Blood & Cardiology Flashcards
Unfractionated heparin
Anticoagulant
MOA: Binds to and activates antithrombin. Activated antithrombin inactivates Xa and IIa.
Indications:
- Treatment and prophylaxis of DVT or PE (post-op patient who is obese who has to stay in bed)
- Drug of choice during pregnancy (does not cross placenta)
Toxicities:
1) Severe bleeding
- Discontinue
- Give protamine sulfate (binds heparin and prevents its antithrombin interaction)
- “HElP me, PlS”!
2) Thrombocytopenia OR
3) Thrombosis:
- UFH binds platelet factor 4 and can initiate immune response OR promote platelet aggregation
4) Osteoporosis
- Chronic use only
- Must monitor therapy (because of variability between patients and bleeding risk)
- Only used parenterally (IV or SC)
Low Molecular Weight Heparin (LMWH)
Anticoagulant
MOA: Binds to and activates antithrombin. Inhibits factor Xa BUT NOT IIa (lacks thrombin binding site).
Indications:
- Similar to UFH, but is the DRUG OF CHOICE for:
- Prophylaxis and treatment of DVT and PE
- Management of acute coronary syndrome
Toxicities:
1) Bleeding
2) Lower incidence of thrombocytopenia than UFH
- Advantage over UFH: Less binding to plasma and EC proteins
- More predictable response
- Less patient-patient variations
- Less need for monitoring
*Given IV or SC
Warfarin (Coumadin)
Anticoagulant
MOA: Inhibits epoxide reductase so that vitamin K cannot gamma carboxylate clotting factors 2, 7, 9, 10.
Note: Protein C also decreased
Indications:
- For prolonged anticoagulant action
- Prevent recurrence of DVT and PE (often following heparin)
- Prophylaxis of thrombotic complication re atrial fibrillation, post MI
Toxicities:
1) Bleeding
- Interacts with everything so monitor after you begin a new drug, new diet, or new disease
2) Skin lesions/Tissue necrosis
- Due to thrombus formation from protein C inhibition.
3) DO NOT USE IN PREGNANCY
- Abortion, birth defects, etc.
- UFH or LMWH alternatives
*Given orally
Fondaparinaux
New Anticoagulant
MOA: Factor 10a inhibitor
Indications:
- Prophylactic DVT and PE treatments (patient undergoing hip replacement)
- Treats acute DVT and PE
Dabigatran
New Anticoagulant
MOA: Factor 2a inhibitor
Indications:
- Warfarin alternative. Since warfarin has tons of drug-drug interactions, 50% of atrial fib patients do not receive it.
- Give this to prevent stroke in AF patients who cannot take Warfarin.
Rivaroxaban
New Anticoagulant
MOA: Factor 10a inhibitor
Indications:
- Prophylactic DVT and PE treatments (patient undergoing hip replacement)
- Treats acute DVT and PE
Aspirin
Antiplatelet Drug
MOA: Irreversible inhibition of COX-1 (AA –> Thromboxane A2)
Indications:
- Primary prevention for those at HIGH risk for ischemic disease
- Secondary prevention of recurrent MI or stroke
Toxicities:
- Bleeding
Clopidogrel
Antiplatelet Drug
MOA: Irreversible inhibition of P2Y-12 ADP receptor
Indications:
- Secondary prevention of recurrent MI or stroke
Toxicities:
- Bleeding
Abciximab
Antiplatelet Drug
MOA: Blocks GP 2b-3a
Indications:
- Stent placement
- Used with heparin and aspirin
Toxicities:
- Bleeding
- Thrombocytopenia
Streptokinase
Thrombolytic Drug (Clot Buster)
MOA: Promote plasminogen conversion to plasmin.
- No intrinsic enzymatic activity.
- Instead, binds to plasminogen, exposes active site, and promotes conversion.
- Give bolus to overwhelm antibody response
- Can cause anaphylaxis
Indications:
- Rapid lysis of occlusive thrombi
- For MI, PE, and ischemic stroke, give within 3 hours of onset!
Toxicities:
- Life threatening bleeding by lysing “physiologic” thrombi
- Aminocaproic acid can treat bleeding (binds plasminogen and plasmin –> blocks access to fibrin)
Tissue plasminogen activator (t-PA)
Thrombolytic Drug (Clot Buster)
MOA: Promote plasminogen conversion to plasmin
- Naturally occurring serine protease
- Give as bolus followed by constant infusion
Indications:
- Rapid lysis of occlusive thrombi
- For MI, PE, and ischemic stroke, give within 3 hours of onset!
Toxicities:
- Life threatening bleeding by lysing “physiologic” thrombi
- Aminocaproic acid can treat toxic bleeding (binds plasminogen and plasmin –> blocks access to fibrin)
Tenecteplase
Thrombolytic Drug (Clot Buster)
MOA: Promote plasminogen conversion to plasmin
- Genetically engineered t-PA
- 3 point mutations introduced to increase half-life and increase activity
- Only have to give as one bolus (as opposed to t-PA)
Indications:
- Rapid lysis of occlusive thrombi
- For MI, PE, and ischemic stroke, give within 3 hours of onset!
Toxicities:
- Life threatening bleeding by lysing “physiologic” thrombi
- Aminocaproic acid can treat bleeding (binds plasminogen and plasmin –> blocks access to fibrin)
Dipyridamole
Antiplatelet Drug
MOA:
- Adenosine Reuptake inhibitor (ADP and ATP).
- Inhibits thromboxane synthase
- Results in less ADP and TxA2 release.
NovoSeven
Recombinant factor 7a
Treats Glanzman’s Thrombasthenia
Cytarabine
Antineoplastic
Subclass: Antimetabolite
MOA: Pyrimidine antagonist
- Converted to ara-CMP, which is converted to ara-CDP and ara-CTP.
- The triphosphate (CTP) is the main cytotoxic metabolite.
- Ara-CTP competitively inhibits DNA polymerases and is incorporated into RNA and DNA.
Toxicity:
- Myelosuppression
- Arthralgia
- Cerebellar neurotoxicity
- Ocular toxicity
*S-phase specific
Fludarabine
Antineoplastic
Subclass: Antimetabolite
MOA: Purine antagonist
*S-phase specific
5-Fluorouracil
Antineoplastic
Subclass: Antimetabolite
MOA:
- Incorporates into RNA + DNA
- Covalently binds and inhibits thymidylate synthase
Toxicity:
- Mucositis
- Myelosuppression
- Hand-foot syndrome
- S-phase specific
- Leucovorin enhances activity
Irinotecan
Antineoplastic
MOA: Inhibits Topoisomerase I, a key enzyme responsible for DNA replication.
Toxicity:
- Myelosuppression
- Transaminitis
- Explosive diarrhea (fix acute diarrhea with atropine; fix delayed with loperamide)
*S-phase specific
Methotrexate
Antineoplastic
Subclass: Antimetabolite
MOA: Inhibits DHF reductase
- DHF reductase reduces DHF to THF. THF helps create thymidylate. Thymidylate involved in DNA and RNA synthesis.
Toxicity:
- Renal (do not use if patient has kidney problem or is on another nephrotoxic)
- S-phase specific
- Leucovorin prevents harmful effects of methotrexate
Paclitaxel
Antineoplastic
Subclass: Microtubule Inhibitor
MOA: Stabilize MT so they cannot disassemble
Toxicity:
- Hypersensitivity reactions (premedicate with steroids)
*M-phase specific
Vincristine
Antineoplastic
Subclass: Microtubule Inhibitor
MOA: Inhibits MT polymerization (disrupts assembly)
*Lagaan. PacliTAXel does one thing. We “vin”!!!!! does the opposite. Taxing vs. Vinning in cricket lol.
Toxicity:
- ***Neuropathy & Constipation
*M-phase specific
Bleomycin
Antineoplastic
Subclass: Antibiotic
MOA:
- Has DNA and Iron binding domains at opposite ends.
- Oxidizes iron atom and sends off electrons to nip at the local DNA.
- **Toxicity:
- Pulmonary toxicity
- Hypersensitivity
- Mucositis
*S/G2-Phase specific
Carmustine
Antineoplastic
Subclass: Alkylating agent
Toxicity:
- Bone marrow suppression (administer every 6-8 weeks)
Cyclophosphamide
Antineoplastic
Subclass: Alkylating agent
Toxicity:
- Bone marrow suppression
- Cystitis
- Cardiac (high doses)
- Immunosuppression
*Acrolein, a byproduct, causes severe hemorrhagic cystitis. MESNA is used to protect against this.
