Pharmacology
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Parenteral Dilantin® (Phenytoin Sodium Injection, USP) WARNING
1 Parenteral Dilantin (Phenytoin Sodium Injection, USP) WARNING: CARDIOVASCULAR RISK ASSOCIATED WITH RAPID INFUSION The rate of intravenous Dilantin administration should not exceed 50 mg per minute in adults and 1-3 mg/kg/min (or 50 mg per minute, whichever is slower) in pediatric patients because of the risk of severe hypotension and cardiac arrhythmias. Careful cardiac monitoring is needed during and after administering intravenous Dilantin. Although the risk of cardiovascular toxicity increases with infusion rates above the recommended infusion rate, these events have also been reported at or below the recommended infusion rate. Reduction in rate of administration or discontinuation of dosing may be needed (see WARNINGS and DOSAGE AND ADMINISTRATION). DESCRIPTION Dilantin (phenytoin sodium injection, USP) is a ready-mixed solution of phenytoin sodium in a vehicle containing 40% propylene glycol and 10% alcohol in water for injection, adjusted to pH 12 with sodium hydroxide. Phenytoin sodium is related to the barbiturates in chemical structure, but has a five-membered ring. The chemical name is sodium 5,5-diphenyl-2, 4- imidazolidinedione represented by the following structural formula: CLINICAL PHARMACOLOGY Mechanism of Action Phenytoin is an anticonvulsant which may be useful in the treatment of generalized tonic clonic status epilepticus. The primary site of action appears to be the motor cortex where spread of seizure activity is inhibited. Possibly by promoting sodium efflux from neurons, phenytoin tends to stabilize the threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient. This includes the reduction of posttetanic potentiation at synapses. Loss of posttetanic potentiation prevents cortical seizure foci from detonating adjacent cortical areas. -
Dilantin (Phenytoin Sodium) Extended Oral Capsule Three Times Daily and the Dosage Then Adjusted to Suit Individual Requirements
Dilantin® (Phenytoin Sodium) 100 mg Extended Oral Capsule DESCRIPTION Phenytoin sodium is an antiepileptic drug. Phenytoin sodium is related to the barbiturates in chemical structure, but has a five-membered ring. The chemical name is sodium 5,5-diphenyl-2, 4-imidazolidinedione, having the following structural formula: Each Dilantin— 100 mg Extended Oral Capsule—contains 100 mg phenytoin sodium. Also contains lactose monohydrate, NF; confectioner’s sugar, NF; talc, USP; and magnesium stearate, NF. The capsule body contains titanium dioxide, USP and gelatin, NF. The capsule cap contains FD&C red No. 28; FD&C yellow No. 6; and gelatin NF. Product in vivo performance is characterized by a slow and extended rate of absorption with peak blood concentrations expected in 4 to 12 hours as contrasted to Prompt Phenytoin Sodium Capsules, USP with a rapid rate of absorption with peak blood concentration expected in 1½ to 3 hours. CLINICAL PHARMACOLOGY Phenytoin is an antiepileptic drug which can be used in the treatment of epilepsy. The primary site of action appears to be the motor cortex where spread of seizure activity is inhibited. Possibly by promoting sodium efflux from neurons, phenytoin tends to stabilize the threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient. This includes the reduction of posttetanic potentiation at synapses. Loss of posttetanic potentiation prevents cortical seizure foci from detonating adjacent cortical areas. Phenytoin reduces the maximal activity of brain stem centers responsible for the tonic phase of tonic-clonic (grand mal) seizures. The plasma half-life in man after oral administration of phenytoin averages 22 hours, with a range of 7 to 42 hours. -
667783-Atenolol (ACC-UK)06-16-SPC-PIL
Artwork No. - Colours Used Customer Accord Pantone Black Description Atenolol Market UK Language English Size 170 x 550 mm PIL Min. Font Size 9.5 Version No. 13 (Page 1 of 2) (06-16-Atenolol SPC) Date 07_05_16 (Atenolol (ACC-UK)06-16-SPC-PIL) Prepared By Checked By Approved By Regulatory Affairs Regulatory Affairs Quality Assurance You must consult your doctor if you are If you forget to take Atenolol Tablets 6. Contents of the pack and other planning to combine Atenolol tablets with the If you forget to take a dose of the Atenolol information medicines listed below: Tablet, take it as soon as you remember, PACKAGE LEAFLET: INFORMATION FOR • Clonidine (for high blood pressure or unless it is time for your next dose. What Atenolol Tablet contains THE USER migraine). If you are taking clonidine and Do not take a double dose to make up for a • The active ingredient is Atenolol. Atenolol 25 mg Tablets Atenolol tablets together, do not stop taking forgotten dose. • The other ingredients are Heavy clonidine unless your doctor tells you to do Magnesium Carbonate, Maize Starch, Atenolol 50 mg Tablets so. If you have to stop taking clonidine, your If you stop taking Atenolol Tablets Sodium Lauryl Sulphate, Gelatin, doctor will give you careful instructions Do not stop taking Atenolol Tablets without Magnesium Stearate, Microcrystalline Atenolol 100 mg Tablets about how to do it. talking to your doctor. In some cases, you may Cellulose and Purified Talc. (Atenolol) • Verapamil, diltiazem and nifedipine (for high need to stop taking it gradually over 7-14 days blood pressure or chest pain). -
Bradycardia; Pulse Present
Bradycardia; Pulse Present History Signs and Symptoms Differential • Past medical history • HR < 60/min with hypotension, acute • Acute myocardial infarction • Medications altered mental status, chest pain, • Hypoxia / Hypothermia • Beta-Blockers acute CHF, seizures, syncope, or • Pacemaker failure • Calcium channel blockers shock secondary to bradycardia • Sinus bradycardia • Clonidine • Chest pain • Head injury (elevated ICP) or Stroke • Digoxin • Respiratory distress • Spinal cord lesion • Pacemaker • Hypotension or Shock • Sick sinus syndrome • Altered mental status • AV blocks (1°, 2°, or 3°) • Syncope • Overdose Heart Rate < 60 / min and Symptomatic: Exit to Hypotension, Acute AMS, Ischemic Chest Pain, Appropriate NO Acute CHF, Seizures, Syncope, or Shock Protocol(s) secondary to bradycardia Typically HR < 50 / min YES Airway Protocol(s) AR 1, 2, 3 if indicated Respiratory Distress Reversible Causes Protocol AR 4 if indicated Hypovolemia Hypoxia Chest Pain: Cardiac and STEMI Section Cardiac Protocol Adult Protocol AC 4 Hydrogen ion (acidosis) if indicated Hypothermia Hypo / Hyperkalemia Search for Reversible Causes B Tension pneumothorax 12 Lead ECG Procedure Tamponade; cardiac Toxins Suspected Beta- IV / IO Protocol UP 6 Thrombosis; pulmonary Blocker or Calcium P Cardiac Monitor (PE) Channel Blocker Thrombosis; coronary (MI) A Follow Overdose/ Toxic Ingestion Protocol TE 7 P If No Improvement Transcutaneous Pacing Procedure P (Consider earlier in 2nd or 3rd AVB) Notify Destination or Contact Medical Control Revised AC 2 01/01/2021 Any local EMS System changes to this document must follow the NC OEMS Protocol Change Policy and be approved by OEMS 1 Bradycardia; Pulse Present Adult Cardiac Adult Section Protocol Pearls • Recommended Exam: Mental Status, HEENT, Skin, Heart, Lungs, Abdomen, Back, Extremities, Neuro • Identifying signs and symptoms of poor perfusion caused by bradycardia are paramount. -
Hypovolemic Shock
Ask the Expert Emergency Medicine / Critical Care Peer Reviewed Hypovolemic Shock Garret E. Pachtinger, VMD, DACVECC Veterinary Specialty & Emergency Center Levittown, Pennsylvania You have asked… What is hypovolemic shock, and how should I manage it? Retroperitoneal effusion in a dog The expert says… hock, a syndrome in which clinical deterioration can occur quickly, requires careful analy- All forms of shock share sis and rapid treatment. Broad definitions for shock include inadequate cellular energy pro- a common concern: Sduction or the inability of the body to supply cells and tissues with oxygen and nutrients and remove waste products. Shock may result from a variety of underlying conditions and can be inadequate perfusion. classified into the broad categories of septic, hemorrhagic, obstructive, and hypovolemic shock.1-3 Regardless of the underlying cause, all forms of shock share a common concern: inadequate per- fusion.1,2 Perfusion (ie, flow to or through a given structure or tissue bed) is imperative for nutri- ent and oxygen delivery, as well as removal of cellular waste and byproducts of metabolism. Lack of adequate perfusion can result in cell death, morbidity, and, ultimately, mortality. Hypovolemic shock is one of the most common categories of shock seen in clinical veterinary medicine.4 In hypovolemic shock, perfusion is impaired as a result of an ineffective circulating blood volume. During initial circulating volume loss, there are a number of mechanisms to com- pensate for decreases in perfusion, including increased levels of 2,3-Bisphosphoglycerate, result- ing in a rightward shift in the oxyhemoglobin dissociation curve and a decreased blood viscosity. -
Update on Volume Resuscitation Hypovolemia and Hemorrhage Distribution of Body Fluids Hemorrhage and Hypovolemia
11/7/2015 HYPOVOLEMIA AND HEMORRHAGE • HUMAN CIRCULATORY SYSTEM OPERATES UPDATE ON VOLUME WITH A SMALL VOLUME AND A VERY EFFICIENT VOLUME RESPONSIVE PUMP. RESUSCITATION • HOWEVER THIS PUMP FAILS QUICKLY WITH VOLUME LOSS AND IT CAN BE FATAL WITH JUST 35 TO 40% LOSS OF BLOOD VOLUME. HEMORRHAGE AND DISTRIBUTION OF BODY FLUIDS HYPOVOLEMIA • TOTAL BODY FLUID ACCOUNTS FOR 60% OF LEAN BODY WT IN MALES AND 50% IN FEMALES. • BLOOD REPRESENTS ONLY 11-12 % OF TOTAL BODY FLUID. CLINICAL MANIFESTATIONS OF HYPOVOLEMIA • SUPINE TACHYCARDIA PR >100 BPM • SUPINE HYPOTENSION <95 MMHG • POSTURAL PULSE INCREMENT: INCREASE IN PR >30 BPM • POSTURAL HYPOTENSION: DECREASE IN SBP >20 MMHG • POSTURAL CHANGES ARE UNCOMMON WHEN BLOOD LOSS IS <630 ML. 1 11/7/2015 INFLUENCE OF ACUTE HEMORRHAGE AND FLUID RESUSCITATION ON BLOOD VOLUME AND HCT • COMPARED TO OTHERS, POSTURAL PULSE INCREMENT IS A SENSITIVE AND SPECIFIC MARKER OF ACUTE BLOOD LOSS. • CHANGES IN HEMATOCRIT SHOWS POOR CORRELATION WITH BLOOD VOL DEFICITS AS WITH ACUTE BLOOD LOSS THERE IS A PROPORTIONAL LOSS OF PLASMA AND ERYTHROCYTES. MARKERS FOR VOLUME CHEMICAL MARKERS OF RESUSCITATION HYPOVOLEMIA • CVP AND PCWP USED BUT EXPERIMENTAL STUDIES HAVE SHOWN A POOR CORRELATION BETWEEN CARDIAC FILLING PRESSURES AND VENTRICULAR EDV OR CIRCULATING BLOOD VOLUME. Classification System for Acute Blood Loss • MORTALITY RATE IN CRITICALLY ILL PATIENTS Class I: Loss of <15% Blood volume IS NOT ONLY RELATED TO THE INITIAL Compensated by transcapillary refill volume LACTATE LEVEL BUT ALSO THE RATE OF Resuscitation not necessary DECLINE IN LACTATE LEVELS AFTER THE TREATMENT IS INITIATED ( LACTATE CLEARANCE ). Class II: Loss of 15-30% blood volume Compensated by systemic vasoconstriction 2 11/7/2015 Classification System for Acute Blood FLUID CHALLENGES Loss Cont. -
Management of Alcohol Withdrawal
Management of alcohol withdrawal Q2: What interventions are safe and effective for the management of alcohol withdrawal, including treatment for alcohol withdrawal seizures and prevention and treatment for acute Wernicke's encephalopathy? Background Alcohol withdrawal can be uncomfortable and occasionally life threatening. Pharmacological management of alcohol withdrawal is an essential component of alcohol dependence. Benzodiazepines (BZDs), non-sedating anticonvulsants and antipsychotics are commonly used in the treatment of alcohol withdrawal. Given that they are all potentially toxic medications, what is the evidence that the benefits of their use justify the risks? Which is more effective? Population/Intervention(s)/Comparison/Outcome(s) (PICO) Population: people with alcohol dependence commencing alcohol withdrawal Interventions: benzodiazepines anticonvulsants (non sedating i.e. non barbiturates and not chlormethiazole) antipsychotics Comparison: placebo and/or active treatment Outcomes: severity of withdrawal complications of withdrawal (seizures, delirium) completion of withdrawal death 1 Management of alcohol withdrawal List of the systematic reviews identified by the search process INCLUDED IN GRADE TABLES OR FOOTNOTES Ntais C et al (2005). Benzodiazepines for alcohol withdrawal. Cochrane Database of Systematic Review, (3):CD005063. Polycarpou A et al (2005). Anticonvulsants for alcohol withdrawal. Cochrane Database of Systematic Reviews, (3):CD005064. Mayo-Smith MF (1997). Pharmacological management of alcohol withdrawal. A -
Guideline for Preoperative Medication Management
Guideline: Preoperative Medication Management Guideline for Preoperative Medication Management Purpose of Guideline: To provide guidance to physicians, advanced practice providers (APPs), pharmacists, and nurses regarding medication management in the preoperative setting. Background: Appropriate perioperative medication management is essential to ensure positive surgical outcomes and prevent medication misadventures.1 Results from a prospective analysis of 1,025 patients admitted to a general surgical unit concluded that patients on at least one medication for a chronic disease are 2.7 times more likely to experience surgical complications compared with those not taking any medications. As the aging population requires more medication use and the availability of various nonprescription medications continues to increase, so does the risk of polypharmacy and the need for perioperative medication guidance.2 There are no well-designed trials to support evidence-based recommendations for perioperative medication management; however, general principles and best practice approaches are available. General considerations for perioperative medication management include a thorough medication history, understanding of the medication pharmacokinetics and potential for withdrawal symptoms, understanding the risks associated with the surgical procedure and the risks of medication discontinuation based on the intended indication. Clinical judgement must be exercised, especially if medication pharmacokinetics are not predictable or there are significant risks associated with inappropriate medication withdrawal (eg, tolerance) or continuation (eg, postsurgical infection).2 Clinical Assessment: Prior to instructing the patient on preoperative medication management, completion of a thorough medication history is recommended – including all information on prescription medications, over-the-counter medications, “as needed” medications, vitamins, supplements, and herbal medications. Allergies should also be verified and documented. -
Pms-ATENOLOL Atenolol Tablets, BP 25 Mg, 50 Mg and 100 Mg
- PRODUCT MONOGRAPH Pr pms-ATENOLOL Atenolol Tablets, BP 25 mg, 50 mg and 100 mg Beta-adrenergic receptor blocking agent PHARMASCIENCE INC. Date of Revision: 6111 Royalmount Ave., Suite 100 November 3, 2017 Montreal, Quebec H4P 2T4 www.pharmascience.com Submission Control No: 201217 PRODUCT MONOGRAPH NAME OF DRUG Prpms-ATENOLOL Atenolol Tablets, BP 25 mg, 50 mg and 100 mg THERAPEUTIC CLASSIFICATION Beta-adrenergic receptor blocking agent ACTIONS AND CLINICAL PHARMACOLOGY Atenolol is a beta1-selective, beta adrenergic blocking agent, devoid of membrane stabilizing or intrinsic sympathomimetic (partial agonist) activities. It is a racemic mixture and the beta1 properties reside in the S (-) enantiomer. Beta1-selectivity decreases with increasing dose. The mechanism of the antihypertensive effect has not been established. Among the factors that may be involved are: a) competitive ability to antagonize catecholamine-induced tachycardia at the beta-receptor sites in the heart, thus decreasing cardiac output b) inhibition of renin release by the kidneys c) inhibition of the vasomotor centres The mechanism of the anti-anginal effect is also uncertain. An important factor may be the reduction of myocardial oxygen requirements by blocking catecholamine-induced increases in heart rate, systolic blood pressure, and the velocity and extent of myocardial contraction. In man atenolol reduces both isoproterenol- and exercise-induced increases in heart rate over the dose range of 50 to 200 mg. At an oral dose of 100 mg the beta1 blocking effects persist for at least 24 hours; the reduction in exercise-induced heart rate increase being about 32% and 13%, 2 and 24 hours after dosing, respectively. -
Towards Non-Invasive Monitoring of Hypovolemia in Intensive Care Patients Alexander Roederer University of Pennsylvania, [email protected]
University of Pennsylvania ScholarlyCommons Departmental Papers (CIS) Department of Computer & Information Science 4-13-2015 Towards Non-Invasive Monitoring of Hypovolemia in Intensive Care Patients Alexander Roederer University of Pennsylvania, [email protected] James Weimer University of Pennsylvania, [email protected] Joseph Dimartino University of Pennsylvania Health System, [email protected] Jacob Gutsche University of Pennsylvania Health System, [email protected] Insup Lee University of Pennsylvania, [email protected] Follow this and additional works at: http://repository.upenn.edu/cis_papers Part of the Computer Engineering Commons, and the Computer Sciences Commons Recommended Citation Alexander Roederer, James Weimer, Joseph Dimartino, Jacob Gutsche, and Insup Lee, "Towards Non-Invasive Monitoring of Hypovolemia in Intensive Care Patients", 6th Workshop on Medical Cyber-Physical Systems (MedicalCPS 2015) . April 2015. 6th Workshop on Medical Cyber-Physical Systems (MedicalCPS 2015) http://workshop.medcps.org/ in conjunction with CPS Week 2015 http://www.cpsweek.org/2015/ Seattle, WA, April 13, 2015 An extended version of this paper is available at http://repository.upenn.edu/cis_papers/787/ This paper is posted at ScholarlyCommons. http://repository.upenn.edu/cis_papers/781 For more information, please contact [email protected]. Towards Non-Invasive Monitoring of Hypovolemia in Intensive Care Patients Abstract Hypovolemia caused by internal hemorrhage is a major cause of death in critical care patients. However, hypovolemia is difficult to diagnose in a timely fashion, as obvious symptoms do not manifest until patients are already nearing a critical state of shock. Novel non-invasive methods for detecting hypovolemia in the literature utilize the photoplethysmogram (PPG) waveform generated by the pulse-oximeter attached to a finger or ear. -
Migraine Headache Prophylaxis Hien Ha, Pharmd, and Annika Gonzalez, MD, Christus Santa Rosa Family Medicine Residency Program, San Antonio, Texas
Migraine Headache Prophylaxis Hien Ha, PharmD, and Annika Gonzalez, MD, Christus Santa Rosa Family Medicine Residency Program, San Antonio, Texas Migraines impose significant health and financial burdens. Approximately 38% of patients with episodic migraines would benefit from preventive therapy, but less than 13% take prophylactic medications. Preventive medication therapy reduces migraine frequency, severity, and headache-related distress. Preventive therapy may also improve quality of life and prevent the progression to chronic migraines. Some indications for preventive therapy include four or more headaches a month, eight or more headache days a month, debilitating headaches, and medication- overuse headaches. Identifying and managing environmental, dietary, and behavioral triggers are useful strategies for preventing migraines. First-line med- ications established as effective based on clinical evidence include divalproex, topiramate, metoprolol, propranolol, and timolol. Medications such as ami- triptyline, venlafaxine, atenolol, and nadolol are probably effective but should be second-line therapy. There is limited evidence for nebivolol, bisoprolol, pindolol, carbamazepine, gabapentin, fluoxetine, nicardipine, verapamil, nimodipine, nifedipine, lisinopril, and candesartan. Acebutolol, oxcarbazepine, lamotrigine, and telmisartan are ineffective. Newer agents target calcitonin gene-related peptide pain transmission in the migraine pain pathway and have recently received approval from the U.S. Food and Drug Administration; how- ever, more studies of long-term effectiveness and adverse effects are needed. The complementary treatments petasites, feverfew, magnesium, and riboflavin are probably effective. Nonpharmacologic therapies such as relaxation training, thermal biofeedback combined with relaxation training, electromyographic feedback, and cognitive behavior therapy also have good evidence to support their use in migraine prevention. (Am Fam Physician. 2019; 99(1):17-24. -
Jp Xvii the Japanese Pharmacopoeia
JP XVII THE JAPANESE PHARMACOPOEIA SEVENTEENTH EDITION Official from April 1, 2016 English Version THE MINISTRY OF HEALTH, LABOUR AND WELFARE Notice: This English Version of the Japanese Pharmacopoeia is published for the convenience of users unfamiliar with the Japanese language. When and if any discrepancy arises between the Japanese original and its English translation, the former is authentic. The Ministry of Health, Labour and Welfare Ministerial Notification No. 64 Pursuant to Paragraph 1, Article 41 of the Law on Securing Quality, Efficacy and Safety of Products including Pharmaceuticals and Medical Devices (Law No. 145, 1960), the Japanese Pharmacopoeia (Ministerial Notification No. 65, 2011), which has been established as follows*, shall be applied on April 1, 2016. However, in the case of drugs which are listed in the Pharmacopoeia (hereinafter referred to as ``previ- ous Pharmacopoeia'') [limited to those listed in the Japanese Pharmacopoeia whose standards are changed in accordance with this notification (hereinafter referred to as ``new Pharmacopoeia'')] and have been approved as of April 1, 2016 as prescribed under Paragraph 1, Article 14 of the same law [including drugs the Minister of Health, Labour and Welfare specifies (the Ministry of Health and Welfare Ministerial Notification No. 104, 1994) as of March 31, 2016 as those exempted from marketing approval pursuant to Paragraph 1, Article 14 of the Same Law (hereinafter referred to as ``drugs exempted from approval'')], the Name and Standards established in the previous Pharmacopoeia (limited to part of the Name and Standards for the drugs concerned) may be accepted to conform to the Name and Standards established in the new Pharmacopoeia before and on September 30, 2017.