Clopidogrel-Induced T: A Case Study

Warfarin is used most often for long-term prophylaxis of thrombosis. “Specific indications are (1) prevention of venous thrombosis and associated pulmonary embolism, (2) prevention of thromboembolism in patients with prosthetic heart valves, and (3) prevention of thrombosis during atrial fibrillation.”(Lehne, 2010, p. 605). Warfarin is the oral anticoagulant of choice for these indications. The drug has also been used to reduce the risk of recurrent transient ischemic attacks (TIA) and recurrent myocardial infarction (MI).(Lehne, 2010).

many different medicines are used to treat coronary heart disease. Usually they aim to reduce blood pressure or widen your arteries. For example antiplatelet are a type of medicine that can help reducing the risk of a heart attack by thinning your blood and preventing it from clotting. However there are also side effects after taking the medication like dizziness, diarrioah, nose bleeds and abdominal pain.

Coumadin (non specific name: warfarin) is an anticoagulant, or blood diminishing drug, that is endorsed to numerous patients who are at danger for creating blood clusters that could bring about heart assaults or strokes. Warfarin is near the most astounding purpose recently and simultaneous investigations of medications that provoke ER visits and occurring an expansion in healing center based offices with the affirmation of patients. Anticoagulation treatment stances perils to patients and over and over prompts unfavorable solution events in light of complex dosing, fundamental ensuing watching, and clashing patient consistence. As a result, various patients who meet current evidence based principles for warfarin treatment are not being managed

In Cardone presentation, His main focus was on Platelet-rich plasma (PRP), (plasmas that come from the patient’s body, and is centrifuged to increase the concentration of platelets combined with remaining blood). He also discussed the potential advantages as well as potential drawbacks and uncertainties regarding the use of PRP injections to treat

The clinical practice project I chose to write about and research is dual antiplatelet therapy. Dual antiplatelet therapy is the combination of aspirin and a P2Y12 inhibitor such as Plavix, Effient, or Brillinta after stent placement in patients who have experienced an ischemic event such as a myocardial infarction or stroke (AHA, 2016). I chose this topic because I work on a telemetry unit that cares for patients who have experienced a myocardial infarction and have undergone stent placement. Part of their post-op care is initiation of dual antiplatelet therapy and education regarding its importance. I feel like more educational materials are needed to assist patients and nurses with this education.

Screen the individual for any and all drugs which interfere with clotting of blood and would cause strokes or interferences with cascade of the clotting factors.

Acute coronary syndrome (ACS) is the most common form of cardiovascular disease.1 In 2006, about 733,000 ACS patients were discharged from hospitals costing the United States $150 billion annually.2 Eighty percent of these cases were either unstable angina (UA) or no ST- elevation myocardial infarction (NSTEMI), and the remaining 20% were ST-elevation myocardial infarction (STEMI).

October 17, 2009, my world changed. My little brother, Brennan, was diagnosed with idiopathic thrombocytopenia purpura, in short known as ITP. Normally, platelets are made in bone marrow and make their way through the blood stream and filtered out by the spleen. In Brennan’s case, his platelets are destroyed by his body causing his platelet count to drop to life threatening levels. Brennan’s platelet count from 2009, to today in 2016, has never gotten higher than 20,000; which means that he is at risk for spontaneous bleeding at any time. Due to this, Brennan is not allowed to participate in sports and many other physical activities.

Clopidogrel is a second-generation thienopyridine antiplatelet agent used in humans and other species including cats to reduce the risk of thromboembolic diseases secondary to cardiovascular diseases and other systemic diseases. Once it’s converted to clopidogrel active metabolite by Cytochrome P450 isoenzymes, clopidogrel irreversibly inhibits one of the platelet ADP receptors leading to an inhibition of platelet activation and aggregation. Several large clinical trials revealed that clopidogrel administration in human patients significantly reduced the platelet activation and aggregation in vivo, and decreased the frequency of developing thromboembolic events (Sabatine MS et al. JAMA 2005, Yusuf S et al. NEJM 2001, Chen ZM et al. Lancet 2005).

The period entered for the search was from January 2002 to August 2015. The Search terms were: “dual antiplatelet therapy”, “shortened DAPT”,”, “clopidogrel”, “early discontinuation”, “Drug-eluting stenting in diabetes mellitus AND Dual Antiplatelet Therapy”, “extended DAPT”, “prolonged DAPT”, “gastroenteritis AND clopidogrel”, “Delayed eosinophilic gastroenteritis and gastroenteritis”, “thienopyridine”, “P2Y12”, “premature cessation “drug eluting stents AND diabetes” , “duration of dual antiplatelet therapy”. The search had to be modified to include patient’s co-morbidities, medications and medical condition. The search initially started with optimal duration of dual antiplatelet therapy in patients after drug-eluting stent revascularization, and then the search was broadened to include diabetic patients with drug-eluting stent. Lastly I included gastroenteritis to unearth any relation between clopidogrel and Mrs GL’s hospital admittance.

Clopidogrel can be prescribed prophylactically to high-risk patients or to those who have experienced atherothrombotic events such as strokes, acute coronary syndrome, peripheral arterial diseases or any other thrombi-producing illnesses (Cheek, 2013). Clopidogrel works by inhibiting the binding of adenosine diphosphate to platelet receptors, thus, disrupting the process of platelet formation and preventing platelet aggregation and thrombi formation. However, in order to inhibit the binding of ADP, clopidogrel has to be converted to its active form by the enzyme CYP2C19*1. Unfortunately, some people have lost the ability to produce enzyme CYP2C19*1 and instead produce a variant form known as CYP2C19*2. CYP2C19*2 cannot convert clopidogrel to its active form, making clopidogrel useless in patients who carry gene CYP2C19*2. Providentially, pharmacogenomics can identify variant genes with DNA sequencing prior to prescribing medications in order to assure the effectiveness of pharmacologic therapy. This also helps health care providers to prescribe alternate medications when appropriate.

We will obtain 6 milliliters and 5 milliliters of blood samples following verification of a diagnosis of HCM and after approximately 14 days of clopidogrel administration, respectively. The blood samples will be obtained from all cats from femoral or cephalic venipuncture using a 21 to 23-gauge needle or butterfly needle. The blood sample will be stored into red-top serum, EDTA, and sodium citrate tubes. The serum sample will be used to evaluate the biochemistry panel. The EDTA whole blood sample will be used to extract genomic DNA and the plasma to measure clopidogrel active metabolite/clopidogrel acid concentrations. The citrated whole blood will be used to perform platelet aggregometry and flow cytometry analyses of platelet function.

Thrombolytic therapy is the use of drugs to break up or dissolve blood clots, which are the main cause of both heart attacks and stroke.

Choice “D” is the best answer. The therapy of choice for TTP is plasma exchange with fresh frozen plasma. Given that only a few patients present with the classic TTP pentad, the presence of microangiopathic hemolytic anemia (schistocytes, elevated LDH, and indirect hyperbilirubinemia) and thrombocytopenia is considered clinical sufficient to begin infusions with fresh frozen plasma. In patients who do not improve with plasma exchange,

Other side effects include cloudy urine, proteinuria, irregular heartbeats, and chest pain. Angioedema involving the extremities, face, lips, mucous membranes, tongue, glottis or larynx has been seen in patients treated with ACE inhibitors, including captopril (Capoten, 2014). If these effects happen nurses should be ready to administer epinephrine to reduce swelling. Other adverse effect according to Karch (2014) include, “CV: Tachycardia, angina pectoris, heart failure, MI, Raynouds syndrome, hypotension in salt-or volume depleted patients.”