Syndrome (ACS) initial management
18
Q

HEPARIN

key characteristics of heparin

A
  • binds to endothelium and plasma proteins
  • unpredictable anticoagulant response
  • requires monitoring and titration during use
    - aPTT (or INR)
    - anti-factor Xa plasma levels
    - at high doses, use activated clotting time (ACT)
19
Q

HEPARIN

adverse effects

A
  • multiple “very uncommon” toxicities
  • hyperkalemia (uncommon, but may be seen in practice)
    (hyperkalemia observed when pts are on other drugs that increase serum potassium)
  • Heparin-Induced Thrombocytopenia (HIT)
20
Q

What is HIT?

A

Heparin-Induced Thrombocytopenia =
pro-thrombotic antibody mediated process triggered by antibodies directed against heparin-Platelet Factor 4 bound complex
- IgG antibodies
- binding activates platelets
- most common w/ unfractionated heparin
- common in surgical pts
- usually manifests as venous thrombosis
- pt can have acute rxn up to 90 days after heparin was administered (the antibodies hang out for that long)

21
Q

HEPARIN

How do we reverse heparin?

A

with salmon sperm!

Protamine Sulfate

  • better for unfractionated heparin
  • MOA: “complexing with the strongly acidic heparin to form a stable complex devoid of anticoagulant action”
  • onset of action = 5 minutes
  • match it to the heparin dose
22
Q

HEPARIN

compare unfractionated heparin vs low molecular weight heparins

A

UNFRACTIONATED =

  • Factor II and Xa via antithrombin
  • long long tail of >18 polysaccharides
    - all the better to wrap up and bind thrombin
  • needs to be monitored, titrated

LMWH =

  • Factor Xa
  • shorter tail = lower molecular wt
  • more predictable bioavailability
  • min need for monitoring
  • cleared by kidneys (almost exclusively)
  • lower risk of HIT
23
Q

List the 4 classes of parenteral anticoagulants referenced by Dr. Norgard

A

unfractionated heparin
low molecular wt heparin
synthetic pentasaccharides
direct thrombin inhibitors

24
Q

What is the synthetic pentasaccharide discussed by Dr. Norgard?

A

Fondaparinux (Arixtra)

25
Q

characteristics of the synthetic pentasaccharide Fondaparinux

A
  • affects FACTOR X
  • bioavailability = 100%
  • dependent on renal excretion
    • watch out for renal impairment, monitor GFR
  • does not affect PT, aPTT, or bleeding time
  • SIDE EFFECT: thrombocytopenia (2.9%)
  • CONTRAINDICATED: CrCl < 30 mL/min, black box warning (epidural hematomas)
26
Q

What is the black box warning for LMWH and synthetic pentasaccharide Fondaparinux?

A

pts who get spinal puncture or epidurals may get a big fat hematoma which could cause long-term or permanent paralysis!!

27
Q

What are the two Direct Thrombin Inhibitors referenced by Dr. Norgard?

A
  • Argatroan

- Bivalirudin

28
Q

Compare the two Direct Thrombin Inhibitors referenced by Dr. Norgard -

A

ARGATROBAN:

  • univalent
  • trtmnt for HIT
  • metabolized by hepatic CYPs, excreted in bile (watch out for pts with hepatic insufficiency!)
  • prolongs the INR

BIVALIRUDIN:

  • bivalent (i.e. two binding spots)
  • dosed based on pt’s renal fxn
  • IV infusion is used as an alternative to heparin in pts undergoing Percutaneous Coronary Intervention (PCI)
29
Q

PARENTERAL ANTICOAGULANT MEDS for Norgard:

A

unfractionated heparin

protamine sulfate (reversal)

LMWH (Lovenox, Fragmin, Innohep (trade names))

synthetic pentasaccharide (Fondaparinux)

Direct Thrombin Inhibitors (Argatroban, Bivalirudin)

30
Q

what are the oral anticoagulants?

A

Warfarin (aka Coumadin)
NOACS
(dabigatran, rivaroxaban, apixaban, endoxaban)

31
Q

What are the common clinical uses for oral anticoagulants (Warfarin and NOACS)?

A
  • venous thromboembolism (VTE) treatment and prophylaxis
  • pulmonary embolism treatment and prophylaxis
  • stroke and VTE prevention in pts with atrial fibrillation
32
Q

Categorize the NOACS

A 
NOACS
     Direct Thrombin Inhibitor
                dabigatran
     Factor Xa Inhibitors
                 rivaroxaban
                 apixaban
                 edoxaban
33
Q

Sargramostim/Leukine: MOA, Use, AE

A

MOA: Recombinant GM-CSF, stimulates myeloid progenitors to differentiate –> increased monocytes, neutrophils, eosinophils, and basophils.

Use: Used after bone marrow transplant, chemo, radiation, etc to correct neutropenia.

AE: possible anaphylaxis, “first dose effect” (SOB, fainting, dizziness, tachycarida)

34
Q

Filgrastim: MOA, Use, AE

A

Recombinant G-CSF: induces the maturation of myeloblasts into neutrophils

Use: in any disease that results in neutropenia (leukeia, myelofibrosis, radiation/chemo, etc)

AE: MSK pain in large bones. Allergic reactions are rare.

35
Q

Romiplostim: MOA, Use, AE

A

Recombinant thrombopoietin; stimulates the maturation of stem cells –> megakaryocytes –> platelets

Use: treatment of thrombocytopenia

AE: increased risk of clot formation

36
Q

Eltrombopag: MOA, Use, AE

A

MOA: agonist of thrombopoietin receptor: stimulates production of megakaryocytes

Use: treatment of thrombocytopenia

AE: Liver toxicity; severe bleeding

37
Q

Oprelvekin: MOA, Use, AE

A

MOA: Recombinant IL-11; stimulates megakaryocyte maturation/platelet production

Use: After chemo to promote platelet production

AE: edema, palpitations, N&V

38
Q

Epoetin: MOA, Use, AE

A

MOA: Recombinant EPO - stimulates new RBC production

Use: treat anemia in the setting of chronic renal failure, leukemia, anemia of chronic disease

AE: HTN, risk of clot formation

Needs several weeks of therapy before [RBC] rises, also need to replete iron stores

Hematology (3 decks)

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