Term
| What is the difference between a thrombosis and an embolism? |
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Definition
Thrombosis: the formation of a clot inside a blood vessel or in a chamber of the heart, obstructing the flow of blood through the circulatory system
Embolism: a thrombus is dislodged from the vessel wall and travels through circulation and occludes a smaller vessel in other parts of the body |
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Term
| What is the mechanism of action of Aspirin (ASA)? |
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Definition
| ASA in low doses inhibits the synthesis of TXA2 without having much effect on prostacyclin. It does this by irreversibly inhibiting cyclooxygenase-1. This means that COX-1 is inhibited for the life of the platelet. The platelet has no nucleus and is unable to make more COX-1 to compensate for this. |
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Term
| What is the mechanism of action of Dipyridamole? |
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Definition
| Dipyridamole inhibits PDE3 and causes an increase in intracellular cAMP (this will increase contractility of the heart). Dipyridamole also increases extracellular adenosine by inhibiting cellular reuptake and by inhibiting adenosine breakdown. Adenosine binds to GPCR and causes an increase in intracellular cAMP. It also reduces activation and expression of cell surface GPIIb/IIIa receptors. It is also a coronary vasodilator (increases intracellular levels of cGMP via inhibition of PDE5) |
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Term
| Name two antiplatelet drugs that require conversion to active thiol metabolites. |
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Definition
| Clopidogrel and Ticlopidine |
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Term
| What is the mechanism of action of clopidogrel/ticlopidine? |
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Definition
| The active metabolites of clopidogrel and ticlopidine inhibit platelet aggregation by irreversible blockade of adenosine diphoshpate (ADP) receptors on the platelet membrane. |
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Term
| What is a drug that is used less often due to the possible side effect of neutropenia (abnormally low neutrophils)? |
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Definition
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Term
| What is the mechanism of action of Abciximab? |
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Definition
| Abciximab reduces platelet aggregation by binding irreversibly to GP IIb/IIIa receptors and blocking the binding of fibrinogen. Abciximab is a combination of the Fab region of a murine (rodent) monoclonal antibody and the human Fc region. Abciximab can reduce platelet aggregation by more than 90%. |
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Term
| What is the mechanism of action of tirofiban and eptifibatide? |
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Definition
| Tirofiban and eptifibatide are glycoprotein IIb/IIIa antagonists. They are competitive reversible inhibitors of fibrinogen binding to GP IIb/IIIa receptors. They are primarily used in unstable angina and MI. Both of these agents have short half lives and are given as IV loading doses followed by maintenence infusion. |
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Term
| What are tissue factor II and IIa also known as? |
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Definition
II = prothrombin
IIa = thrombin |
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Term
| What does antithrombin do? |
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Definition
| Antithrombin inhibits the activity of cofactors II (thrombin), VIIa, IXa, Xa, XIa, and XIIa. It is also the binding site for UFH, LMWH, and fondaparinux. |
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Term
| What is the mechanism of action of warfarin? |
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Definition
| Warfarin inhibits epoxide reductase and this blocks the reduction of oxidized vitamin K and thereby prevents the post-translational carboxylation of clotting factors VII, IX, X, and II. |
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Term
| Why does warfarin have a drug interaction with broad-spectrum antibacterial agents? |
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Definition
| Broad spectrum antibacterial agents suppress the production of vitamin K by the gut bacteria. This will lead to an increase in the anticoagulant effect of warfarin. |
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Term
| What are some vitamin K rich foods? |
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Definition
| Kale, collards, spinach, and other green leafy vegetables. |
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Term
| Why do NSAIDs have a drug interaction with warfarin? |
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Definition
| NSAIDs displace warfarin from proteins in the plasma. This will lead to more free warfarin in the blood and will increase the effects of warfarin. |
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Term
| What is used to perform dose adjustments of warfarin? |
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Definition
| PT/INR is used to adjust doses of warfarin. |
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Term
| What does prothrombin time (PT) measure? |
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Definition
| Prothrombin time (PT) is a measure of the extrinsic (tissue factor) pathway of coagulation. It is used to determine the clotting tendency of blood. It is also used to calculate the INR. |
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Term
| What is a normal INR and what is a therapeutic INR? |
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Definition
Normal INR = 1
Therapeutic INR = 2-3 (Ideal is 2.5) |
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Term
| What is activated partial thromboplasin time (aPTT)? |
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Definition
| Activated partial thromboplastin time (aPTT) is a measure of the intrinsic pathway of coagulation. It is used to determine the clotting tendency of blood. It can also detect abnormalities of blood clotting and is used to monitor the effects of heparin. |
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Term
| What is the mechanism of action of heparin? |
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Definition
| Heparin inactivates clotting factors by potentiating the activity of an endogenous anticoagulant (antithrombin III). It increases the activity of antithrombin III by a thousand fold. Antithrombin III inhibits clotting factors II (thrombin), VIIa, IXa, Xa, XIa, and XIIa. |
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Term
| What can be used to neutralize heparin? |
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Definition
| Protamine can be used to neutralize heparin. Upon contact with heparin, protamine forms a salt. This neutralizes the anticoagulant effect of both drugs. |
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Term
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Definition
| Bivalrudin is a direct thrombin inhibitor (DTI). It is a synthetic derivative of hirudin. Hirudin is a polypeptide produced by the salivary gland of the medicinal leech. |
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Term
| What is the mechanism of action of alteplase? |
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Definition
| Alteplase is a recombinant tissue-plasmin activator also known as a fibrinolytic agent. These drugs are enzymes that convert plasminogen to plasmin. Plasmin then degrades fibrin to fibrinogen and thereby causes clot dissolution. Alteplase is indicated for both STEMI and stroke. |
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Term
| How is streptokinase different from alteplase and reteplase? |
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Definition
| Alteplase and reteplase are both recombinant plasminogen activators (t-PA). Streptokinase must combine with plasminogen to form an activator complex that converts inactive plasminogen to plasmin. |
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Term
| What is aminocaproic acid? |
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Definition
| Aminocaproic acid is an antifibrinolytic agen that is used in the treatment of bleeding. It inhibits fibrinolysis by competitively blocking plasminogen activation to plasmin and by blocking the binding of plasmin to fibrin. |
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Term
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Definition
| Tranexamic acid is an antifibrinolytic agent that is used in the treatment of bleeding. It competitively inhibits the inactivation of plasminogen to plasmin. |
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Term
| What is the difference between ischemia and infarction? |
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Definition
Ischemia - the restriction in blood supply with resultant damage or dysfunction to tissue (precursor to infarction)
Infarction - necrosis of tissue due to upstream obstruction of blood flow |
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Term
| What is the single most important risk factor for ischemic stroke? |
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Definition
| Hypertension is the most important risk factor for ischemic stroke. |
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Term
| What is the difference between a stroke and a transient ischemic attack (TIA)? |
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Definition
Stroke - abrupt onset focal neurologic lasting more than 24 hours and of presumed vascular origin
Transient Ischemic Attack (TIA)- same as above, but lasting less than 24 hours (usually less than 30 mins) |
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Term
| How should you counsel patients to recognize stroke? |
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Definition
Act F.A.S.T
-Face: ask the person to smile. Does one side of the face droop?
-Arms: ask the person to raise both arms. Does one arm shift?
-Speech: ask the person to repeat a simple sentence. Are the words slurred? Can he/she repeat the sentence correctly?
-Time: If the person shows any of these symptoms, time is important! Call 911 or get to the hospital FAST! |
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Term
| Why is glucose a concern in a stroke patient? |
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Definition
| There is a positive correlation between elevated glucose and death down the line in stroke patients. |
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Term
| When should blood pressure be treated in a ischemic stroke patient? |
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Definition
| Blood pressure should only be treated if it is above 220/120 mmHg. You do not want to decrease perfusion in the brain. |
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Term
| What should be the first line drug of choice for the secondary prevention of stroke in a patient with documented cardioembolic stroke (with an emphasis on those with atrial fibrillation)? |
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Definition
| Warfarin is the first line drug of choice for the secondary prevention of stroke in a patient with documented cardioembolic stroke (Per ASA Stroke Guidelines 2007 & ACCP "Chest" Guidelines 2008) |
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Term
| What are the first line agents for blood pressure control in the secondary prevention of stroke? |
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Definition
First line agent for BP control is an ACE-inhibitor + thiazide diuretic (PROGRESS study & JNC VII guidelines; 43% stroke risk reduction)
Patients unable to tolerate ACE-inhibitor should receive Angiotensin II Receptor Antagonist (LIFE study & JNC VII guidelines; 24% stroke risk reduction) |
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Term
| What are the three corners of Virchow's Triangle and what do they mean? |
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Definition
Venous Stasis - altered or decreased blood flow in the deep veins
Vascular Injury - injury or damage due to mechanical/chemical trauma. this injusy exposes the subendothelium and allows platlets to adhere to the subendothelium.
Hypercoagubility - increased clotting of the blood |
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Term
| What clotting factor begins the common pathway? |
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Definition
| Factor X is the start of the common pathway. |
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