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Clinical Pharmacy - Science topic

Explore the latest questions and answers in Clinical Pharmacy, and find Clinical Pharmacy experts.
Questions related to Clinical Pharmacy
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Hello! What are the oldest literary sources you know that would mention pharmaceutical salts? I am aware of the first cocrystal [benzoquinone + hydroquinone] (1:1) investigated in 1844, but I could not find any mention of the first (or even the first described) pharmaceutical salt (Wohler, F. Untersuchungen über das Chinon / F. Wohler // Ann. Chem. Pharm. – 1844. – V. 51. – P. 145-163). If you know of such sources, please share them. Thanks in advance
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As far as I understand, at the turn of the 19th and 20th centuries, there were enough chlorides and sodium salts of the API. However, it is not yet clear when salts with organic counterions began to be used. Perhaps someone has such information?
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Someone was taking Daflon 500 mg (450 mg Diosmin, 50 mg Hesperidin) twice daily for her varicose veins. Now, the manufacturer makes Daflon 1000 mg (900 mg Diosmin, 100 mg Hesperidin).
Now, the Q is, if she takes the new dosage form 1000 mg once daily, will this dose be equivalent to 500 mg once daily or the pharmacokinetics and the therapeutic effects will be different?
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based on a double-blind, multicenter, RCT comparing 1,000 mg tabs vs 500 mg tabs (same daily dose) in acute hemorrhoid, the authors concluded that "We have been demonstrated that the new single MPFF 1000 mg tablet has clinical acceptability and a good safety profile, comparable to that of MPFF 500 mg tablets. MPFF 1000 mg was as effective as MPFF 500 mg in reducing anal pain and bleeding. The new dose regimen should lead to better treatment adherence and consequently to better management of hemorrhoidal disease."
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Kindly, explain your answer. Thanks in advance.
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I agree with my colleaques answer espically focus dysfunction of parathyroid gland and level of excreated calcium
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Respected Sir/Madam,
Just I wanna a discussion on the topic that how we can use the Conceptual Framework in Pharmacy practice research or Clinical pharmacy research? is there any books, references, articles or any comprehensive discussions on it?
Thanks and kind regards
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Dear colleque,
Thank you very much for intresting question.
I shoud inform you that I have the book only related with pediatric disseases because I am pediatration and delivered lectures, but my articles research related with Clinical Pharmacology because of my interest in this field of medicine.
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I'm a community Pharmacist and I'm interested in writing, especially writing scientific papers. I'm offering my help and assistance in case you need a hand with your current research. My areas of interest: Pharmacotherapy, psychology, neurology, psychiatry. So send me a message in case you need help.
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I am interested...Kindly contact me after two weeks...
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When you read about the treatment goals for Glaucoma, you'll find for example : the target IOP is determined by factors like baseline IOP, Rate of disease progession, etc... I want to know which branch of pharmacy the above Q relates to? The treatment targets and goals aren't clinical Pharmacology, so what branch if I want to delve deeper (How these goals are set, why these goals specifically) I should read?
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I am a clinical Pharmacy Specialist with about 4 years of experience. Mostafa Elsersy
To get this straight, the treatment goal is addressed under pharmacotherapy one area of clinical pharmacy. Unless you have a measurable goal or pre-defined goals (sign or symptoms improvements) it is difficult to assess whether the treatment is adequate or not. Specific to your question, the main goal of Glaucoma treatment is to halt or slow down the disease progression or to prevent further deterioration of the vision. Lowering IOP help to decrease the disease progression or prevents glaucoma in patients with ocular hypertension (without optic nerve damage). If you want to dig more you can read standard textbooks such as Pharmacotherapy: A pathophysiologic approach (Joseph T. Dipiro) or Applied Therapeutics: The Clinical Use of Drugs (Caroline S. Zeind)
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I read that diabetic retinopathy can affect people with type 1 and 2 diabetes, especially those who have uncontrolled blood sugar and have diabetes for a long time. How can uncontrolled blood sugar cause diabetic retinopathy? and how is the treatment for diabetic retinopathy patients? thank you.
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Initially, the main treatment was laser treatment to coagulate leaking retinal blood vessels. Today, intravitreal injections from the group of anti-VEGF drugs are standard in the treatment of both macular edema and diabetic retinopathy. The injections are given after local anesthesia with drops through the sclera and are completely painless. Treatment is carried out monthly for several months or years. With the help of these injections, better results are achieved than after laser treatment because the laser also damages the surrounding healthy tissue. Improvement of vision is often achieved, and not only stabilization of existing vision. After improving vision with injections, the treatment is supplemented with classic laser treatment, which then permanently preserves the existing condition. In our Clinic we have the most modern laser photocoagulator Pascal which is significantly less painful
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How can a patient safely taper off bisoprolol 2.5 mg who used it once daily? What schedule can he follow to taper off gradually? Any reference/paper/textbook for doing this?
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Dear Seyed Ruhollah Musavinsab. I fully agree with you. But ocassionally patients need to be individualized.Excepting renal failure, I prefer to give drugs at usual interval.
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When I viewed the PK parameters of both warfarin and candesartan, I found that both medications have 99% plasma protein binding. I then went to check and confirm there will be PK interaction through resources and I was surprised when I found no interaction! So can it be? Any explanation?
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Hi
Conclusion about no interactions probably cover lack of meaningful PD observations see:
" Candesartan cilexetil produced a 7% decrease in trough plasma warfarin concentration but this had no effect on prothrombin time. "
So in some cases pharmacokinetic interaction can exist but have no impact on clinical findings. Probably this is why you find conclusions about lack of interaction. Finally protein binding in blood plasma not must be most important aspect of interactions between both drugs
from another hand:
" Candesartan had no effect on S-warfarin 7-hydroxylation. In contrast, S-warfarin inhibited candesartan metabolism by the wild-type (K = 17microM) greater than by the Leu359 variant (Ki = 36 microM). These findings suggest that CYP2C9*3 may change not only the metabolic activity but also the inhibitory susceptibility compared with CYP2C9*1. "
Best regards
Tomasz
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Is there any reference/Book/Software that shows only the pharmacokinetic parameters of all medications available? For example, if I want to know the absorption, metabolism of acetaminophen, I should open the monograph in this reference and see all the information I need, the same goes for omeprazole, cetirizine, any medication. Is there such a resource/reference?
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Hi
To be onest from my point of view best are FDA documents related to specific drug submission its better than any database (for example drugbank https://go.drugbank.com/drugs/DB00341) ....
for example
google, key words: fda cetirizine pharmacokinetics accedata
Or maybe such books will be better
Best regards
Tomasz
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If someone with allergic rhinitis developed epistaxis after using intranasal steroids (Fluticasone propionate) and Azelastine, what should be the correct action to be taken? Stop taking them until bleeding stops and then re-initiate taking them or stop taking them forever as they may cause complications if they caused bleeding initially? What would be your chouce?
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The reason for bleeding in the majority of cases is misdirection of the spray towards the septum, active management in the first instance is stop the spray for a few days and use aseptic or a local lubricating spray. Either lubrication should be applied with the 'non-touch' technique as patients often use their finger or a cotton bud to install the ointment which defeats the purpose.
Prevention is best especially if the intranasal steroids are necessary so I advise the use of the X-Factor approach which is directing the spray laterally towards the medial cants of the eye on the same side thus optimising delivery of the medication to the turbinates and avoiding the septal mucosa as much as possible. This advice which is liked by children was based on a clinical nugget that I received from an experienced German ORL college some year ago which was to present the spray to the right nostril with the left hand and vice versa. This method by crossing fingers for the nose while instructing her led to one of my adolescent patients first suggesting the X-Factor
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  • What is the time taken for steady state to be established in adults for ( Mycophenolate mofetil ) ?
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Please bear in mind that there is a large interindividual variability in the bioavailability and therefore the plasma concentration of parent mycophenolate and active metabolite. The variation can b as large as 30%. You may consider checking the plasma concentration in critical cases.
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Background: it needs to be solved for IV administration to pavians and the current information we have is that it is soluble in DMSO (dimethylsulfoxid). If you don't know a different solvent maybe someone knows a little more about 'safe' concentrations for administration. Many thanks for your help!
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1,4-dideoxy-1,4-imino-D-Arabinitol (DAB) is soluble in DMSO. For obtaining a higher solubility ,it is necessary to warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
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The same route of administration, dosage form, and the strength of the biological product ?
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If developed to the standards of the FDA, and EMA, the answer is 100% "yes." Products with the same structure and function will have the same effect. Head-to--head comparisons of reference and biosimilars are required at multiple levels to confirm the match in clinically important parameters. That having been said, there are products available in less developed countries that claim to be biosimilars but are not developed to the same standards and may not match the structure of the reference. Some of these products are still OK in terms of safety and efficacy (although I would not call them "biosimilars"), but others less so.
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Does taking many medications make a load on the kidney, liver and stomach affecting them negatively?
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We must look to prescribe as little drugs as possible to manga well all the problems and to get a good relationship between risk/benefit for all patients
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We know common symbols of pharmacy;
  • Rx means you take, represents drug dispensing.
  • Bowl of Hygeia, represents medicines that are potent.
  • Mortar and Pestle, represents the compounding of medications.
As pharmacy practice is becoming more clinically focussed, pharmacists need a more relevant symbol like;
  • Stethoscope of doctors
  • Syringe of nurses
  • _______ of pharmacists
I hope this future symbol will drive change and help in achieving clinical pharmacy mission in the future. That will be included in the next edition of my book;
Kindly suggest.
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It should be like magnifying glass on the prescription pad ...or any symbol resembles monitoring of the treatment
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I have a question related to severity assessment of ADR and that is if a patient is hospitalized due to some ADR caused by drug and has reported 6 adverse drug reactions for example, neutropenia, pancreatitis, bladder cancer, headache, rash, cough, then how would I be able to tag the ADR or classsify the ADR on the basis of Hartwig and Seigel scale or how would I be able to find that which individual ADR caused hospitalization as there are multiple ADR in practicing?
I have to put the ADR into Level 1, Level 2 and so on. (hartwig and seigel scale)
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Level 2
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Metronidazole 500mg/100ml Intravenous Infusion should be infused intravenously at an approximate rate of 5 ml/minute (or one bag infused over 20 to 60 minutes) ?
Why this slow rate of infusion?
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ADVERSE EFFECTS OF METRONIDAZOLE OVERDOSAGE
System Organ Class (SOC)
Blood and Lymphatic System Disorders
Leukopenia
Agranulocytosis
Pancytopenia
Neutropenia
Thrombocytopenia
Eosinophilia
uncommon
Immune System Disorder
Anaphylactic shock
Jarisch-Herxheimer reaction
Hypersensitivity
rare
Metabolism and Nutrition Disorders
Decreased appetite
Psychiatric Disorders
Hallucinations
Depression
Confusional state
Insomnia
rare
Nervous System Disorders
Dysgeusia
Headache
Encephalopathy
Meningitis aseptic
Seizure
Somnolence
Neuropathy peripheral
Ataxia
DizzinessDysarthria
Hypoaesthesia
Paraesthesia
common
rare
Eye Disorders
Optic neuropathy
Diplopia
Myopia
rare
rare
rare
Cardiac Disorders
Tachycardia
Palpitations
RARE
Respiratory, Thoracic and Mediastinal Disorders
Dyspnoea
not known
Gastrointestinal Disorders
Glossitis
Stomatitis
Dry mouth
Pancreatitis
Abdominal pain upper
Diarrhoea
Nausea
Vomiting
Constipation
Tongue discoloration
common
common
common
rare
rare
rare
rare
rare
Hepatobiliary disorders
Jaundice cholestatic
rare
Skin and Subcutaneous Disorders
Stevens-Johnson syndrome
Toxic epidermal necrolysis
Angioedema
Erythema multiforme
Pruritus
Swelling face
Urticaria
Hyperhidrosis
Rash
rare
rare
rare
rare
not known
not known
not known
not known
not known
Musculoskeletal and Connective Tissue Disorders
Myalgia
Muscle spasms
Arthralgia
common
not known
not known
Renal and urinary disorders
Chromaturia
Dysuria
rare
not known
General and Administration Site Conditions
Asthenia
Mucosal inflammation
Pyrexia
Injection site reaction
Malaise
Face oedema
Oedema peripheral
Chest pain
Chills
uncommon
rare
rare
not known
not known
not known
not known
not known
not known
Investigations
Hepatic enzyme increased
not known
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It takes 1 min to translate everything but it takes 25 years to know if it has translated correctly. I had a client, a pharmacy graduate, called Dr. Grand (for ethic's sake, I'm gonna call her Grand). she had prepared a text extracted from her thesis, clinical pharmacy, and sent it to me for translation and manuscript preparation. she was all good and bargaining like crazy to get a discount. I liked clinical pharmacy, so I accepted to write at for a little amount of money because she was sb I knew. so, I started translating and finished in time and sent it to her to read. In my opinion, it was a well-written DRAFT, so I told her not to worry about the text and that it was going to be revised several times. what this young lady did was, she called me after 5 months, telling me that her supervisors thought that it was a simple text! To be honest, until today, I don't know how to make really basic research with no proper literature review sound sophisticated?! DO YOU PREFER A REALLY COMPLICATED TEXT WITH SO many JARGON IN IT? that is my question. After too many revisions, She texted me angrily that Her English is way better than me and she could write a better manuscript than me. She was so rude in her texts, telling me that she is a Dr. and I'm nothing. Dr. Grand!!
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We will express things as long in a complicated manner as we do not understand them fully;
in a gradual process, we can learn to formulate complicated things as simple as possible, in terms of (scientific) creativity.
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4.5 half life are required in order for the medication to be eliminated from the body right? Thus in order for the cefipime to be eliminated from the body 2 days (t1/2= 12 hour)? I'm asking because if someone stopped taking the medication for one day, can he continue the medication afterward?
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basically their is no any clinical evidence of accumulation of the drug when injected tid mean while the total elimination of cefepime in the body is 2hrs independent of the dose administered to the patient or the volunteers during the clinical trials of the drug
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If someone was taking Cefipime IM 1 gm/ 12 hours for 10 days (The course is supposed to be 14 days) for complicated urinary tract infection (Cystitis) then he suddenly stopped taking the medication for one day. Can he continue the medication afterwards or he needs to adjust the dose?
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Patient should containue dose as prescribed
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In hypertensive patients, is there recommended diluent ( Ns, dextrose, Ringer, or any isotonic solution) used in drug dilution for intravenous administration?
which one is preferred or restricted?, with explain plz.
Thanks...
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following
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Is there any website that can tell me when this adverse reaction will occur? For example, will this adverse reaction occur after repeated exposure? Or can occur after first dose? Or can be delayed?
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How can I assess the medication effect on the liver? Should I check the frequency of the adverse event? And if common, go further by checking the mechanism and measures to minimize it? If so, what resource I should check SmPC and USPI or Livertox? Or you check by severity of the injury of the medication? If so, what resource do you use to assess the severity of injury caused by the medication?
For example, what will be your approach if I assigned you clindamycin? What will be your comment if my Q is, is Clindamycin entirely safe medication if the liver is the only organ in Q?
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Mostafa Elsersy The CIOMS/RUCAM scale is a tool to predict whether liver damage can be attributed to a particular medication.
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How is neomycin is precribed in second degree burn and it is contraindicated in broken skin because of the systemic absorption?!!
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Neomycin is used in prophylaxis of skin infection in minor injury , the main side effects of this drug may aggrevate the severity of burn because already it may cause:
  • irritation
  • burning
  • redness
  • rash
  • itching
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Which resource or what is the most reliable reference/website/textbook to check when looking for the safety of medications during pregnancy?
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Food Drug Administration USA ( USA), Harrison's principles of internal medicine
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Is there any reference/resource that can explain the reason behind the contraindications? I'd like to know so I can be sure that if the patient can take the medication (no alternatives available) safely despite the presence of one of the contraindications.
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Mostafa: Within the contraindications there are different types . Depending on what you look for you can find information in one way or another: Contraindications for side effects: that refer to an unintended consequence that is part of the pharmacological action of a medication; for example, dry mouth in the course of a treatment with anticholinergics. Think of, a patient with s. Sjogren, who sees his symptoms worsened by taking anticholinergics. It could also be a non-selective beta-blocker and an asthmatic patient. The physiological mechanism of bronchial relaxation is through beta2 agonism, if you block it you can trigger asthma attacks. You can usually find the cause by looking at the physiology of the mechanism of action and physiology of the side effect.Also books of clinical pharmacolgy usually explain this.
Secondary effect, on the other hand, is an unintended manifestation that arises as a consequence of the fundamental action of a medicine, but that is not an inherent part of it. By way of example, hypokalemia may occur that occurs in the course of treatment with thiazide diuretics. You can also evaluate it depending on the mechanism of action of the drug. Adverse reaction or undesirable effect, finally, refer to the unwanted effects that, in addition, are harmful. In these the cause of the adverse reaction is not usually known . You know the frequency of appearance, the characteristics of the population that it affects ... in these cases the information can be found in pivotal trials, or in safety drug monitoring agencies, and drug technical data sheets. Physiologically justify why they appear is difficult, if a patient taking ibuprofen suffers a syndrome of Steve Johnson, you may say that it is a very rare adverse reaction, but not why this patient, its idiosyncrasic.
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What will happen if the patient used carbamide peroxide to remove earwax when there is dizziness? I know dizziness could indicate inner ear problem, but what if the patient used carbamide peroxide while he is complaining of dizziness? Will there be adverse reactions like hydrogen peroxide could affect the inner ear?
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Donna, I have two Qs. Firstly, how can I know the rationale behind the contraindications? Is there any draft that explains so? Because I'd like to know if the contraindication in Q can be managed or it is absolutely not. Secondly, can I rephrase what you said with regard to dizziness? You mean that if the patient used carbamide peroxide while he is suffering tymanic membrane perforation, will suffer vertigo? Is that the rationale behind the contraindication?
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The Health Technology Assessment (HTA) unit of the CHU de Québec – Université Laval is currently working to get data on integrated early rehabilitation interventions in pediatric intensive care unit.
We define «integrated early rehabilitation interventions» as physical, functional, nutritional, psychological, communicational, social or spiritual rehabilitation activities initiated during the first days of admission of a patient in the pediatric intensive care unit and delivered by each professional according to an intervention plan that has been developed beforehand as a team by these same professionals.
Are early interdisciplinary rehabilitation interventions an established practice in the pediatric intensive care unit of your hospital?
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Currently I am living in Bolivia and most of the Hospital don´t count with those services in ICU.
In Brazil there is a law that determine the presence of some of those professional (PT for example) 24/7. But that doesn´t translate into practice.
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Interdisciplinary research (IDR) is a mode of research by teams or individuals that integrates information, data, techniques, tools, perspectives, concepts, and/or theories from two or more disciplines or bodies of specialized knowledge to advance fundamental understanding or to solve problems whose solutions are beyond the scope of a single discipline or area of research practice.
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Mohamed, check out this journal. You might find it interesting. I’m a review for it: https://commons.pacificu.edu/hip/about.html
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Will you initiate Daflon with this list of medications or not?
Medical History:
Atrial Fibrillation (Managed with 2.5 mg bisoprolol once daily)
Allergic Rhinitis (Managed with 10 mg cetirizine once daily)
Vaginal Hysterectomy (Post-operation medications to prevent surgical site infection include : Clindamycin 300 mg 3 times per day, Cefixime 400 mg once daily along with topical treatment Clindamycin vaginal cream along with Betadine® (Povidone-iodine))
The operation (Vaginal Hysterectomy) was done on 14/3/2019 and she was precribed Enoxaprin 40 (once daily) two days consequently prior to the operation and she did take Enoxaprin on the day after the surgery also.
My Q is: Can she take Daflon one tablet daily for managing chronic venous insufficiency as she used to prior to the operation or taking Daflon can increase the risk of bleeding? Should she wait till she finish the post-op medications?
Medications administered during her stay in Hospital:
meropenem, Levofloxacin 500 mg , Acetaminophen.
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Hesperidin has moderate drug interactions with:
  • Bisoprolol: leading to increased blood pressure lowering effect and this interaction may lead to hypotension.
  • Enoxaparin: hesperidin in combination with diosmin may increase fibrinogen levels and clotting time and increased risk of bleeding.
Diosmine has moderate drug interactions with:
  • Clindamycin: diosmine inhibits the metabolism of clindamycin and might increase the risk of infection with C. diff.
  • Enoxaparin: taking diosmin with other anticoagulant/antiplatelet drugs might increase the risk of bleeding
Thanks
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When do you go the medical literature (primary - journal articles) instead of going to well known databases like Lexicomp, PDR, etc..with regard to adverse reactions/effects?
Is it when you check OTC medications? Herbal Medications? Or what?
The data of castor oil are conflicting unfortunately! And I'm not sure if it is safe or not!! What is your recommendation?
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The medical literature may be an earlier reporting of new outcomes, positive and negative.
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For example , Clindamycin 300 mg three time daily and Cefixime 400 mg once per day have the potential to cause liver injury or the likelihood is low? I read both monographs but can't make decision whether this combination is safe or harmful on the liver?
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I agree with previous comments, that LiverTox is a great resource for information on DILI, but that LiverTox does not claims to answer all questions.
Still it is a very good starting point.
When it comes to the question if any drug is safe to use, DILI is unlikely to occur, usually only in the range of 1 in 1000 or fewer people (Exceptions are ie Isoniazid [INH] where monitoring is recommended).
If a patient had a DILI reaction in the past to a certain medication, I would avoid such medication, unless clinically absolutely necessary due to lack of alternative therapies.
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53 Y F is taking bisoprolol 2.5 mg once daily (Before sleep), Cetirizine 10 mg once daily , Cefixime 400 mg once daily along with Clindamycin 300 mg 3 times per day. Tamsulosin 0.4 mg is going to be added to this drug regimen. Which time you prefer to administrate Tamsulosin since Tamsulosin may interact with bisoprolol and lower blood pressure even more? I suggested to take both medications at different times during the day, Bisoprolol before sleep and Tamsulosin in the morning because I don't want to lower blood pressure too much during sleep (with no monitoring available during sleep time). What do you think? Agree?
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Beta blockers are preferred during day time and avoided during night mostly as during sleep there is increased parasympathetic drive which reduces the resting heart rate.
Better to give bisoprolol in morning.
Tamsulosin is a selective alpha blocker and has minimal effect on the alpha 1 receptors present in the blood vessels which reduces it's chances of causing hypotension as expected from a non selective alpha blocker like prazocin.
So continue Tamsulosin at night and consider bisoprolol at morning
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The partnership is growing between clinical pharmacy education, practice and research areas related to practice of pharmacist. This integration is the highlight in new Elsevier textbook https://www.sciencedirect.com/book/9780128142769/clinical-pharmacy-education-practice-and-research. All clinical pharmacy teachers need to be practitioners and practice with research is evidence-based.
Professor Dixon Thomas
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Pharmaceutical Care, Medication Therapy Management (MTM), and Pharmacists' Patient Care Process (PPCP) are discussed well in the Elsevier textbook Clinical Pharmacy Education, Practice and Research. Authors include global leaders in MTM and PPCP;
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We made a Clinical Pharmacy glossary (more than 5000 terms) and wright the book - The History of Clinical Pharmacy.
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I believe they are offering their research contribution, if the project is still developing.
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I have been working with my juniors for final year project of clinical pharmacy, the topic assigned is self-medication trend among general population. The topic is generally weak. What intervention or parameters, can I seek to improvise my research in this area.
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Self-medication is a common human behaviour in response to minor discomfort, many people who practice self-medication hold positive perception toward this practice. There are certain medical problem where self-medication is very common like dental pain (read our paper on self medication in dental pain here:
You can look at specific group of people (e.g. elderly), as for different age groups reasons may vary. I feel going into behavioural side would be difficult for final year students.
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I want to detect various neurotransmitters in various biological samples. Please suggest a simple, accurate and economic method for determination of these neurotransmitter. like UV method.
It is very important in my research work. Please.
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Following
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I do have some time available within my day, and I was wondering if there is any research project that needs collaboration?
I can collaborate, and my field of interest is Clinical pharmacy , Toxicology, Herbal Medicine or other Pharmaceutical related Fields.
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I am interested to join Dr Mauro
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If someone has been taking Candesartan 4 mg one tablet daily for a year and want to take Diclofenac 25 mg for occassional pain, How can I eliminate the interaction between both (Aside from monitoring blood pressure and renal function)? Is there a way where I can separate the interaction. I read that half life of diclofenac is 2 hours so can he take Candesartan after 2 hours from ingesting Diclofenac or it (Candesartan) already in the blood as he has been taking it for a year, so the interaction will inevitably occur?
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Just have a look at candesartano drug-drug interactions at the link below
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Dear all,
Could you please recent Textbooks on drug-drug interactions covering all or most aspect of this issue.
Thanks
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Hi Ahmed
I think these books may help to find your queries
1. Drug-drug interactions in pharmaceutical development/ [edited by] Albert P. Li : Wiley,2008.
2.Drug-drug interactions /edited by A. David Rodrigues: Informa Healthcare,2008.
3. Drug-membrane interactions: analysis, drug distribution, modeling/ Joachim K. Seydel and Michael Wiese: Wiley,2002.
4. Meyler's side effects of drugs: the international encyclopedia of adverse drug reactions and interactions/ editor, J.K. Aronson: Elsevier,2016.
5. Drug facts and comparisons
6. Drug-Drug interactions with an emphasis on psychiatric medications / Sheldon H Preskorn: Professional Communications,2018.
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Good evening all,
Please suggest me any society or agency who provide fund specially for CLINICAL PHARMACY project??
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You can try the United Kingdom Clinical Pharmacy Association (UKCPA)
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What is the evidence based protocol for tapering off topical Corticosteroids? And when to consider tapering off instead of discontinuing abruptly? After 2 months for example?
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I think it depends on the type of that topical steroid, potency, duration, combination with other drugs... but in general tapering may be needed after 1 month of it use to be on the safe side.
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Dear all
I'm looking for the recent standards HF knowledge test primarily used in HF clinics led by pharmacists. Thanks
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Echo and chest X- ray.
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I see some Healthcare Professionals recommend Coenzyme Q10 supplementation because Beta Blockers deplete it. I tried to find evidence for this, and I didn't find except this paper.
So my Q, as a Pharmacist, do I have to supplement someone who is taking Bisoprolol or not? Because I didn't find also Bisoprolol mentioned in this paper.
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Hi Mostafa,, I totally agreed with answar of Dr Koshy. There are some suggestions that propranolol may reduce level of Co enzyme Q. But supplementation is not required. Bisoprolol is very unlikely to cause Co enzyme Q depletion. Following article might help you... Thanks
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Advertising may shape purchase behaviour and attitudes towards (or knowledge about) the products. I wonder whether such link exists between susceptibility to advertising dietary supplements and knowledge about them (or attitudes towards them). I searched the literature, but found no relevant data. Do you know about any research in this field? Could you please provide any literature? Negative responses are also welcomed :)
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You may start with this article. This is primarily about theory but you may find it helpful (full text posted):
Susceptibility to Advertising: an Individual Difference With Implications For the Processing of Persuasive Messages
Best wishes!
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As a Pharmacist, which resource do you use to check whether the Excipients are safe for your patients or not? I have read in some references that Saccharin is hepatotoxic, and when I checked "Handbook of Pharmaceutical Excipients, Sixth Edition", I found nothing about that! So, can you help me with this dilemma?
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For excipients used in pediatrics see the Safety and Toxicity of Excipients for Paediatrics (STEP) database provided by the European Pediatric Formulation Initiative (EUPFI)
Best regards
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I am not much into pharmaceutics and drugs manufacturing , I rather enjoy being a part of the health care system in real life and dealing with patients is something I long for. But I also don't want to be deviated from the core of pharmacy( medications and pharmacotherapy).
So my question is: would a master in community and public health be a good choice or better options are there?
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Clinical Pharmacist is an active member of healthcare team providing direct patient care. American College of Clinical Pharmacy describes role of a Clinical Pharmacist as working directly with physicians, other health professionals, and patients to ensure that the medications prescribed for patients contribute to the best possible health outcomes. This role provides opportunity for a Clinical Pharmacist to apply core of pharmacy in patient care.
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I'm working on a project; a pharmacoeconomics study, I want to know the exact no of patients to take into my study, given that:
My study is a cost effectiveness analysis that, I'll do on patients.
So, I used G Power, but, the main problem is how to know the effect size?.
The previous studies were done on a large samples and only mentioning confidence interval and RR, OR.
Can anyone guide me for an easy way to calculate the effect size?
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You mentioned you found a meta-analysis study that provided the result as mean difference. That study should also have provided the pooled variance. Divide the mean difference by the square root of the variance (aka standard error). That should give you the effect size. Hope this helps.
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As a community Pharmacist, which guideline or resource do you follow for differential diagnosis of common ailments like common cold, allergic rhinitis, and other mild cases ? As well as the established pathway for OTC products to recommend in each of the above mentioned cases ? Do you follow "handbook of nonprescription drugs" or " community pharmacy symptoms diagnosis and treatment" or both combined or something else ?
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There are no guidelines or standards widely accepted for OTC medicines used in community pharmacies, as minor illnesses vary from one region to another. However, you may follow the WHO's brief guidance as you wish. In the UK, three reference books have been used by most pharmacy students and pharmacists:
1. Symptoms in the pharmacy: a guide to the management of common illness. 7th ed. Blenkinsopp A, Paxton P, Blenkinsopp J. Oxford: Wiley-Blackwell; 2014.
*** This book is recommended for pharmacy students and pharmacists, as it provides many good disease and medication points, esp. when to refer patients.
2. Community pharmacy: symptoms, diagnosis and treatment. 4th ed. Rutter P. Edinburgh: Elsevier; 2017.
*** Professor Rutter is an experienced community pharmacist himself and he spent many years writing this book to meet all purposes.
3. Minor illness or major disease. 6th ed. Addison B, Brown A, Edwards R, Gray G. London: Pharmaceutical Press; 2016.
*** It is interesting to see some OTC and P medicines used for both minor and major diseases.
Hope this helps.
Dr Win
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How is this possible ? One of the images shows that the first dose didn't produce the therapeutic effect !! Aren't we suppose to feel the effect even after the first dose ? Isn't the first dose suppose to cross the MEC ?
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Gee, you'd best ask a clinician that. They get feedback from their patients as to onset of effects. Probably varies amongst the various anxiolytics and patients.
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Isn't Css the same as the plasma therapeutic level ? Because if so, in the case of Acetaminophen, just one dose of 500 mg would reach the Css, and there would be no need for 4-5 half life ?
if we want to reach the Css from one dose(Loading dose), we will use this equation Dose (Oral)=Vd*Css divided by the Bioavailability. Here are the info. The volume of distribution is about 70 L for someone who weigh 70 K.g and the oral bioavailability is about 70%, and the therapeutic level is 10 to 20 mcg/mL so a simple calculation would yield 500 mg to be the dose which is common in practice. So, how is this possible ? Aren't we suppose to reach the Css after 4-5 half life, not just from one dose ? Am I getting this right ? Or there is a difference between the therapeutic level and the Css ?
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Mostafa,
Note that Css is the steady state level that is reached after several half-lives following regular multiple dosing. The therapeutic level is simply the blood concentration that will result in a therapeutic response which (for certain drugs) can be reached just from a single dose.
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Will they have the same magnitude of therapeutic effect ? Or do I have to check for bioequivalence studies before choosing the brand name ?
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I think we need to remember we are treating a patient. If the person really needs a treatment we should not deny them simply because we can't find the same brand. Most of the time the differences between brands are smaller than the differences between individuals, so It is entirely logical to give the patient a trial of a different brand and to watch what happens. So, my recommendation is to switch brands ( my own GP does it all the time) but ensure that the patient knows and is on the lookout for any differences that could be due to a change in pharmacokinetics such as an initially more intense effect (eg: Higher Cmax in an antihypertensive) or delayed effect (Later Tmax).
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Do all drugs need to achieve the steady state concentration after 4-5 half life in order to see the therapeutic effect ? Doesn't ibuprofen produce its effect from a single dose without 4-5 half life ?
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Half life is the time duration required by a drug to get reduced in plasma by half of its initial concentration. For example if the plasma concentration is 100mg now what time it will take to remain 50 mg then 25mg and so on. A drug needs 4-5 half life toget elliminated or excreted completely from body not to acheive a steady state . Actually steady state is an equlibrium mantained by frequent doses of drugs. A single dose may acheive a minimum effective concentration in plasma and effects will be observed but a single dose will not acheive the steady state concentration.
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Take this example (Bisoprolol is the mentioned example ) : assuming that 5 mg is the minimum effective dose
dosing with 5 to 20 mg, and mean peak values range from 16 ng/mL at 5 mg to 70 ng/mL at 20 mg. So 5 mg dose will give a range of concentrations that are therapeutically active ranging from 16 ng/ml to 8 ng/ml , etc.. So how they are equating both terms minimum effective and minimum effective concentration although 5 mg will give a range of concentrations that will be active not like mec which is below which no activity ?
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Minimal effective concentrations is obtained 5mg so the response will be produced but the magnitude of effects is dependent on receptor occupied whileincreasing the dose to 20mg will raise the plasmaconcentrationof the drug that will occupy most of the receptors so the magnitude of effects will be increased .
further you can read from the Katzung basicand clinical pharmacology or further elaborate your question.
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I have researched, and there are many available ways to manage cough in community pharmacy setting, so which resource or reference do you use ?
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I do have some time available within my day, and I was wondering if there is any research project that needs collaboration?
I can collaborate, and my field of interest is Clinical pharmacy , Toxicology, Herbal Medicine or other Pharmaceutical related Fields.
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I am also interested in this field.
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I was wondering How do you utilize medicinal chemistry in your daily practice as a community Pharmacist ? or you are no longer utilizing it in any form in your daily practice ?
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If you know one drug is a free acid or free base you can predict what it will react with/precipitate out with in IV solution. Since some community pharmacy practices interface with home infusion, this can be a possible circumstance in which medchem would come into play.
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Does medicinal chemistry in general or knowing the Pharmacophore to be specific will help in the practice of Pharmacists in community Pharmacy ? If so, may you give examples to illustrate this point ? Because I think medicinal chemistry is all related to scientific research and Pharmaceutical companies, not related to the practice of Pharmacists.
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In my opinion it is helpful to know the general structure of the compound classes to understand interactions, side effects etc. For example, if you understand, that the antibiotic tetracyclines are good chelatic binders because of their structure, you will remember more easily to warn the patient to not take it together with 2+ charged ions like Ca2+ and Mg2+. Another example are antihistaminic drugs: If you are familiar with the structure, you will realize the similarity to cholin, meaning these drugs, especially the first generation, show cholinergic action, which explains a lot of the side reactions.
So in my opinion it is important and useful to know the pharmacophore, or at least to be able to recognize and know important key elements of the structure. But of course in the time of databases and computers, which are of course used in the community pharmacy, one could argue that you don't need to know anymore. But honestly I prefer a pharmacist who is not just selling you drugs but also understands their action and side effects.
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Is it just you go check graded dose response curve for comparing different pharmaceutical agent ? Or there is another fast quick method ? Lets say you want to give the most available otc analgesic ? which method do you follow (regardless of side effects now) ?
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Firstly, I don't think you should disregard side effect profiles when comparing pharmaceutical agents for the same indication. Side effects are a very important factor to consider when selecting among different drugs. They can cause harm to the patient, or they can cause the patient to cease taking the drug.
To compare different otc analgesics, you will have to set up a double-blind trial with placebo control. You will have to decide on the most appropriate dose(s) of each drug. Then you will have to come up with a readout, which in the case of analgesics is the subjective experience of pain upon application of some painful but harmless stimulus. You will have to include enough subjects to achieve sufficient statistical power to detect a difference between the effectiveness of the drugs of the desired size.
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In this scenario, I'm interested in Daflon (Trade name). Could misdiagnosis be harmful and turn the Pharmacological and therapeutic effect of a drug (Daflon) into an adverse reaction? We know that Daflon is used in case of chronic venous insufficiency as it helps with capillary permeability, etc..But is it dangerous for someone with healthy veins to ingest Daflon? Does decreasing capillary permeability in case of healthy veins(someone who is healthy) affect it in a negative way? And if so, is it imperative that drug shouldn't be given unless we are 100% sure of the diseased state, so when given the drug, it'll return normal? And how can I know when the drug pharmacological effect can be turned into an adverse reaction?
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The undesirable effects that may appear are those well described: digestive disorders (frequent), nervous system (rare) and immuno-allergic (rare). They are related to flavonoids.
The pharmacological effects are likely to be expressed in the healthy subject (AGRAWAL AD, 2011. Pharmaceutical activities of flavonoids: a review. International Journal f Pharmaceutical Sciences and nanotechnology). In my opinion, they will not have any clinical expression.
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According to the attached image, no therapeutic window is there with regard to diclofenac potassium, because the maximum tolerated dose ( 150 mg/day PO ) is the same as the minimum effective dose ( 50 mg PO 3 to 4 times daily. ) for pain management?
Or there is something I miss, and the minimum effective dose isn't 150 mg (50 three times per day)?
And I have another Q, if there is hepatic impairment, it is said to initiate therapy at the lowest dose, so isn't 50 mg (3 times per day) the lowest dose possible with regard to pain management?
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I think Diclofenac potassium is not at all a drug of choice for oral intake to give relief from pain. It is generally used at local application as a pain reliever due to probable toxicity in oral use.
Paracetamol is the drug of choice for oral use to relief pain, as far my knowledge goes. As the Pain center and Thermo-regulatory center are staying very near in Hypothalamus, interaction in effects are seen in almost all the drugs used in related purposes.
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The maximum dose is 10 mg/day, so why let it available while having such narrow therapeutic window?
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The therapeutic index of cetirizine is not indicated by the recommended maximum dose of 10 mg/day. I belive the recommended dose was chosen to be 10 mg/day since it had the same efficacy as 20 mg/day in several randomized controlled trials. Not due to any toxicity.
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I'm not sure why d they mention rare adverse reactions? Any idea, of what purpose does this serve? Like here in the case of Cetirizine
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When a side effect is listed as “common,” what does that mean? What are the odds of a “rare” side effect happening to me? It was news to me that these terms are actually very specific. The World Health Organization (WHO) defines categories as:
  • Very common means 1 in 10 — 1 out of every 10 people (or more) taking that medicine will experience that side effect.
  • Common means more than 1 in 100 — between one in 10 and one in 100 people are affected
  • Uncommon means more than 1 in 1,000 — between one in 100 and one in 1,000 people are affected
  • Rare means more than 1 in 10,000 — between one in 1,000 and one in 10,000 people are affected
  • Very Rare means more than 1 in 10,000+ — fewer than one in 10,000 people are affected
I found these definitions to be comforting. After all, a rare effect that happens to 1 in 1,000 to 10,000 seems safe. Then I pulled out my calculator. As an example, Crestor is one of the most prescribed drugs in America, through June 2015. It “rarely” causes liver damage (among other things). 21 million prescriptions for Crestor were written from July 2014-June 2015. Doing the math reveals that it’s possible that between 2,100 and 21,000 people in the US suffered new onsets of liver damage from taking Crestor each year.
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We know that natural products aren't regulated by the FDA, so when checking the safety of natural products/Herbs, should I check for adverse reactions and toxic dose only? Or should I also check for carcinogenic capability? Or carcinogenic capability will be listed as a default under adverse reactions? (I mean whether this product is carcinogenic or not)
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Natural products are a very important class of medicinal drugs. Roughly 25% of all drugs are derived from natural sources. For your particular product, a good starting point would be the products history. If people have been taking this product for many centuries (eons?), then the risk of adverse effects is very low. However, standard toxicity tests and carcinogen tests should be performed. Beyond this, I would recommend testing for heavy metals and persistent environmental toxins (pcbs, etc.). Also, there are requirements in the US for vitamins (not sure how much supplements apply). These are listed in the DSHEA standards.
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So like the attached image. There should be a purpose behind mentioning rare adverse reactions, otherwise why they would mention it.
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The frequency (whether rare or very rare) speaks to how likely the adverse effect is to be a problem. If an adverse event is rare/very rare, then the benefits of the drug is likely going to outweigh the risk. This is especially when the disease condition is serious.
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I do have some time available within my day, and I was wondering if there is any research project that needs collaboration?
I can collaborate, and my field of interest is Clinical pharmacy , Toxicology, Herbal Medicine or other Pharmaceutical related Fields.
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Dear Dr Toske, please send me details on gslavekar@gmail.com.
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In other words, which websites list the adverse reactions of the drugs instead of listing the adverse events (no causality established)? I know of https://www.medicines.org.uk/emc/ which lists SmPC, any other websites?
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LexiComp is the as it give an up to date information and I find very handy and user friendly.
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Reference that can list side effects according to cause & effect relationship, so I can know with certainty that this drug will be the cause of the side effect. Do you use Meyler's Side Effects of Drugs as your reference?
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Micromedex®
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Why most websites report frequency of adverse reactions of drugs(In terms of common, rare, etc..)? Does this indicate causal relationship? Like common adverse reactions is established to be induced by the drug and not as an adverse event? Like here in the case of cetirizine or reporting the frequency serves another purpose?
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CIOMS generally gives this classification :
  • Very common ADR occurs in more than 1/10 patients who take the drug
  • Common (frequent) > = 1/100 and < 1/10
  • Uncommon (infrequent) >= 1/1000 and < 1/100
  • Rare >= 1/10000 and < 1/1000
  • Very rare < 1/10000
The frequency of ADR is often determined during the clinical trials, although clinical trials are more designed to assess efficiency than to detect side effects (as clinical trials do not include more than 3000, it is for example impossible to see very rare ADR).
During those clinical trials ADR are assessed with an imputability method, as it is done in real life with pharmacovigilance.
When a patient has a symptom, those data helps health professionals to see if it could be or not an ADR, and if so stop or not the drugs if needed (and ask an expertise).
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I have come across two different tools in my preliminary searching
1) The quality use of medications in dementia (QUM-D) tool by Peisah et al.
2) The Appropriate Psychotropic drugs use In Dementia (APID) index by van der Spek et al.
I was just wondering if anyone knows of any other tools, preferably validated in a long term care setting.
Additionally does anyone have any experience of applying any of these tools?
Many thanks.
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We used the UK Alzheimer's Society guidelines for MEDREV (see protocol published in BMJ Open- http://bmjopen.bmj.com/content/6/3/e010279) - only use anti-psychotics if risk of harm to the person or others.
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Their is always a confusion in international graduates about the field of Clinical Pharmacy and Pharmacy Practice.
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Pharmacy practice is a term that was introduced long time ago but just adopted to explain the evolution of pharmacy profession by Hepler and Strand in 1989. The evolution with three stages includes:
1. Traditional pharmacy practice (or product-oriented practice). At this stage, pharmacists are all involved in technical or product-related practice, such as dispensing, inventory control, sterile and non-sterile drug manufacturing, etc.
2. Clinical pharmacy practice (or service-oriented practice). Pharmacists at this stage try to get close to patients on the ward or OPD by providing clinical pharmacy services, e.g. DIS, ADR monitoring, TDM, iv drug admixture, etc.
3. Pharmaceutical care practice (or patient-focused practice). It is called medication therapy managment (MTM) in the US, or medicines management/optimisation in the UK. Pharmacists need to optimize the use of medicines in terms of benefits and risks by working closely with other healthcare professionals and patients.
To put it in short, pharmacy practice nowadays is a broad term that embraces all traditional practices, clinical pharmacy and pharmaceutical care regardless of settings. In the UK, to many pharmacists pharmacy practice is more involved in community pharmacy, whereas clinical pharmacy is mostly hospital-based or GP practice-based.
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In real clinical practice some patients are treated with combination of clozapine and another depot antipsychotic. Although we have a positive evidence of clozapine combination with some antipsychotics, clozapine should not be combined with depot antipsychotics, because of several adverse events, which can not be discontinued very easy in patients treated with depot. In clinical practice we often have problem that we have positive symptoms (residual) with only clozapine and therefore combinations could be used. In my point of view many combinations should be used first (e.g. combination with lamotrigine, combination with another antipsychotic non-depot, combination with N-acetylcysteine) before this potentially risky combination.
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Before combining with other antipsychotics, it might be helpful to control serum levels, because particularly in clozapine, non-compliance or only partial compliance is a frequent cause of treatment resistance.
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It's beyond doubt tailor made treatment options for a specific diseases and patients will help the health care system better. Amongst other things individual therapy by gene IS a viable alternative. But for the economic aspects. 
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Do you make money more important than patient's life? Don't you care about the accumulated drugs' toxins in the environment and patient's prescription drugs are adding more and more?
Even bargain for lower drug's price. Eventually, in overall, you make more money.
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Light sensitive medications are to be stored in proper conditions and it is a challenging task for the pharmacist and health care team. 
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In developing countries one of the major issues is linked to falsified drugs and fake medicine which results in important health issues in those countries.
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I'm doing the population pharmacokinetics modelling with a Tacrolimus database and I found out that in some patients, there is a period of 5 days without administration, (for ex, at time after dose: 0, 12, 24, 36, 48, 60, the corresponding concentration was 17, 14.5, 14, 10.5, 8.7, 7.3). 
As we cannot verify the source of information and I do not have real clinical experience with this drug, I wonder is it possible to have this kind of kinetics (that the drug remained very long in the patient body) or we can assume that there is maybe some dose that was not recorded?
If by chance anyone has looked at/ modelled real-life TDM data of tacrolimus, can you please share your opinion?
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