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112 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Hematologic Drugs
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p. 305
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p. 305
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heparin
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p. 305
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Catalyzes activation of ____________, decreases ________ and __________. It has a ____t1/2. check PTT
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catalyzes the activation of antithrombin III, decreases thrombin and Xa. It has a short t1/2
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p. 305
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It is used for immediated anticoagulation for pulmonary embolism,_______, _______, MI, and ________. Follow PTT
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used for pulmonary embolism, stroke, angina, MI, and DVT.
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p. 305
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T/F: Is used during pregnancy
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true: it is used during pregnancy because it does not cross the placenta.
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p. 305
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It can cause bleeding,___________, and drug-drug interactions.
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thrombocytopenia
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p. 305
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___________ is used for rapid reversal of heparization (it is a _______ charged molecule that binds the ________ charged heparin)
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protamine sulfate is used for rapid reversal of heparinization (it is a positively charged molecule that binds the negatively charged heparin).
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p. 305
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Newer________________ (enoxaparin) act more on _____, have better bioavailability and 2-4 times longer t1/2. Can be administered subcut and (with/without) lab monitoring.
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lower-molecular-weight heparins (enoxaparin) act more on Xa, have better bioavailabitlity and 2-4 times longer half-life. Can be adm. Subcut and without lab monitoring.
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p. 305
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warfirin (coumandin)
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p. 305
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p. 305
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Interferes with normal synthesis and gamma-carboxylation of vitamin K-dependent factors ___, ___, ___, and ___, also, ___ and ___ via ______ antagonism.
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Interferes with normal synthesis and gamma-carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X, protein C and S via vitamin K antagonism.
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p. 305
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t1/2 (short/long)
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long
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p. 305
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Used for _______ anticoagulation. Follow PT
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WEPT - Warfirin affects the Extrinsic pathway and prolongs PT
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p. 305
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T/F: is used during pregnacy
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False! (warfarin, unlike heparin, can cross the placenta).
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p. 305
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Toxicity: bleeding, _________, drug-drug interactions
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teratogenic
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p. 305
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heparin vs. warfarin
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p. 305
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p. 305
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Heparin is a (large/small) _____charged acicid polymer while Warfarin is (large/small) (charged/neutral) molecule
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Heparin is a large negatively charged acidic polymer while Warfarin is a small neutral charged lipid-soluble molecule
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p. 305
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T/F: Heparin is given orally while warfarin is given SC/IV
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False! Heparin is given IV/SC and warfarin is give oral
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p. 305
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Site of action: heparin _________, warfarin ______
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heparin's site of action is the blood; warfarin's site of action is the liver (synthesises clotting factors)
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p. 305
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Onset of action of _________ is slow; the onset of action of ______ is rapid
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onset of action of heparin is rapid (secs) and the onset of action of warfarin is slow, limitd by t1/2 of normal clotting factors.
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p. 305
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Warfarin works by imparing the synthesis of _______ dependent factors __, ___, ___, and ___ also _____, and ____; heparin activates _____, ____ and ___
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Warfarin works by imparing the synthesis of vitamin K dependent factors II, VII, IX, and X also protein S and protein C; heparin activates ATIII, Iia (thrombin) and Xa.
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p. 305
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Heparin 's duration of action is (acute/chronic); warfarin's duration of action is (actue/chronic)
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Heparin's duration of action is actute and warfarin's duration of action is chronic.
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p. 305
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Tx of acute OD: Heparin = _________; warfarin=______
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Tx of heparin OD is protamine sulfate; Tx of warfarin= IV vit. K and fresh frozen plasma.
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p. 305
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Warfarin is monitored by _________ while Heparin is monitored by ___________.
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Warfrin is monitored by PT (extrinsic pathway) (WEPT) and heparin is monitored by PTT (intrinsic pathway)
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p. 305
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Thrombolytics
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p. 306
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p. 306
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questions from diagram at bottom of page
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p. 306
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plasmin is the major ___________ enzyme. It breaks down both _______ and _______
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fibrinolytic enzyme. It accelerates breaks down of both fribin and fibrinogen yielding fibrin splip products and degradation products, respectively.
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p. 306
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Fibrinogen is converted to fibrin by _________
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thrombin
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p. 306
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tPA and urokinase promote the converson of ______ to ________ thereby increasing fibrinolysis.
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plasminogen to plasmin
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p. 306
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Various stimuli activate a blood proactivator to a blood activator that promotes conversion of _________ to blank thereby increasing fibrinolysis
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plasminogen to plasmin
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p. 306
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Streptokinase and anistreplase both activate and Activator that increases convesion of plasminogen to plasmin.
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p. 306
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Aminocaproic acid:____________ fibrinolysis.
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inhibits fibrinolysis by inhibition of plasminogen conversion to plasmin.
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p. 306
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4 examples of thrombolytics include: ________, _________, _____________, and ___________
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Streptokinase, urokinase, tPA(altepalse), APSAC (anistreplase)
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p. 306
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work by directly or indirectly aiding the conversion of ___________ to __________, which cleaves ______ and ________ clots. tPA specifically coverts _______________ to plasmin
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Directly or indirectly aid conversion of plaminogen to plasmin, which cleaves thrombin and fribrin clots. It is claimed that tPA specifically coverts fribrin-bound plasminogen to plasmin.
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p. 306
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T/F: clinical use is for DVTs
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False: used for early MI
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p. 306
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pts. receiving this medication are at most risk for: ______
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bleeding
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p. 306
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Hematologic Drugs
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p. 306
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p. 306
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mechanism of antiplatelet interaction
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p. 306
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questions from diagram at top of page
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p. 306
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When a break in the endothelium occurs _________ and _________ are exposed.
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collagen and vWF
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p. 306
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Platelets are activated by binding to the above macromolecules. The two structures expressed by the platelets involved in this process are __________ and _________ and they bind to _________ and __________, repectively
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Platelets bind to collagen and vWF. The two structures expressed by platelets that are involved in this process are GP 1a and GP 1b. GP 1a and GP 1b bind to collagen and vWF, respectively.
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p. 306
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After platelet activation _________ is expressed on their surface. What is the role of this structure?
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after platelets are activated they express GP IIb/IIIa. This molecule is important in platlelet-platelet aggregation.
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p. 306
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_________ and _________ interaction is needed in order for platelet aggregation to occur.
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GP IIb/IIIa and fribinogen
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p. 306
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5-HT, _______, and ________ are molecules that play a role in the glycoprotein expression of activated platelets.
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5-HT, ADP, and TxA2 are molecules that play a role in the glycoprotein expression of activated platelets.
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p. 306
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Aspirin acts by inhibiting production of ________ that in turn inhibits glycoprotein expression in activated platelets.
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TxA2
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p. 306
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ADP production is inhibited by the drug _________.
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ticlopidine
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p. 306
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This antibody drug targets the _______ on platelets.
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Abciximab
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p. 306
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Copidogrel, ticlopidine
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p. 307
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p. 307
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What drug inhibits platele aggregation by irreversibly inhibiting the ADP pathway involved in the binding of fibrinogen
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Clopidogrel, ticlopidine
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p. 307
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Clopidogrel, ticlopidine is used for ______ ________ syndrome, coronary _______, and it has been shown to decrease the incidence or recurrence of___ ____.
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it is used for acute coronary syndrome, coronary stenting. Decreases incidence or recurrence of thrombotic stroke
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p. 307
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Ticlopidine is associated with_________ as a side effect.
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Ticlopidine causes neutropenia and it is reserved for those who cannot tolerate aspirin.
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p. 307
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Abciximab
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p. 307
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p. 307
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What drug is a monoclonal antibody that binds to __________ on activated platelets.
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Abciximab, gp IIb/Iia
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p. 307
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Abciximab is used for ___________ and ________ _________ ___________ ___________
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acute coronary syndromes and percutanous transluminal coronary angioplasty
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p. 307
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Toxiciites of abciximab are _______ and ________
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bleeding and thrombocytopenia
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p. 307
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Aspirin
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p. 307
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p. 307
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It ________ and (reversibly/irreversibly) inhibits COX1 and COX2 to prevent the conversion of _______ to prostaglandins.
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acetilates and irreversably inhibits COX-1 and COX-2
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p. 307
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T/F: aspirin has an effect of PT, PTT
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false it has no effect but increases bleeding time
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p. 307
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What are the 4 A's of aspirin and NSAIDS in general
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Antipyretic, Analgesic, Anti-inflam, antiplatelet
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p. 307
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Important toxicities of Aspirin include _________, bleeding, hyperventilation, __________- in children, and CN ____ toxicity
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gastric ulceration, bleeding, hyperventilation, Reyes syndrome and tinnitus (CNVIII).
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p. 307
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Oncologic Drugs
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pg 307-310
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p. 307
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What are the cell cycle specific oncologic drugs (6)
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antimetabolites (MTX, 5-FU, 6-MP), vinca alkaloids, stroid hormones, bleomycin, paclitaxel, etoposide
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p. 307
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What are the cell cycle Nonspecific oncologic drugs?
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alkylating agents and antibiotics (dactinomycin, doxorubicin, bleomycin)
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p. 307
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What class of drugs inhibits with cell division by interfering with the S phase (DNA synthesis)
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Antimetabolites (MTX, 5-FU)
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p. 308
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What drug acts on boht the S phase and the G2 phase of the cell cycle?
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Etoposide
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p. 308
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What drug specifically acts on the G2 phase of the cell cycle?
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Bleomycin
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p. 308
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What two classes of drugs interfere with the M phase of the cell cycle?
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Vinca alkaloids and taxols
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p. 308
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What is an S-phase-specific antimetabolite that is a folic acid analog that inhibits dihydrofolate reductase, resulting in a decrease dTMP (thymidine and purines) and therefore decreased DNA and protien synthesis
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Methotrexate
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p. 308
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What is the mechanism of action of Methotrexate
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Methotrexate is an S-phase-specific antimetabolite. Folic acid analog that inhibits dihydrofolate reductase, resulting in a decrease dTMP (thymidine and purines) and therefore decreased DNA and protien synthesis
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p. 308
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What anti-cancer drug is a folic acid analogue?
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Methotrexate
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p. 308
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Methotrexate effects what part of the cell cycle?
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S-phase
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p. 308
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What anti-cancer drug inhibits dihydrofolate reductase?
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Methotrexate (folic acid analogue)
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p. 308
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Used to treat leukemias, lymphomas, choricarcinoma, sacromas, rheumatoid arthritis, psoriasis, and can be an abortifacient; it may lead to myelosuppression
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Methotrexate
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p. 308
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What is Methotrexate used for (7)
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Used to treat leukemias, lymphomas, choricarcinoma, sacromas, rheumatoid arthritis, psoriasis, and can be an abortifacient; it may lead to myelosuppression
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p. 308
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What are the toxicities of Methotrexate?
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meylosuppression, which is reversbiel by leucovorin (folinic acid) "rescue." Macrovesicular fatty chage in the liver.
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p. 308
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What is the effect of Methotrexate on the liver?
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Macrovesicular fatty chage in the liver.
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p. 308
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____is an S-phase-specific anti-metabolite that is a pyrmidine analog which complexed to folic acid, inhibiting thymidylate synthase, decreasing dTMP and decreasing DNA/protein synthesis
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5-Fluorouracil (5-FU)
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p. 308
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What is the mechanism of action of 5-Fluorouracil (5-FU)
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5-Flourouacil (5-FU) is an S-phase-specific anti-metabolite BIOACTIVATED TO 5F-dUMP that is a pyrmidine analog which complexed to folic acid, inhibiting thymidylate synthase, decreasing dTMP and decreasing DNA/protein synthesis
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p. 308
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Myelosuppression by methotrexate is reversible with ____
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leucovorin (folinic acid) rescue
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p. 308
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What is the clinical use for 5-Flourouracil?
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Colon cancer and other solid tumors, basal cell carcinoma (topical).
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p. 308
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What drug works well on solid tumors?
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5-Flourouracil (5-FU)
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p. 308
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What drug works synergistically with 5-FU?
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Methotrexate (MTX)
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p. 308
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What drug is works welll in colon cancer?
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5-Flourouracil (5-FU)
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p. 308
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Leucovorin (folinic acid) is counteract what drug side-effect
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meylosuppression due to methotrexate
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p. 308
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What are the toxicities of 5-Flourouracil?
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myelosuppression (NOT reversible with leucovorin) and photosensitivity
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p. 308
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What drug inhibits thymiylate synthase?
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5-Flourouracil (5-FU)
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p. 308
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Used to treat colon cancer and other solid tumors, basal cell carcinoma (topically)
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5-Fluorouracil (5-FU)
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p. 308
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Myelosuppression by 5-FU is ______
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Not reversible
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p. 308
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Which drug blocks purine synthesis and is used to treat leukemias, lymphomas (not CLL or Hodgkins)
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6-mercaptopurine (6-MP)
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p. 309
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What is the mechanism of 6-mercaptopurine?
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Blocks de novo purine synthesis. Activated by HGPRTase.
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p. 309
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What drug is commonly used to treat leukemias and lymphomas (not CLL or Hodgkin's)?
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6-mercaptopurine (6-MP)
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p. 309
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6-mercaptopurine (6-MP) is used for what cancers?
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leukemias and lymphomas (not CLL or Hodgkin's)?
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p. 309
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What drug increases the toxicity of allopurinol and how?
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6-mercaptopurine (6-MP) because it is metabolized by xanthine oxidase
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p. 309
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What are the side effects of 6-mercaptopurine (6-MP)?
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Bone marrow, GI, liver, increased tox of allopurinol
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p. 309
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This drug used to treat Leukemias and Lymphomas is metaboilized by xanthine oxidase
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6-mercaptopurine (6-MP)
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p. 309
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Which drug inhibits DNA polymerase and is used to treat AML?
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cytarabine (ara-C)
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p. 309
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This drug used to treat AML may lead to leukopenia, thrombocytopenia, megaloblastic anemia?
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cytarabine (ara-C)
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p. 309
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What are the side effects of cytarabine (ara-C)
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Leukopenia, thrombocytopenia, megaloblastic anemia
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p. 309
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What cancer drug inhibits DNA polymerase?
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cytarabine (ara-C)
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p. 309
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These alkylating agents can cause myelosuppression and hemorhagic cystitis
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cyclophosphamide, ifosfomide
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p. 309
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What drugs are alkylating agents?
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cyclophosphamide, ifosfomide
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p. 309
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What is the mechanism of action of alkylating agents (cyclophosphamide and ifosfomide)?
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Alkylating agents ; covalentsly x-link (interstrand) DNA at guanin N-7. Require bioactivation by the liver.
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p. 309
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Where is cyclophosphamide and ifosfonide activated?
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liver
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p. 309
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What drug can be used to prevent the side effects of alkylating agents (cyclophosphamide and ifosfomide)?
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mesna
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p. 309
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What are cyclophosphamide and ifosfamide used for?
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Non-Hodgekin's lymphoma, breast and ovarian carcinomas. Also immunosuppressants?
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p. 309
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What drugs are used to treat Non-Hodgekin's lymphoma, breast and ovarian carcinomas.
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cyclophosphamide, ifosfomide
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p. 309
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What cancer agents can be used as immunosuppressants
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cyclophosphamide, ifosfomide
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p. 309
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What drugs alkylate DNA after bioactivation and can cross the BBB and treats brain tumors (glioblastoma multiforme)
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Nitrosoureas (Carmustine, lomustine, semustine, streptozocin)
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p. 309
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Name 4 Nitrosoureases
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Carmustine, lomustine, semustine, streptozocin
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p. 309
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What class of drugs are Carmustine, lomustine, semustine, streptozocin
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Nitrosoureas
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p. 309
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What class of drugs is used to treat brain tumors (including gioblastoma maltiforme)
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Nitrosoureas (Carmustine, lomustine, semustine, streptozocin)
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p. 309
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What anti cancer drugs causes CNS toxicity (dizziness and ataxia)
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Nitrosoureas (Carmustine, lomustine, semustine, streptozocin)
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p. 309
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What are the side effects of Nitrosoureas (Carmustine, lomustine, semustine, streptozocin)
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CNS toxicity (dizziness and ataxia)
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p. 309
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