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69 Cards in this Set

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  • Back
What is the mechanism of heparin?
Enhances antithrombin III activity

2) Decreases thrombin and Xa.

So inhibits thrombin from converting fibrinogen to fibrin.
What are the clinical uses of heparin?
Immediate anticoagulation for PE, stroke, angian, MI, DVT.
What drug heparin or warfarin can be used during pregnancy?
Heparin because it does not cross the placenta!
What is the best way to monitor heparin?
PTT time.
What are the side effects of heparin?
Bleeding, thrombocytopenia.
What is the antidote for heparing overdose?
Protamine sulfate (positively charged molecule that acts by binding negatively charged heparin) --> rapidly reverses heparinization.
What is the name of the new LOW MOLECULAR WEIGHT HEPARIN?
What is action of enoxaparin?
Acts more on blocking Xa

Xa converts prothrombin to thrombin!
What are the advantages/disadvantages of using enoxaparin vs heparin?
1) Enoxaparin --> better bioavailability, 2-4x longer half life, can be administered SubQ and without lab monitoring.

Disadvantage: enoxaparin overdose cannot be easily reversed with protamine sulfate!
What is mechanism of warfarin (coumadin)?
Inhibits vitamin K epoxide reductase. You therefore cannot convert Vit K to its active form.

Active vit K --> needed for gamma carboxylation of glutamate residues of factors, 2, 7, 9, and 10, and protein C and S.
What is the best way to monitor warfarin?
PT time. Affects Extrinsic pathway.

Long half life.
What drugs increase the degree of anticoagulaiton by inhibiting cytochrome p450?
cimetidine, disulfuram, and chlroamphenicol.
What drugs decrease teh degree of anticoagulation by activating cytochrome p450?
What is the clinical use of warfarin?
Chronic anticoagulation. Not used in pregnant women (because warfarin unlike heparin, can cross the placenta).

What is the structure of heparin?
Large anionic polymer, acidic (so cant cross the placenta)
What is the structure of warfarin?
Small lipid-soluble molecule (so can cross the placenta).
What is the site of action of heparin?
What is the site of action of warfarin?
What is the duration of action of heparin?
Acute (hours)
What is the duration of action of wafarin?
Chronic (weeks or months).
Which drug inhbits coagulation in VITRO?
What drug does not inhibit coagulation in vitro?
How do you treat wafarin overdose?
IV vitamin K and for acute bleeding --> fresh frozen plasma.
What are the classes of thrombolytics?
Streptokinase, urokinase, tPA (alteplase), APSAC (anistreplase)
What is the mechanism of streptokinase, urokinase, tPA?
Aids in the conversion of plasminogen to plasmin.

Plasmin can then cleave thormbin and fibrin clots!
When do you use streptokinase, tPA?
Early ischemic stroke

Early MI.
What is the toxicity of streptokinase, tPa?
Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleed, recent surgery, or severe hypertesion.
Lets say you overdose a patient on streptokinase or tpa. How would you reverse this?
Aminocaproic acid, an inhibitor of fibrinolysis.
What is the mechanism of aleptase (tissue plasminogen activator)?
Converts plasminogen BOUND TO FIBRIN within a clot to plasmin which cleaves fibrin and lyses the thrombus. But TPA only binds plasminogen already bound to fibrin.
What is the mechanism of action of streptokinase?
Converts plasminogen to plasmin. Streptokinase can lead to hypersensitivity, since it is a foreign protein (unlike urokinase which is not foreign).
What can plasmic act on?
Plasmin can degrade fibrinogen into its products

2) Plasmin can also break down fibrin into its split products.
What is mechanism of action of aminocaproic acid?
Inhibits conversion of plasminogen to plasmin.
What is mechanism of aspirin?
Aceylates and irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) to prevent conversion of arachidonic acid to prostaglandins.
What effect does aspirin have on patient?
Increases bleeding time.

Normal PT and PTT.
What is the clinical use for aspirin?



What is the toxicity of aspirin?
Gastric ulceration, bleeding, hyperventilation, Reye's syndrome, tinnitus.

Causes mixed acid-base disorder: first respiratory alkalosis then metabolic acidosis.
What is clopidogrel mechanism of action?
1) Blocks ADP receptors --> inhibit platelet aggregation

2) Prevents glycoprotein IIb/IIIa expression --> inhibits fibrinogen binding.
When is clopidogrel/ticlopidine used?
acute coronary syndrome; coronary stenting.
What is major side effect of ticlopidine?
Neutropenia, agranulocytosis, so use clopidogrel instead.
What is the mechanism of action of abciximab?
Monoclonal antibody that binds to glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation. Prevents fibrinogen binding!
What is the mechanism of dipyramidole?
Inhibits adenosine deaminase and phosphodiesterase.

1) Accumulation of adenosine/cAMP

Adenosine and cAMP inhibit platelet aggregation.
What is mode of action of methotrexate and 5FU?
Decrease thymidine synthesis
What is MOA of 6-MP?
Decreases purine synthesis
What is MOA of dactinomycin and doxorubicin?
DNA intercalation
What is mechanism of bleomycin?
strand breakage and DNA intercalation
What is mechanism of action of enoxaparin?
Actually inhibits ATIII --> this leads to a conformation change of ATIII that actually allows it to rapidly combine with and inhibit thrombin. This prevents conversion of fibrinogen to fibrin.
What is advantage of enoxaparin?
1) Easier to administer: SubQ
2) Longer half life
COX 1. Explain
COX-1 expressed constitutively in platelets and the GI tract.
COX 2. Explain
Expressed preferentially at sites of inflammation.
What effect does COX-2 inhibitors have?
Dont impair platelet function b/c platelets predominantly express COX-1.
What is HIT?
Heparin induced thrombocytopenia. Leads to paradoxical thrombus! Autoimmune reaction with antibodies formed against platelet factor 4 (PF4), neutrophil-activating peptide 2 (NAP-2) and interleukin 8 (IL8) which form complexes with heparin,
What is best way to treat HIT?
Direct thrombin inhibitors!!

Hirudin, leipirudine, argatroban: inhibit thrombin.

(Thrombin normally converts fibrinogen to fibrin)
What is mechanism of action of hirudin, and argatroban?
Directly inhibit thrombin. Drug of choice for HIT!! They bind to thrombin active site.
What are the risk factors for DVT during pregnancy?
1) increase level of clotting factors
2) Decrease protein S
3) Pressure of uterus on IVC allows for stasis
4) Presents as unilateral leg pain, swelling, and warmth.
What is effect of PGE2 in infants?
Keeps the patent ductus arteriosus open.
How can you close a ductus arteriouss pharmacologically?
Indomethacin or aspirin because they inhibit COX preventing formation of prostaglandin E.
What is mechanism of aspirin?
Non-selective irreversible inhibition of COX, causing decreased prostaglandin and thromboxane production. If block prostaglandins at thermoregulatory centers in hypothalamus, asprin, and other NSAIDs act as antipyretics.
What is action of prostaglandin in pain and fever?
Prostaglandins sensitive pain receptors to chemical and mechanical stimuli, and also acts on thermoregulatory center to cause fever.
What is mechanism of ibuprofen and indomethacin?
Reversible, non selective inhibitor of COX....

What is mechanism of action of celecobix and rofecoxib?
Selective Cox II inhibitors.

Fewere side effects on GI and on bleeding.
What is the side effect of indomethacin?
It has 100% hypersensitivity cross-reactivity with aspirin. The hypersensitivity consists of rashes, urtricaria, and acute asthmatic attacks!
constitutively expressed in platelets.

2) COX1 products are responsible for mucous secretion of gut.
Why does acetominophen have no local anti-inflammatory effects?
It is inactivated in peripheral tissues.
What is mechanism of action of colchicine?
Used in acute attacks of gout. Acute!!

1) Blocks mitotic spindles
2) Blocks tubulin which decreases mobility of granulocytes to affected areas
What are side effect of colchicine?
Agranulocytosis, aplastic anemia.
What is probenecid and sulfinpyrazone used for?
Used to prevent attacks of gout.
What MOA of probenecid and sulfinpyrazone?
Inhibits uric acid reabsorption

It also blocks tubular secretion of penicillin, so used to increase the antibiotic.
What is MoA of allopurinol?
Inhibits xanthine oxidase, and used for chronic suppression of gouty attacks.
Why should allopurinol NOT be given during acute attacks?
If given during gouty attack, allopurinol has the potential to actually exacerbate the condition.