pcm powerpoints

  

15 slides including title and reference page with speaker notes

PLAG free 

Intext citation

PCM PLEASE READ INSTRUCTIONS CAREFULLY

Assignment Scenario

After graduating from nursing school and passing your boards, you accepted a position as an RN in the emergency center at PCM. In the weeks ahead, your emergency center plans to implement a new initiative where clients diagnosed with low-risk deep vein thrombosis (DVT) will be sent home on 3 months of oral anticoagulation therapy with rivaroxaban.

Historically, clients diagnosed with DVTs in the emergency center were admitted to the hospital’s observation unit. However, when surveyed about their experiences, many clients reported that this was costly, time-consuming, and inconvenient. Under PCM’s new program, emergency center nurses will be responsible for educating clients about their new medication and administering the first dose to the client before discharge.

As part of this new initiative, all emergency center nurses at PCM must be trained to properly educate these clients on all aspects of their new medication regimen. Because you have demonstrated a keen interest in pharmacology, your manager has asked you to develop the educational tools that will be used to train the nurses at PCM.

It’s worth noting that the standard dosing for all low-risk DVTs is as follows:

· 15 mg BID, 12 hours apart, for 21 days

· After 21 days, use 20 mg once per day

· After 90 days, the client will follow up in the thrombosis clinic to evaluate if they meet criteria for discontinuing the medication

Assignment Instructions

Your manager explained that all of the emergency center nurses PCM will be educated in small groups through a short, in-service training session. You have been asked to develop a professional-looking PowerPoint presentation that the trainers will use to guide the in-service sessions. Your PowerPoint will need to:

1. Be professional-looking, have a title slide, and 10-15 content slides.

2. Use the Speaker Notes feature in PowerPoint to reduce the amount of text that appears on the content slides.

3. The Speaker Notes for each slide will contain the text that will guide what the trainer will say while presenting the slides during the in-service.

4. The content slides themselves should be clear and easy to understand; they serve as an outline so the audience can follow along with what is being presented.

5. Be written using proper spelling/grammar and at a level that would be appropriate for the audience.

6. Remember the purpose of the training is to help nurses learn to educate their clients about the use of a medication. With that in mind, it may be helpful to provide examples of how to explain the information to a client in an easy to understand way without complicated, technical terms.

7. Include APA formatted in-text citations for at least 3 scholarly references and present the sources in APA format on a References slide.

8. Contain content addressing the items below.

9. Pharmacotheraputics

10. State the drug name and its therapeutic category

11. Pharmacodynamics (how does this drug work to achieve its intended response)

12. Pharmacokinetics (how is this drug absorbed, distributed, metabolized, and excreted).

13. Discuss dosage, scheduling, route, and length of therapy.

14. Describe what clients can expect regarding their therapeutic response and when it should develop

15. Introduce nondrug measures that clients can do to enhance their therapeutic response (e.g., specific diet to follow, exercise requirements, substances to avoid, special precautions to take, etc.)

16. Side Effects, Adverse Effects, and Interactions

17. Explain the symptoms of common side effects, and what clients can do to minimize any discomfort

18. Explain the symptoms of any major adverse effects, and what clients should do if they experience them

19. List the major adverse drug-drug interactions and drug-food interactions that clients need to be made aware of

20. Follow-up Care

21. Provide information regarding when clients should call their doctor for advice (e.g., questions, non-urgent symptoms, unpleasant side effects, etc.)

22. Emphasize any symptoms for which clients should seek immediate care (e.g., when to go to the emergency center or call 911)

Note: When developing a professional-looking presentation, it’s important to be mindful of how you layout your content. The slides should present key points, arranged in a logical manner, without extraneous information contributing to a cluttered look. Using the Speaker Notes feature in PowerPoint is a great way to include relevant details without overloading the slides.

15 slides including title and reference page

PLAG free

Intext citation

Due 9/3/22

Get information from link below, ATI and one drug book

Kreutz, R. (2012). Pharmacodynamic and pharmacokinetic basics of rivaroxaban. Fundamental & clinical pharmacology, 26(1), 27-32.

Rosenthal, J.B. L. ([Insert Year of Publication]). Lehne’s Pharmacology for Nursing Care (11th Edition). Elsevier Health Sciences (US). 

https://ambassadored.vitalsource.com/books/9780323825245

Direct Factor Xa Inhibitors

Rivaroxaban

Actions and Uses

Rivaroxaban [Xarelto]

is an oral anticoagulant that causes selective inhibition of factor Xa (activated factor X). Rivaroxaban binds directly with the active center of factor Xa and thereby inhibits production of thrombin. Compared with warfarin, our oldest oral anticoagulant, rivaroxaban has several advantages: rapid onset, fixed dosage, lower bleeding risk, few drug interactions, and no need for INR monitoring. Rivaroxaban has four approved uses: (1) prevention of DVT and PE after total hip or knee replacement surgery, (2) prevention of stroke in patients with atrial fibrillation, (3) prevention of recurrent DVT and PE, and (4) treatment of DVT and PE unrelated to orthopedic surgery. Contrasts with warfarin are shown in Table 55.6.

Pharmacokinetics

Rivaroxaban is administered orally, and bioavailability is high (80% to 90%). Plasma levels peak 2 to 4 hours after dosing. Protein binding in blood is substantial (92% to 95%). Rivaroxaban undergoes partial metabolism by CYP3A4 (the 3A4 isoenzyme of cytochrome P450) and is a substrate for P-glycoprotein, an efflux transporter that helps remove rivaroxaban from the body. Rivaroxaban is eliminated in the urine (36% as unchanged drug) and feces (7% as unchanged drug), with a half-life of 5 to 9 hours. In patients with renal impairment or hepatic impairment, rivaroxaban levels may accumulate.

Adverse Effects

Bleeding

Bleeding is the most common adverse effect and can occur at any site. Patients have experienced epidural hematoma, as well as major intracranial, retinal, adrenal, and GI bleeds. Some people have died. Bleeding risk is increased by other drugs that impede hemostasis. How does rivaroxaban compare with warfarin? The risk of hemorrhagic stroke and other major bleeds is significantly lower with rivaroxaban.

In the event of overdose, we have no specific antidote to reverse this drug’s anticoagulant effects. However we can prevent further absorption of ingested rivaroxaban with activated charcoal (see Chapter 109). Treatment with several agents—recombinant factor VIIa, prothrombin complex concentrate (PCC), or activated PCC—can be considered. Preliminary studies of PCC have been promising, but more testing must be completed. Because rivaroxaban is highly protein bound, dialysis is unlikely to remove it from the blood.

Spinal/Epidural Hematoma

Like all other anticoagulants, rivaroxaban poses a risk of spinal or epidural hematoma in patients undergoing spinal puncture or epidural anesthesia. Prolonged or permanent paralysis can result. Rivaroxaban should be discontinued at least 18 hours before removing an epidural catheter; once the catheter is out, another 6 hours should elapse before rivaroxaban is restarted. If a traumatic puncture occurs, rivaroxaban should be delayed for at least 24 hours. Anticoagulant-related spinal/epidural hematoma is discussed further earlier in this chapter (see “Adverse Effects” under “Heparin”).

Drug Interactions

Levels of rivaroxaban can be altered by drugs that inhibit or induce CYP3A4 and P-glycoprotein. Specifically, in patients with normal renal function, drugs that inhibit CYP3A4 strongly and also inhibit P-glycoprotein (e.g., ketoconazole, itraconazole, ritonavir) can raise rivaroxaban levels enough to increase the risk of bleeding. Similarly, in patients with renal impairment, drugs that inhibit CYP3A4 moderately and also inhibit P-glycoprotein (e.g., amiodarone, dronedarone, quinidine, diltiazem, verapamil, ranolazine, macrolide antibiotics) can raise rivaroxaban levels enough to increase the risk of bleeding. Conversely, drugs that induce CYP3A4 strongly and also induce P-glycoprotein (e.g., carbamazepine, phenytoin, rifampin, St. John’s wort) may reduce rivaroxaban levels enough to increase the risk of thrombotic events. Of note, rivaroxaban itself does not inhibit or induce cytochrome P450 enzymes or P-glycoprotein, and hence is unlikely to alter the effects of other drugs.

Because of the risk of bleeding, rivaroxaban should not be combined with other anticoagulants. Concurrent use with antiplatelet drugs and fibrinolytics should be done with caution.

Precautions

Renal Impairment

Renal impairment can delay excretion of rivaroxaban and can thereby increase the risk of bleeding. Accordingly, rivaroxaban should be avoided in patients with severe renal impairment, indicated by a CrCl below 30 mL/min. In patients with moderate renal impairment (CrCl 30 to 50 mL/min), rivaroxaban should be used with caution. If renal failure develops during treatment, rivaroxaban should be discontinued.

Hepatic Impairment

In clinical trials, rivaroxaban levels and anticoagulation were excessive in patients with moderate hepatic impairment. Accordingly, in patients with moderate or severe hepatic impairment, rivaroxaban should not be used.

Pregnancy

Rivaroxaban appears unsafe in pregnancy. The drug increases the risk of pregnancy-related hemorrhage and may have detrimental effects on the fetus. When pregnant rabbits were given high doses (10 mg/kg or more) during organogenesis, rivaroxaban increased fetal resorption, decreased fetal weight, and decreased the number of live fetuses. However, dosing of rats and rabbits early in pregnancy was not associated with gross fetal malformations. Rivaroxaban should be used only if the benefits are deemed to outweigh the risks to the mother and fetus.

Reversal of the Direct Oral Anticoagulants

Although the risk of bleeding is less than with warfarin, the main concern with use of the DOACs remains bleeding. When these drugs first emerged, there were no known specific antidotes. Lack of an antidote led to an uneasiness regarding care of the patient with bleeding, overdose, or of patients requiring emergent surgical procedures. As the use of DOACs increased, two antidotes have been approved: idarucizumab and andexanet alfa. These and other options for reversal are shown in

Table 55.8

.

Table 55.8

Approved Direct Oral Anticoagulant Reversal Agents

Drug Reversal Agent Mechanism of Reversal Agent Suggested Dosing Approved Indication

Apixaban [Eliquis] Andexanet alfa [Andexxa] Binds and sequesters the Xa inhibitors 400–800 mg IV bolus followed by 4–8 mg/min infusion depending on last DOAC dose For life-threatening or uncontrolled bleeding

Rivaroxaban [Xarelto]

Dabigatran [Pradaxa] Idarucizumab (Praxbind) Monoclonal antibody fragment that binds to dabigatran 5 gm IV once, may repeat dose ×1

Emergency surgery or urgent procedures

Life-threatening or uncontrolled bleeding

DOAC, Direct oral anticoagulant; IV, intravenously.

Antiplatelet Drugs

Antiplatelet drugs suppress platelet aggregation. Because a platelet core constitutes the bulk of an arterial thrombus, the principal indication for the antiplatelet drugs is prevention of thrombosis in arteries. In contrast, the principal indication for anticoagulants (e.g., heparin, warfarin) is prevention of thrombosis in veins.

There are four major groups of antiplatelet drugs: aspirin (a “group” with one member), P2Y12 ADP receptor antagonists, PAR-1 antagonists, and GP IIb/IIIa receptor antagonists. As indicated in Fig. 55.1, aspirin and the P2Y12 ADP receptor antagonists affect only one pathway in platelet activation, and hence their antiplatelet effects are limited. In contrast, the GP IIb/IIIa antagonists block the final common step in platelet activation, and hence have powerful antiplatelet effects. Properties of the major classes of antiplatelet drugs are shown in Table 55.9.

Rosenthal, J.B. L. ([Insert Year of Publication]). Lehne’s Pharmacology for Nursing Care (11th Edition). Elsevier Health Sciences (US). 

https://ambassadored.vitalsource.com/books/9780323825245

Clinical pharmacokinetic and pharmacodynamic profile of rivaroxaban

Wolfgang Mueck

 

1

, 

Jan Stampfuss

, 

Dagmar Kubitza

, 

Michael Becka

Affiliations expand

· PMID: 23999929

 

· PMCID: 

PMC3889701

 

· DOI: 

10.1007/s40262-013-0100-7

Free PMC article

Abstract

Rivaroxaban is an oral, direct Factor Xa inhibitor that targets free and clot-bound Factor Xa and Factor Xa in the prothrombinase complex. It is absorbed rapidly, with maximum plasma concentrations being reached 2-4 h after tablet intake. Oral bioavailability is high (80-100 %) for the 10 mg tablet irrespective of food intake and for the 15 mg and 20 mg tablets when taken with food. Variability in the pharmacokinetic parameters is moderate (coefficient of variation 30-40 %). The pharmacokinetic profile of rivaroxaban is consistent in healthy subjects and across a broad range of different patient populations studied. Elimination of rivaroxaban from plasma occurs with a terminal half-life of 5-9 h in healthy young subjects and 11-13 h in elderly subjects. Rivaroxaban produces a pharmacodynamic effect that is closely correlated with its plasma concentration. The pharmacokinetic and pharmacodynamic relationship for inhibition of Factor Xa activity can be described by an E max model, and prothrombin time prolongation by a linear model. Rivaroxaban does not inhibit cytochrome P450 enzymes or known drug transporter systems and, because rivaroxaban has multiple elimination pathways, it has no clinically relevant interactions with most commonly prescribed medications. Rivaroxaban has been approved for clinical use in several thromboembolic disorders.