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.
What a finished NU559 Unit 2 mechanism to therapy map looks like
One wide page in two lanes, with a half page of prose beneath. The upper lane follows a platelet from adhesion at exposed collagen through activation to aggregation, and the lower lane runs the coagulation cascade from tissue factor to fibrin. Drug classes sit in boxes at the step each interrupts: [aspirin] at cyclooxygenase-1 and thromboxane A2, [clopidogrel] at the P2Y12 receptor, [apixaban] at factor Xa. Agents the patient is not taking, including [heparin], [warfarin] and a direct thrombin inhibitor, appear in gray at their own steps so the whole set is visible. A legend separates irreversible from reversible blockade, and a narrow column on the right explains which kind of clot each lane produces and where in this patient it would form.
How a 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.
Two lanes, one crossing
Platelet and coagulation pathways are drawn separately, then joined where thrombin cleaves PAR-1 receptors on the platelet surface. That single crossing arrow explains why an anticoagulant also dampens platelet activation somewhat, and why the lanes cannot be treated as independent systems.
Slow flow and high shear
A red, fibrin-rich thrombus in the appendage and a white, platelet-rich thrombus at the stent are contrasted in a small inset. The inset gives the reason the patient needs both drug families at once, and it appears before any drug does.
Irreversible, marked differently
[Aspirin] acetylates cyclooxygenase-1 for the life of the platelet, roughly [seven to ten] days, and the active metabolite of [clopidogrel] binds P2Y12 permanently. Hatched boxes mark both, setting them apart from [apixaban], whose effect falls as its level falls.
Gray boxes for absent drugs
[Heparin] at antithrombin, [warfarin] at vitamin K epoxide reductase and [dabigatran] at thrombin are shown faded. Including them demonstrates the full pathway without implying that any of them belongs in this regimen.
Bleeding traced to the same steps
Each drug's bleeding risk is traced to the same point it interrupts, and the combined risk of three blockades is stated plainly. A bracketed note records that the length of combined therapy is set by the prescribing team and by current cardiology guidance.
Where marks go in NU559 Unit 2
Placement is what graders read first: a drug pinned to the wrong step, [clopidogrel] at cyclooxygenase or [apixaban] at thrombin, costs more than any omission, because the map exists to show position. Maps that list drugs in a sidebar with no arrow to a step score as inventories. The fibrin-versus-platelet distinction is the second thing a strong map carries and a weak one lacks; without it the regimen looks redundant, and the paper cannot explain why both families appear. Unlabeled arrows cost marks in most rubrics, as does a legend that fails to separate reversible from irreversible blockade. A crowded figure that shows every clotting factor at equal weight costs a little, as do bleeding risk listed apart from its mechanism and any duration presented as the author's recommendation.
Get a 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.
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.