Pharmacology Glyceryl - Essay Example

?Pharmacology Question 1. Glyceryl trinitrate is a vasodilator that has an effect on both veins and arteries. Nitro lingual Pump spray is a dose spray that is metered and contains Glyceryl trinitrate. Each metered dose has a delivery of 400µg for every spray emission and the product conveys Glyceryl trinitrate as spray droplets below the tongue. No inhalation of the spray should take place. An initial one-metered dose ought to be sprayed below the tongue at an attack’s onset, followed by another metered dose within a period of five minutes should pain relief not occur. It is recommended that it should not exceed two metered doses. To prevent exercise-induced angina and other precipitation-related conditions, at least one metered dose should be sprayed beneath the tongue shortly before the event. The highest number of Nitrolingual Pumpspray doses administered per day should be determined considering the full medical history of the patient, the angina severity, and any concurrent medication (Coyne 2008 p34). 2. The patient is complaining of discomfort and pain, which are angina’s main symptoms. It includes squeezing, pressure, tightness and burning in the chest, with the discomfort and pains starting from behind the breastbone. The patient is also complaining of nausea, shortness of breath, as well as a pale and cold skin, all which point to angina. The shortness of breath is common with elderly patients of angina, and the pain may make the patient feel as if he is suffering from indigestion or an uncomfortable feeling in the stomach. The blood pressure is also a factor to consider, as the patient was recorded to have 148mmHg, which is way above the recommended 100mmHg for a normal person. Additionally, the patient’s last oral intake was tea and biscuits, which indicates that within the previous 24 hours he did not consume sildenafil (Neal 2012 p34). Question 2 1. The main glyceryl trinitrate’s pharmacological action is that it relaxes vascular smooth muscle, and then vasodilates peripheral arteries and veins, with veins vasodilating more than arteries. Post-capillary vessels’ dilation that also includes large veins promotes blood peripheral flooding and reduces preload. A relaxation in the arteries significantly decreases afterload (arterial pressure and systematic vascular resistance). The reduced systolic wall tension and less ventricular radius reduce the oxygen requirements and the myocardial energy. This decrease in the filling pressures of the heart enhances subendocardial wall layer perfusion that ischemia threatens. Glyceryl trinitrate’s therapeutic doses may decrease diastolic, systolic and average blood pressure in the arteries. This helps in maintaining coronary perfusion pressure. However, should blood pressure reduce, or an increase in the heart rate lowers the diastolic filling time, it can be highly compromised (Coyne 2008 p34). 2. GNT is a prodrug that should be denitrated first so that it can produce NO (the metabolite nitric oxide that is active). Nitro vasodilators are nitrates that undergo denitration to produce NO in the body. NO being a potent activator of GC (Guannyl Cylase) with the help of mechanisms that are heme-dependent, its activation results in the formation of cGMP from cGTP (cyclic guanosine triphosphate) (Bersten 2009 p938). 3. When glyceryl trinitrate is administered sublingually, it is absorbed rapidly from the mouth’s mucosa and bypasses the liver to reach the vascular system. It is metabolized in the liver and other cells such as erythrocytes with cleavage of several nitrate groups. Numerous inter-individual as well as intra-individual variations can be seen after the sublingual administration, for the plasma concentration. Glyceryl trinitrate, together with its metabolites, is eliminated principally, with less than 1% excreted with no change (Broyles, Reiss & Evans 2012 p.437). 4. The application of glyceryl trinitrate in any form during acute myocardial infarction’s early days requires attention to be particularly paid to clinical status and hemodynamic monitoring. Reducing the systolic blood pressure to less than 90mmHg should be avoided. Question 3 In the interpretation of the ECG, lead II is the 12 leads of reference. The pulse rate can be seen to be 66 beats per minute (300/45), calculated from the division of 300 by the number of 1mm boxes that are located between the QRS boxes. Since the P wave can be seen, the rhythm can be observed to be a sinus rhythm, meaning that ectopic sources of electrical activity are not present in the heart. There is notable ST elevation in the leads between V2 and V5, with reciprocating depressions in leads aVR and lead III. This is an indication of an acute anterior lateral MI. The patient should be transported to a hospital on a stretcher that is strapped to the ambulance to avoid dizziness and fainting that are associated with sitting and standing (McKenry & Salemo 1998 p. 281). Question 4 1. Aspirin can be beneficial to patients who are already experiencing angina, a heart attack, peripheral vascular disease, or a stroke, or those who have had procedures the likes of bypass or angioplasty. 2. Generally, aspirin that is of immediate release is usually wholly absorbed from the GI (gastrointestinal) tract. After it is absorbed, it is hydrolyzed to salicylic acid, with the acid’s peak plasma levels occurring within a period of about two hours after administration. Salicylic acid is distributed to all fluids and tissues such as the central nervous system. Aspirin is hydrolyzed rapidly to salicylic acid in the plasma (Coyne 2008 p.515). 3. The mechanism of action of aspirin Aspirin inhibits Prostaglandin Synthase ‘s action, which is also known as Cyclooxygenase or COX. Prostaglandin Synthase catalyses the conversion of arachidonate within the prostaglandin H2, which happens to be a precursor of some other prostaglandins such as thromboxane that mediates when the inflammation process takes place, such as fever and pain. Thromboxane takes part in the mechanism of coagulation that facilitates the activation of platelets. Since the Prostaglandin Synthase activity is inhibited by aspirin, it leads to a decrease in the production of prostaglandin H2 together with its derivatives. This forms an explanation for the anticoagulant and anti-inflammatory effects of aspirin (Bryant & Knights, 2012 p.398). 4. Aspirin may cause gastrointestinal distress, gastrointestinal bleeding and may contribute to the increase in bleeding severity or disorders of bleeding. Additionally, low-grade toxicity may lead to headaches, ringing in the ears, dizziness, tachycardia, and flushing. It is advised that aspirin not administered if the patient is unable to swallow or chew, or is allergic to aspirin and products that contain aspirin or similar products. 5. Some of the advice that should be given to Leonard is an explanation of the procedure to him, including that needs to chew the aspirin and not swallow it. He should be advised to take the correct dosages of between 160 and 325mg. The patient can be allowed to self-administer the aspirin and if he is not able to do so, and should not be allowed to take any fluids by mouth (Neal, 2012 p.619). Question 5 1. Clopidogrel is an ADP-receptor antagonist that is irreversible, and it inhibits the aggregation of platelet that is mediated by decreased glycoprotein receptor IIb/IIIa activation. Clopidogrel, when combined with aspirin, has been known to be superior to aspirin alone when it comes to the treatment of unstable angina, but its recipients have exhibited rides in blood loss, reoperation rates, and transfusion requirements following a cardiac surgery. 2. Clopidogrel used in the prevention of strokes and heart attacks in patients suffering from angina and heart disease. It is applied together with aspirin worsening chest pains that may be an indication of unstable angina and for the prevention of blood clots and keeping blood vessels open following certain procedures. 3. Action Mechanism Clopidogrel falls among thienopyridines that are administered orally. It is a prodrug whereby 85 per cent of it undergoes metabolism through esterases to form a derivative of carboxylic acid that is inactive. The remaining 15 per cent undergoes activation via hepatic metabolism. Thiol etabolite, which is active, binds ADP receptor’s P2Y component in an irreversible process. This leads to platelet activation that is ADP independent to be inhibited and then aggregation takes place. The active metabolite’s peak plasma concentration can be achieved after several hours, with platelet inhibition and increased peak concentration of metabolite occurring upon the administration of a single loading dose is administered of 600 versus 300mg. Platelet aggregation inhibition and its activation lasts for the entire platelets’ lifetime. On the other hand, the platelet recovery function needs an off therapy of approximately five days (Roach & Zorko 2005 p.529). 4. If Clopidogrel is administered before coronary angiography, in a patient undergoing a coronary stent placement it can be applied in the prevention of thrombosis. It can also be used to stem any complications that may arise by acting as a prophylactic medication. However, Clopidogrel may aggravate bleeding during the surgery, and it is thus necessary for the patient to be observed during the surgery as it takes some time for the drug’s anti platelet effects to be achieved. In case of worsening chest pains in the patient that are indications of angina that is unstable, it can be used together with aspirin to reduce the pain. It is also used to keep arteries and veins open to keep the blood flowing and also prevent blood clots following surgery (Bryant & Knights, 2012 p.298). 5. There are some clinical situations that would make it in appropriate for the administration of Clopidogrel to a patient such as Leonard, and they include administration to patients with blood ailments that lead to a prolonged bleeding time. (Bryant & Knights, 2012 p.328). Other situations include administration to patients with GIT problems such as abdominal pains, vomiting, diarrhea, and nausea (Coyne 2008 p.515). Additionally, in the case of patients with peptic ulcers and liver functions that are impaired, it would be in appropriate to be administered with Clopidogrel. Other situations include patients with unstable angina, thrombotic thrombocytopenia purpura, and at the start of a myocardial infarction. Patients who are hypersensitive to Clopidogrel and those on warfin should not be administered (McKenry & Salemo 1998 p. 296). Reference List Bersten, A. D. 2009. Oh's Intensive Care Manual. New Jersey: Elsevier Health Sciences Broyles, B. E., Reiss, B. S. & Evans, M. E. 2012. Pharmacological Aspects of Nursing Care. New York: Cengage Learning Bryant, B & Knights, K. 2012. Pharmacology for Health Professionals. Sydney: Elsevier Health Sciences. Coyne, C. P. 2008. Comparative Diagnostic Pharmacology: Clinical and Research Applications in Living-System Models. New York: John Wiley & Sons McKenry, L. M. & Salemo, E. 1998. Mosby's pharmacology in nursing, Volume 20. New York: Mosby. Neal, M. J. 2012. Medical Pharmacology at a Glance. New York: John Wiley & Sons Roach, S. S. & Zorko, J. 2005. Study Guide for Pharmacology for Health Professionals. New Jersey: Lippincott Williams & Wilkins Read More