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Mark Hanna
May 16, 2021
In General Discussions
https://hbr.org/2021/04/make-time-for-me-time?utm_campaign=hbr&utm_medium=social&utm_source=linkedin
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Mark Hanna
May 11, 2021
In Leadership
Making Joy a priority at work! Great read. #tuesdaymotivation #tuesday #Toliveistolearn https://hbr-org.cdn.ampproject.org/c/s/hbr.org/amp/2019/07/making-joy-a-priority-at-work
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Mark Hanna
Apr 20, 2021
In Pharmacy Forum
This video explains the vaccine development process and how it is possible to achieve a COVID-19 vaccine, with significant domestic and international collaboration, in a much shorter period of time.
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Mark Hanna
Apr 15, 2021
In Tehcnology
Photoshop, it was created in 1980 for people to edit there photos. What started off as a small project by Adobe now became a worldwide English word with billions of photographers using everyday. You may ask how do you use it as it has a high monthly payment of 30 CAD (1166 in the Philippines).First, get a photo from your files in your computer. Second, drag it into the empty black place where it says "Put your photos here) Thirdly , let it render and mess around. As someone who used it. Mess around with it any learn the tools before editing your photo in PS (Photoshop). Once you learn the basics, your on your way to having a endless road of fun editing! The possible with photoshop are endless! -Daniel
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Mark Hanna
Apr 15, 2021
In Tehcnology
Coding, everyone with a computer has heard of it. Some people say it's a waste of time , some don't. But coding is more deeper than that. It is the future of humanity, in fact it's what contribute to rovers, spacecraft and even medical care! You may ask how does work? Well, it runs through a thing called a "Script". Scripts are the place that the code runs in. Code is like a password code, there is a command to it. Such as something like "Wait" and this does it waits for something/time then the code counties. It even has gonna as far to help countries in need! Nasa in 2018 launched a spacecraft that can check the soil in the earth every few days. This helps Countries like Egypt check their soil to see if it is in good condition or not. The possibilities are endless! -Daniel
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Mark Hanna
Mar 31, 2021
In General Discussions
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Mark Hanna
Mar 30, 2021
In Mental Health
The COVID-19 pandemic has had a considerable impact on mental health across the globe particularly due to mitigation measures such as quarantine, isolation, curfews and lockdowns, loss of income, deaths, travel restrictions, as well as disruptions of our daily routine. According to the World Health Organization, the largest impact is in the form of stress and anxiety. There are rising cases of depression, suicide, and alcohol and substance use. On the other hand, we record high rates of divorce cases, domestic violence as well as sexism. KFF Health Tracking Poll conducted research in July 2020 and found out that the majority of adults are reporting negative impacts on their mental health and well-being. People are having difficulty in sleeping, eating, and have worsened chronic conditions due to stress and worry over the coronavirus. Prevention and promotion of mental health Mental disorders affect individual functioning resulting in emotional suffering and reduced quality of life, moreover, stigma and discrimination. The problem extends further into the community resulting in far-reaching economic and social consequences. Therefore, the need to reduce the burden of mental disorders and to pay attention to the prevention and promotion of mental health. The establishment of mitigation strategies to preserve mental well-being is crucial. Prevention is the best strategy to combat mental problems, in addition to, looking after your physical and mental health such as · Eat a balanced diet to help your immune system to function properly · Exercise · Avoid alcohol consumption and cigarette smoking · Use relaxation techniques · Get plenty of rest and sleep
Effects of COVID-19 on Mental Health content media
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Mark Hanna
Mar 30, 2021
In Leadership
https://hbr.org/2021/03/3-tools-to-help-leaders-steady-their-teams-during-a-transition?utm_campaign=hbr
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Mark Hanna
Mar 28, 2021
In Pharmacy Forum
Epidemiology · 2016 US National Survey on Drug Use and Health, 50% of US adults reported using alcohol at least once in the past 30 days · According to the CDC, 25.1% of adults > 18 years of age had at least one heavy drinking day (five or more drinks for men and four or more drinks for women) in the past year. · Alcohol is a significant contributor in up to 40% of all medical admissions and 50% of all surgical Trauma cases · Alcohol use is associated with 85,000 deaths each year in the US alone · Approximately half of patients with alcohol use disorder experience alcohol withdrawal when they reduce or stop drinking · With early identification and appropriate management, mortality from DT is less than 5 percent Pathophysiology · Symptoms of alcohol withdrawal occur because alcohol is a central nervous system depressant. · enhances inhibitory tone (via modulation of gamma-aminobutyric acid [GABA] activity) and inhibits excitatory tone (via modulation of excitatory amino acid activity · Abrupt cessation unmasks the adaptive responses to chronic ethanol use, resulting in overactivity of the central nervous system. GABA · GABA is the major inhibitory neurotransmitter in the brain. · Highly specific binding sites for ethanol are found on the GABA receptor complex · As alcohol tolerance develops, the individual retains arousal at alcohol concentrations that would normally produce lethargy or even coma in relatively alcohol-naïve individuals. · Cessation of alcohol or a reduction from chronically elevated concentrations results in decreased inhibitory tone. Glutamate · One of the major excitatory amino acids · When glutamate binds to the N-methyl-D-aspartate (NMDA) receptor, calcium influx leads to neuronal excitation by binding to the glycine receptor on the NMDA complex · Ethanol inhibits glutamate-induced excitation. Adaption occurs by increasing the number of glutamate receptors in an attempt to maintain a normal state of arousal. · Cessation of alcohol or a reduction from chronically elevated concentrations results in unregulated excess excitation. · Dopamine, also appears to be involved in both alcohol dependence and the manifestations of withdrawal. Increases in dopamine during withdrawal may contribute to hyperarousal • Symptoms of Alcohol withdrawal 6- 36 hours Tremors , mild anxiety, headache, diaphoresis, palpitations, anorexia, gastrointestinal upset Considered Mild withdrawal 6- 48 hours Single or brief flurry of generalized tonic-clonic seizures, status epilepticus (rare) Seizures 12 – 48 hours Visual, auditory, and/or tactile hallucinations with intact orientation and normal vital signs Alcoholic hallucinations 48 hours – 96 hours and up to 10 days Delirium, agitation, tachycardia, hypertension, fever, diaphoresis Delirium Tremens Symptoms of Alcohol withdrawal Alcoholic Hallucinations vs Delirium tremens 1) Alcoholic Hallucinations: · Hallucinations that develop within 12 to 24 hours of abstinence and typically resolve within 24 to 48 hours · Hallucinations are usually visual, although auditory and tactile phenomena are also described. 2) Delirium Tremens: · Typically begins between 48 and 96 hours after the last drink and lasts one to five days Risk Factors for DT : A history of alcohol withdrawal seizures A history of sustained drinking A history of Delirium Tremens (Altered mental status) Age greater than 30 presence of a concurrent illness The presence of significant alcohol withdrawal in the presence of an elevated blood alcohol concentration A longer period since the last drink General Factors to Consider: Quantity of alcoholic intake Duration of alcohol use Time since last drink Previous alcohol withdrawals Presence of concurrent medical or psychiatric conditions Abuse of other agents. Should assess possible complicating medical conditions: Arrhythmias, CHF, CAD, gastrointestinal bleeding, infections, liver disease, nervous system impairment, and pancreatitis. Initial Testing Complete blood count Liver function tests Urine drug screen Determination of blood alcohol and electrolyte levels. CIWA SCORE - Clinical Institute Withdrawal Assessment for Alcohol Criteria: N/V, Anxiety, Paroxysmal sweats, Tactile disturbances, Visual disturbances, tremors, agitation, orientation and cloudiness of the sensorium, Auditory disturbances, Headache Scale for Scoring: Total Score 0 – 9: absent or minimal withdrawal 10 – 19: mild to moderate withdrawal More than 20: severe withdrawal Management Overview 1) Ruling out alternative diagnoses It may be necessary to perform extensive testing, including lumbar puncture and cranial computed tomography (CT), to rule out other diagnostic considerations with confidence Especially, Important when the presentation includes altered mental status and fever. Factors such as infections, trauma metabolic derangements, drug overdose, hepatic failure, and gastrointestinal bleeding can mimic or coexist with alcohol withdrawal A premature diagnosis of alcohol withdrawal can lead to inappropriate use of sedatives, which can further delay accurate diagnosis 2) Supportive Care Benzodiazepines are used to control psychomotor agitation and prevent progression to more severe withdrawal Supportive care, including intravenous IV fluids, nutritional supplementation, and frequent clinical reassessment including vital signs Patients should be placed in a quiet, protective environment. Isotonic IV fluid can be infused rapidly until patients are clinically euvolemic Thiamine (100 milligrams IV) followed by glucose should be administered in order to prevent or treat Wernicke encephalopathy. Multivitamins containing or supplemented with folic acid (Vit B9) should be given routinely, and deficiencies of glucose, potassium, magnesium, and phosphate should be corrected as needed Wernicke’s Encephalopathy Neurologic complication of thiamine (vitamin B1) deficiency Thiamine (B1) protects agents oxidative stress Thiamine has a role in cerebral energy utilization – Deficiency leads to neuronal injury by inhibiting metabolism in brain regions with high metabolic requirements Alcohol leads to reduced absorption as it causes inflammation to the GIT Common Symptoms include: Ataxia, confusion, ocular muscle disturbances Thiamine repletion: Neuronal damage occurs usually after 14 days of deficiency (about 20% below normal) 200-500mg thiamine IV TID until symptom resolution. Replete glucose and magnesium shortly after. Korsakoff Syndrome Usually irreversible condition due to chronic thiamine deficiency resulting in in neuronal death Common symptoms: Amnesia, poor recall, confabulation. Memory disorder despite appearance of no cognitive losses. Recent memory most effected. 50% will have permanent impairment after repletion Even after thiamine repletion 75% of patients will have some long-term changes – permanent impairment (amnesia). Benzodiazepines · Used to treat the psychomotor agitation most patients experience during withdrawal and to prevent progression from minor withdrawal symptoms to major ones · Diazepam (Valium), lorazepam (Ativan), and chlordiazepoxide (Librium) are used most frequently to treat or prevent alcohol withdrawal, but other benzodiazepines may be used . · In general, long-acting benzodiazepines with active metabolites (ex, diazepam or chlordiazepoxide) are preferred because they seem to result in a smoother clinical course with lower chance of recurrent withdrawal or seizures u Lorazepam oral dosing: 2 mg orally every 6 hours for 4 doses, then 1 mg every 6 hours for 8 doses u Lorazepam IV dosing: 2 to 4 mg IV every 15 to 20 minutes u Diazepam IV dosing: 5 to 10 mg IV every 5 to 10 minutes · lorazepam (Ativan) or oxazepam (Serax) are preferred for the treatment of patients with advanced cirrhosis or acute alcoholic hepatitis. · The shorter half-life of lorazepam and the absence of active metabolites with oxazepam may prevent prolonged effects if over sedation occurs. · Chlordiazepoxide has a relatively long half-life and may lead to over sedation in patients with severe liver disease BZD Mechanism of Action · Positive Allosteric modulators. They bind between Alpha and Gamma subunits · When BZD are bound, Cl- channel opens longer, which enhances the amount of Cl- entering the cell · They only work in the presence of GABA. So with prolonged heavy Alcohol use - u Cross tolerance between BZDs and Alcohol. 3 Strategies: 1) Loading Dose Strategy · Uses high doses of longer‐acting benzodiazepines to quickly achieve initial sedation with a self‐tapering effect over time due to their pharmacokinetic properties. · Typically, diazepam 10–20 mg or chlordiazepoxide 100 mg doses are repeated every 1–2 h until the patient reaches adequate sedation with an average of three doses usually required · Possible Benefits: Reducing the total of BZDs needed, and intense monitoring is usually required in the earlier part · Possible Drawbacks: Sedation and respiratory depression- need to intensely monitor (especially in elderly patients or those with hepatic dysfunction). 2) Fixed or Scheduled dosing · Beneficial for patients who will require medication regardless of symptoms, such as in those with a history of seizures or DT · Also used in patients withdrawing from alcohol with comorbid medical illnesses or if unable to assess withdrawal symptoms. · Chlordiazepoxide and diazepam remain the agents of choice because of their long‐acting nature · A ceiling dose of 60 mg of diazepam or 125 mg of chlordiazepoxide is advised per day After 2–3 d of stabilization of the withdrawal syndrome, the benzodiazepine is gradually tapered off over a period of 7–10 days 3) Symptom Triggered therapy · Requires regular assessment of patient's withdrawal symptoms using a validated tool like the CIWA scale · Not applicable in non‐verbal patients · The cutoff for beginning treatment is a score of at least 8 · 5–10 mg diazepam or 25–100 mg chlordiazepoxide · If symptoms persist, doses are repeated hourly until the score is below 8. · Advantages: Lower doses of BZDs used, less sedation, and lower risk of respiratory depression Barbiturates MOA · 1. At low doses: They act like BZD (positive allosteric modulators) as they Increase Cl- entry when they bind between the Alpha and Beta subunits. · 2. At high doses, they can open GABA-A Cl- channels on their own even when GABA is not present. · 3. Barbiturates can inhibit Glutamate (excitatory) neurotransmitters. Antagonists at the AMPA receptors. Phenobarbital · In patients with refractory Delirium tremens or Alcohol withdrawal seizures who require high doses of BZD · Pts with Chronic heavy Alcohol use who have cross tolerance between Alcohol and BZD · Phenobarbital Dosing: 130 to 260 mg IV, repeated every 15 to 20 minutes, until symptoms are controlled Monitoring/ considerations & Precautions u Do not start benzodiazepines after starting phenobarbital u Phenobarbital loading doses may need to be reduced in patients with higher risk of sedation or respiratory compromise u Patients receiving phenobarbital must be on a cardiac monitor with continuous oxygen saturation monitoring Adverse Effects Phenobarbital Adverse Effects: · Somnolence, Syncope, Thrombophlebitis, Megaloblastic anemia, Liver damage, Hypersensitivity reaction, Hallucinations, Angioedema, Respiratory depression Benzodiazepines Adverse Effects: · Hypotension, Muscle weakness, Ataxia, Incoordination, Somnolence Euphoria, Respiratory depression, Fatigue Adjunct Therapy Dexmedetomidine (Precedex) · alpha-2 agonist that decreases release of norepinephrine which decreases sympathetic overdrive. · No controlled trials showing that it prevents the development of seizures or DT. Data so far suggest that may decrease the amount of BZDs used. · 0.2-1.5 mcg/ kg/ hour · Adverse Effects: Bradyarrhythmia, Hypotension, Sinus arrest, Tachycardia, Transient hypertension, Hypoxia, Respiratory depression Clonidine · Consider in patients with significant increase in blood pressure or nearing hypertensive urgency (pressure > 180/120 mm Hg) · Other autonomic symptoms such as tachycardia or tremor · 0.1 mg orally hourly up to 3 times until systolic blood pressure < 140 mm Hg and diastolic pressure < 90 mm Hg Haloperidol · For patients exhibiting agitation despite benzodiazepine therapy, giving haloperidol adjunctively can be beneficial. · Caution is advised because of the potential for a lowering of the seizure threshold, extrapyramidal effects, and risk of QTc prolongation leading to arrhythmias · Baseline electrocardiogram and electrolyte panel should be obtained, with daily electrocardiograms thereafter · Suggested haloperidol dosing is 2 to 5 mg intravenously every 0.5 to 2 hours with a maximum dose of 0.5 mg/kg/24 hours Beta Blockers May be considered in combination with benzodiazepines in patients with persistent hypertension or tachycardia, but not used often. Atenolol commonly used; typical single doses are50 mg if pulse 50-79 beats/minute or 100 mg if pulse ≥ 80 beats/minute Common AE: bradycardia, hypotension, fatigue, dizziness, cold extremities, and depression Prevention and Screening · Consider prophylactic treatment in inpatients admitted for reasons other than alcohol withdrawal (and are without withdrawal symptoms) and have history of either: · Withdrawal seizures or delirium tremens · prolonged, heavy alcohol consumption · typical prophylactic treatment of hospitalized patients at risk of withdrawal consists of chlordiazepoxide 50-100 mg every 6 hours for 1 day · reduce to 25-50 mg every 6 hours for 2 additional days · frequent assessments, and switch to typical treatment regimen if withdrawal symptoms develop References Kattimani S, Bharadwaj B. Clinical management of alcohol withdrawal: A systematic review. Ind Psychiatry J. 2013;22(2):100–108. doi:10.4103/0972-6748.132914 J. Biol. Chem. 2012, 287:40224-40231. doi: 10.1074/jbc.R112.386664 originally published online October 4, 2012 Cresce, Nicole D., et al. “Alcohol Withdrawal Syndrome in Medical Patients.” Cleveland Clinic Journal of Medicine, 15 Aug. 2017, Benzer DG. Management of alcohol intoxication and withdrawal. In: Miller NS, American Society of Addiction Medicine, eds. Principles of Addiction Medicine. Chevy Chase, Md.: The Society; 1994. https://www.cdc.gov/nchs/fastats/alcohol.htm https://www-dynamed-com.ezproxymcp.flo.org/condition/alcohol-withdrawal-syndrome#BENZODIAZEPINE_SELECTION uhttps://www.uptodate.com/contents/management-of-moderate-and-severe-alcohol-withdrawal-syndromes https://hospitalpolicies.ellucid.com/documents/view/18373 https://onlinelibrary.wiley.com/doi/full/10.1111/ane.12671 https://www.uptodate.com/contents/wernicke-encephalopathy?sectionName=TREATMENT&search=alcohol%20withdrawal&topicRef=323&anchor=H14&source=see_link#H4 https://basicmedicalkey.com/sedative-hypnotic-and-anxiolytic-drugs-2/
Alcohol withdrawal content media
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Mark Hanna
Mar 27, 2021
In Pharmacy Forum
Phenytoin Bioavailability (F): · Has a good bioavailability (95%), F can range from 0.90-1 · Completely absorbed from most forms Salt Factor (S): · 0.92 - Phenytoin Na+ (caps, IV) · Phenytoin Acid (tabs, suspension) Volume of Distribution (Vd): · 0.65 L/Kg: Adults – increased in patients with plasma protein binding · 0.7 L/Kg: Children Protein binding: Highly protein bound (90%), mainly bound to albumin, so we would expect issues with patients who have hypoalbuminemia. Time to Peak: · 3-12 hours with regular oral dosing · 20-25 min with IV Metabolism: · Undergoes extensive hepatic metabolism ( CYP 2C19 and CYP 2C9). However, it’s a CYP 3A4 inducer. It is also very important to consider that it is capacity limited. So, in other words, Clearance decreases as concentration increases. Michaelis- Menten Kinetics: · Initially when we load phenytoin naïve patients, it starts as linear Kinetics but once you reach the saturation point, the plasma concentration increases disproportionally so a small change in the dose would have a big impact on the plasma concentration of phenytoin (it would increase). Half-Life (t½): · A function of plasma concentration · Average - 22 hours (range 8 - 60 hours) · Not a constant value since the clearance of Phenytoin changes with the plasma concentration. Once it reaches the saturation point, t ½ becomes longer. Time to Steady State: · Variable but approximately 5 days. Elimination: · Mainly eliminated through the urine Fosphenytoin: Time to Peak : · 20 minutes after a 20 minute infusion · 30 minutes after an IM injection Half-Life (t½): 8 minutes. However, we need to remember that it is a prodrug so it does get metabolized to phenytoin which has a half life of 22 hours. · Based on its PK profile, Fosphenytoin is usually used in patients with poor or absent IV access. It is also important to remember that it does not require propylene glycol for solubilization, which is helpful because propylene glycol can sometimes cause hypotension or tissue necrosis in the case of extravasation. Fosphenytoin Dosing: · Loading Dose is 15-20 mg/kg of PE infused at a rate between 50-150 mg of PE / minute. · Maintenance dose is 4-6 PE/ kg/ day IV · Maximum IM dose is 5 ml. Phenytoin Dosing: · Patients are started with a loading dose · Loading dose is 15,g/kg ( using ABW) rounded to the nearest 50 mg increment. · IV infusion rate should not exceed 25-50 mg/ min. In healthy patients, we usually use the 50 mg/ min but in older patients or in patients with concurrent issues, the 25 mg/ min dose is sometimes used. · If the patient will receive the loading dose orally, we use either the oral solution or the IR formulation, not the ER formulation. · Oral dose should be administered in 3 divided doses separated every 2-4 hours. · Doses greater than 400 mg should be separated to avoid prolonged absorption times and risk of GI AE. Therefore, it is important to remember that the maximum oral dose of phenytoin is 400 mg. · In terms of Maintenance dosing: 5-7 mg/ kg/ day ( using ABW) · Maintenance dosing beings 8 hours after loading dose, and we utilize the ER capsules. The reason for that is because it can be given only once a day. However, if the IV or oral solution form is used, then we have to give it Tid. · Again, Doses greater than 400 mg should be separated to avoid prolonged absorption times and risk of GI AE · When considering dose adjustments, the patient has to be at steady state. It is also important to remember that the maximum change should be no more than 20% of daily dose. · Phenytoin and Fosphenytoin are sring inducers of several enzymes, including CYP2B6, 2C19, 2C8/9, 3A4, P-gp and UGT1A1; they are substrates of CYP2C19 ( major), 2C9 (major) and 3A4 ( minor). · Both drugs can also decrease the concetration of many drugs including other anti epileptics, contraceptives, and warfarin. · Use of an alternative, non hormonal contraceptive is also recommended with chronic phenytoin. · Since both have high protein binding, they can displace other protein bound drugs or be displaced by other highly protein bound drug, cause an increase in levels that can lead to toxicity Incremental Dosing Strategy: · Used when you check the patient’s concentrations and it is not between 10-20 Incremental LD = { (Vd)(Cp desired- Cp initial) } x ABW / ( S*F) · Important to consider that the Bioavailability is always 1 and that we use the IV or oral solution formulations not the ER capsules. Monitoring Serum concentrations: · We sample 2 hours after an IV loading dose · 5-7 days after a regimen dosing change if the patient is on a maintenance dose ( we usually check trough levels) · Also check if patient develops any complications such as seizures, signs and symptoms of toxicity, and addition or deletion of feeding tube administration. · It is also very important to remember that phenytoin is highly Albumin bound (90%), so if there is a drop in serum albumin, there will be an increase in the amount of free phenytoin circulating. · It is also important to remember that dose adjustments are required in patients with renal dysfunction. Adjustments: 1) Adjustments for low Albumin (<3.5g/ dL): Adj concentration = Observed concentration/ (0.2* measured albumin) + 0.1 2) Acute or chronic renal failure (CrCl < 10 ml/min): Adj concentration = Observed concentration/ (0.1* measured albumin) + 0.1 Phenobarbital · Phenobarbital is usually administered orally, IM, or IV · Distribution is less rapid than that of other barbiturates because it is less lipid-soluble, but the drug is found in all tissues and fluids, including adipose tissue and cerebrospinal fluid. · Only unionized drug crosses the blood brain barrier, therefore, acidosis can increase the pharmacologic effects by increasing the concentration of unionized drug. · Phenobarbital has a biphasic distribution. In adults, the volume of distribution of the central compartment (to highly perfused organs) is about 0.3 L/kg; the volume of distribution at steady state ranges 0.5 to 1 L/kg (mean: 0.7 L/kg). · The time to reach steady state phenobarbital levels is 12 to 24 days in the absence of interacting comedication · About 20 to 45% of phenobarbital is bound to plasma proteins. · Phenobarbital is the longest acting of all the commercially available barbiturates; the half-life in adults ranges from 50 to 120 hours (mean: 96 hours). · In the absence of a loading dose, several weeks of therapy may be required to achieve steady-state plasma concentrations. · Therapeutic plasma concentrations (for anticonvulsant activity) are roughly 10 to 40 mcg/mL. · Plasma concentrations > 50 mcg/mL may produce coma or respiratory depression; and concentrations > 80 mcg/mL are potentially fatal. · Roughly 25% of phenobarbital is eliminated unchanged in the urine, but the excretion is pH-dependent. · Increasing the urinary flow rate or alkalinizing the urine will increase the rate of excretion of unchanged phenobarbital. The remainder of the dose (roughly 75%) is inactivated by the liver, primarily via CYP2C9, with minor metabolism by CYP2C19 and 2E1. · Importantly, phenobarbital accelerates the clearance of other drugs metabolized via hepatic enzymes (UGT enzymes, CYP2C-family enzymes, CYP3A-family enzymes, and CYP1A2 · Phenobarbital is inactivated by the liver, primarily via CYP2C9, with minor metabolism by CYP2C19 and 2E1. · Phenobarbital is also a strong inducer of the P-gp drug transporter. · Phenobarbital can also decrease hormonal contraceptive levels significantly. Use of an alternative, non hormonal contraceptive is recommended. Route-Specific Pharmacokinetics: Oral Route · Oral bioavailability is generally good; 95% or higher of an oral dose of phenobarbital is absorbed from the GI tract. · For this reason, total parenteral dosages and oral dosages are often similar on a mg/day basis. · Oral absorption is delayed by the presence of food. Peak serum concentrations are achieved 8 to 12 hours after oral dosing. Intravenous Route · Onset of action after IV administration of phenobarbital is within 5 minutes, reaching a maximum in about 30 minutes. · The peak brain/plasma concentration ratio occurs slowly about 20 to 40 minutes after an IV dose. Intramuscular Route · Onset of action is slightly slower than the less than 5 minutes typical of intravenous administration. Subcutaneous Route · Onset of action is slightly slower than the less than 5 minutes typical of intravenous administration. Rectal route · Phenobarbital is also generally well-absorbed when administered rectally. Additional Considerations: Hepatic Impairment : · Metabolism of phenobarbital may be impaired in patients with hepatic disease. Renal Impairment: · Phenobarbital may accumulate in patients with renal failure or severe renal impairment. Phenobarbital is removed during hemodialysis. Pediatrics Infants and Children: · Peak concentrations are achieved 3 hours after oral administration and 45 minutes to 6 hours after IM administration in infants and children. · The volume of distribution is approximately 0.6 to 0.9 L/kg in infants and 0.6 to 0.7 L/kg in children. · The elimination half-life ranges from 47 to 63 hours in infants and 37 to 69 hours in children. Neonates: · Higher plasma concentrations of phenobarbital are achieved after IM administration than after oral administration in neonates. · Little difference has been reported for other pediatric populations. · Absorption is delayed after oral administration in neonates with a Tmax of 9 hours. After IM administration, the Tmax ranges from 7 to 40 hours in premature neonates and 30 minutes to 27 hours in full term neonates. · Protein binding is 25 to 50% less in neonates compared to older children and is even lower in hyperbilirubinemic neonates; Which would lead to a higher concentration of free Phenobarb and increase the risk of AE. · Volume of distribution in neonates is larger than in other populations (approximately 0.7 to 1.2 L/kg), and is not affected by gestational age or birthweight. · The elimination half-life is highly variable and ranges from 45 to 409 hours. References: https://www-micromedexsolutions-com.ezproxymcp.flo.org/micromedex2/librarian/CS/3B7C50/ND_PR/evidencexpert/ND_P/evidencexpert/DUPLICATIONSHIELDSYNC/30E604/ND_PG/evidencexpert/ND_B/evidencexpert/ND_AppProduct/evidencexpert/ND_T/evidencexpert/PFActionId/evidencexpert.DoIntegratedSearch?SearchTerm=Phenobarbital&fromInterSaltBase=true&false=null&false=null&=null# https://www-clinicalkey-com.ezproxymcp.flo.org/pharmacology/monograph/479?sec=monphar
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Mark Hanna
Jan 02, 2021
In General Discussions
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