Platelet activation and the clotting cascade share one page in this NU559 Unit 2 map, with each of a composite patient's three antithrombotic drugs fixed to the point where it acts. Searches like "nu 559 unit 2 assignment example", "nu559 unit 2 sample" and "nu559 unit 2 example" land here.
Two Lanes, Three Drugs: A Mechanism-to-Therapy Map for Atrial Fibrillation Four Days After a Coronary Stent
[Student Name]
Purdue University Global
NU559: Essentials of Advanced Pathophysiology and Pharmacology
Unit 2 Mechanism to Therapy Map
[Instructor Name]
[Date]
The patient is a composite; drug names in brackets stand for their classes, and the map is not a prescribing recommendation.
The Organizing Contrast
Mr. [N.], 69, has persistent atrial fibrillation and his left anterior descending artery was stented four days ago after an episode of unstable angina. His discharge list includes [aspirin], [clopidogrel] and [apixaban].
Clots in a fibrillating left atrial appendage form in slow-moving blood and are rich in fibrin, so they answer to anticoagulants; clots on a fresh stent form under high shear and are rich in platelets, so they answer to antiplatelet agents. That single contrast explains why he takes drugs from both lanes.
Upper Lane: The Platelet
Read left to right.
1. Adhesion. Exposed collagen and von Willebrand factor at the stent's struts capture platelets through their glycoprotein receptors.
2. Activation. Captured platelets change shape and release their granule contents, including adenosine diphosphate (ADP), and generate thromboxane A2 from arachidonic acid through cyclooxygenase-1.
Drug box: [aspirin] blocks cyclooxygenase-1 irreversibly, so thromboxane A2 cannot form for the life of the platelet, about seven to ten days.
3. Amplification. Released ADP binds P2Y12 receptors on nearby platelets, recruiting them.
Drug box: [clopidogrel], a prodrug activated in the liver, blocks P2Y12 irreversibly. Gray box, not in use: prasugrel and ticagrelor, also P2Y12 inhibitors.
4. Aggregation. Activated glycoprotein IIb/IIIa receptors bind fibrinogen, linking platelets into a plug.
Gray box, not in use: glycoprotein IIb/IIIa inhibitors, used intravenously in the catheterization laboratory.
Lower Lane: Coagulation
Read left to right.
1. Initiation. Tissue factor on damaged tissue binds factor VIIa, activating small amounts of factors IX and X (Hoffman & Monroe, 2001).
2. Amplification. The small amount of thrombin generated switches on factors V, VIII and XI and turns nearby platelets on as well.
3. Propagation. On the surface of activated platelets, large amounts of factor Xa form, converting prothrombin to thrombin in a burst.
Drug box: [apixaban] binds factor Xa directly and reversibly. Gray box, not in use: [warfarin], which reduces the liver's production of functional factors II, VII, IX and X; [heparin], which enhances antithrombin's inactivation of thrombin and Xa.
4. Fibrin. Thrombin converts fibrinogen to fibrin, which stabilizes the clot.
Gray box, not in use: direct thrombin inhibitors, such as dabigatran.
Where the lanes join. Thrombin is the most potent activator of platelets. The arrow from the lower lane's thrombin to the upper lane's activation step marks the point where the two systems stop being separate, which is why an anticoagulant also reduces platelet activation somewhat, and why the two lanes' drugs add to each other's bleeding risk.
Legend
1. Irreversible blockade: [aspirin] and [clopidogrel]. The effect lasts until new platelets are made, about a week after stopping.
2. Reversible blockade: [apixaban]. The effect falls as the drug is cleared, within a day or two of stopping, depending on kidney function.
Where Each Clot Would Form in This Patient
1. Left atrial appendage: in atrial fibrillation, blood stagnates in the appendage, and a fibrin-rich clot can form and travel to the brain. Prevented by [apixaban].
2. The new stent: until the stent's struts are covered by the artery's lining, platelets adhere to them. A platelet-rich clot there would cause a heart attack. Prevented by [clopidogrel] and, early on, [aspirin].
One Drug at a Time
[Aspirin]. Target: cyclooxygenase-1 in platelets. Consequence: less thromboxane A2, less activation. Bleeding risk from the same action: cyclooxygenase-1 also produces prostaglandins that protect the stomach lining, so aspirin increases gastrointestinal bleeding.
[Clopidogrel]. Target: P2Y12. Consequence: less ADP-driven recruitment of platelets at the stent. Bleeding risk: the same weaker platelet plug that protects the stent makes bleeding from any other source harder to stop.
[Apixaban]. Target: factor Xa. Consequence: less thrombin, less fibrin, less clot in the appendage. Bleeding risk: less thrombin also means slower clotting anywhere, and combined with two antiplatelet drugs, the risk adds up.
Why the Combination Is Time-Limited
Three antithrombotic drugs together raise bleeding risk substantially. In a large trial of patients with atrial fibrillation after a coronary syndrome or stenting, apixaban with a P2Y12 inhibitor caused less bleeding than warfarin, and adding aspirin increased bleeding without a clear reduction in ischemic events (Lopes et al., 2019). Expert consensus now favors a short period of triple therapy, often only through the hospital stay or up to about a month, followed by an anticoagulant plus a P2Y12 inhibitor, then the anticoagulant alone after about a year (Angiolillo et al., 2021). The stop date for [aspirin] is a decision for the prescribing team: [date aspirin stops]. The stop date for [clopidogrel] is [date clopidogrel stops].
References
Angiolillo, D. J., Bhatt, D. L., Cannon, C. P., Eikelboom, J. W., Gibson, C. M., Goodman, S. G., Granger, C. B., Holmes, D. R., Lopes, R. D., Mehran, R., Moliterno, D. J., Price, M. J., Saw, J., Tanguay, J.-F., & Faxon, D. P. (2021). Antithrombotic therapy in patients with atrial fibrillation treated with oral anticoagulation undergoing percutaneous coronary intervention: A North American perspective, 2021 update. Circulation, 143(6), 583-596. https://doi.org/10.1161/CIRCULATIONAHA.120.050438
Hoffman, M., & Monroe, D. M. (2001). A cell-based model of hemostasis. Thrombosis and Haemostasis, 85(6), 958-965. https://doi.org/10.1055/s-0037-1615947
Lopes, R. D., Heizer, G., Aronson, R., Vora, A. N., Massaro, T., Mehran, R., Goodman, S. G., Windecker, S., Darius, H., Li, J., Averkov, O., Bahit, M. C., Berwanger, O., Budaj, A., Hijazi, Z., Parkhomenko, A., Sinnaeve, P., Storey, R. F., Thiele, H., ... Alexander, J. H. (2019). Antithrombotic therapy after acute coronary syndrome or PCI in atrial fibrillation. New England Journal of Medicine, 380(16), 1509-1524. https://doi.org/10.1056/NEJMoa1817083
How this NU559 Unit 2 example is structured
The map is organized around a single contrast that explains the whole prescription. Clots in a fibrillating left atrial appendage form in slow-moving blood and are rich in fibrin, so they answer to anticoagulants; clots on a fresh stent form under high shear and are rich in platelets, so they answer to antiplatelet agents. Everything else hangs from that distinction. The upper lane is read left to right, then the lower lane, and arrows join them where thrombin activates platelets, the point at which the two systems stop being separate. Beneath the figure, three short paragraphs take one drug each: its target, the consequence of blocking it, and the bleeding risk that follows from the same action. Closing the prose, a paragraph explains why the combination is usually time-limited, leaving which agent stops first as a bracketed decision for the prescribing team.
Get an NU559 Unit 2 example written to your instructions
Coagulation, inflammation or another system entirely: whichever pathway your NU559 Unit 2 map covers, share it, plus the case when one exists and the layout rules your rubric sets. A sample map comes back in 24-48h with drug classes placed at their steps and agents in brackets. There is no charge for a first request. The paper above is an original model document written by our desk, not a submitted student paper and not an official Purdue University Global document.
NU559 Unit 2 questions, answered
Does the map need a patient, or can it show the pathway alone?
Many prompts accept the pathway alone. Anchoring it to a composite patient helps because it makes the writer decide which steps matter; a map of every clotting factor with no case behind it tends to become a textbook diagram. If your prompt asks for a pure pathway, the drug placements still decide the grade, so keep those precise and label every arrow.
Which software do graders expect for a concept map?
Sections vary, and most accept anything legible: a drawing tool, slide software or a scanned hand drawing. What rubrics tend to specify is content, meaning labeled arrows, a legend and a short narrative. Export to a format the submission area accepts, most often PDF or an image, and confirm that small text survives at the size a grader will view it.
How much prose should accompany the map?
Typically a page or less. The figure carries the structure, and the prose explains what a figure shows poorly: why each drug sits where it does, what its bleeding risk has to do with that position, and how the regimen changes over time. Prose that simply retells the figure in sentences adds length without adding any reasoning a grader can credit.