Eye Care for Computer Users

Computers have become indispensable in work place. Professionals spend more time working at computer workstations. The combination of fixed and constrained body postures, work overload and unsuitable workstations can lead to health problems like aches and pains in the shoulders, forearm, wrist, hand, back & neck pain and eyes strain.

Normal blink rate in human is 16-20 per minute. When this blink rate gets reduced to 6-8 blinks/minute, it results in dry eyes. Near focusing for long hours causes eye strain. Early presbyopia (need for reading glasses) sets in. Other symptoms include headache, eye strain, blurred vision, dry or irritated eyes, double vision, light sensitivity, neck ache, back aches etc.

The pre disposing factors which mainly cause discomfort are:
1.Work place conditions
2.Working habits
3.Visual conditions
4.Nature of work
5.Length of time spent at computer
6.Reduced blinking rate
7.In co ordination between design of work station and design of glasses.

A Good Chair: Feet should rest on the floor. Angle should be of 90 degrees at the knee. Arm rest is desirable. Back rest must support the area from the upper ridge of the pelvis to the shoulder blades. The curve in the back rest must support the hollow in lower back. An adjustable tilt is desirable.

Lighting – Required illumination on the working surface. Lower level illuminance for general areas. (3:1 ratio)
Eye Care Tips for computer users and professionals~
Monitor should be more than 5 inches from the eyes.
Ideal viewing area is 6 inches below the horizontal eye level.
Work with fonts of darker shades on light background.
Attach an anti-glare screen in front of the monitor.
Use screen mounted document holder at the same plane.
Use suspended lights from ceiling & windows with curtains to avoid light hitting directly on eyes.
Avoid sitting in front of AC or in a room with low humidity.

20-20-20 rule – Take short breaks for your eyes every 20 minutes between your work for 20 seconds and look 20 feet away.
Give proper rest to the eyes – Close your eyes for 20 seconds at least every half an hour.
Correct near vision with glasses.
Use of Anti reflective coating glasses can reduce glare from a monitor.
Contact lens users need to lubricate their eyes frequently.
Lastly working at the computer is not harmful to eyes, but make sure to examine your eyes at least once a year.

4 Board Certified Pharmacotherapy Speialist (BCPS) Exam Tips

I get asked quite a few questions nowadays on the BCPS exam, so I put together a quick list of 4 common questions I frequently get asked and give you a few BCPS exam tips.

Question 1: How hard is the exam?  The huge challenge of this exam is the broad scope of information that you could be tested on.  Pediatrics, geriatrics, cardiology, psych, critical care, etc. are all fair game on the BCPS exam and is really what makes it difficult.

Question 2: Are you asked about Brand or Generic names on the exam?  The BCPS uses generic names.  Here’s the statement right from the BPS website – “Official United States Adopted Name (USAN) generic names are used on all BPS examinations for all drug products, when possible.”

Question 3: What types/style of questions are on the exam?  The questions are in one format, and the test is uniform throughout.  You will be asked multiple choice questions with 4 possible answers and only 1 being correct.  No select all that apply, no fill in the blank, and no essay.  Here’s the language on that from BPS “The multiple-choice format is used exclusively. Four possible answers are provided for each question, with only ONE designated as the correct or best choice.”

Question 4: What’s the single most important thing I need to know for the BCPS exam?  It isn’t much of a secret, but if you don’t know basic biostatistics, you dramatically reduce your chances of passing.

CARDIAC ARREST Vs HEART ATTACK

Cardiac arrest vs. heart attack. People often used the terms interchangeably, but they are not the same. http://spr.ly/61848MvCA

Source: American Heath Association

Warfarin and Metronidazole Interaction

A 74 year old female was recently discharged from the hospital with pneumonia.  The latest INR was 2.1.

Current Meds:

• Aspirin 81 mg daily
• Warfarin 2.5 mg daily
• Lamotrigine 25 mg BID
• Ranitidine 150 mg daily
• Carafate 1 gram twice daily
• Loperamide as needed (just recently started)
• Ramipril 5 mg daily
• Amlodipine 10 mg daily
• Metoprolol 100 mg twice daily

About 3 days following discharge she begin to develop foul smelling diarrhea.  It continued for another 2-3 days before going into the clinic to get assessed.

Diagnosis was made as C. Diff infection.  She was initiated on metronidazole for 10 days to treat the suspected infection.  On day 7 of antibiotic therapy, the patient has a nose bleed that she cannot resolve.  She goes to a local urgent care clinic where an INR was checked and it was 9.4.

So, we must ask the question as to what would’ve prevented the warfarin and metronidazole interaction from getting out of control and putting our patient at risk?  Taking warfarin and metronidazole will usually result in increased concentrations of warfarin and increase the risk of elevated INR.  Checking an INR on day 3-5 would have been a plausible option and may have been able to prevent this interaction from getting out of hand.

Another option that I occasionally see in practice is preemptive dose reduction of warfarin.  They recommend about a 30-35% reduction in the warfarin dose for the warfarin and metronidazole interaction.  Here’s a small study with a little further reading on that.

Another alternative would be to identify if the patient is a candidate for a newer oral anticoagulant that might have lower risk of interactions in the future.

Pharmacists: Should you take a board certification?

In Singapore, one of the most common ways to enhance your clinical skills as a pharmacist is to take a Board Certification. Locally, one of the most popular Board Certification is the Board of Pharmacy Specialties (BPS) administered by the American Pharmacist Association (APhA).

BCP was set up in 1976, with the mission of promoting the recognition and value of specialized training, knowledge, and skills in pharmacy and speciality board certification of pharmacists. It is a well know post-licensure certification agency worldwide that operates across the profession to provide speciality certification of pharmacists.

Today, the association recognises eight different specialities areas of Pharmacy: Ambulatory Care Pharmacy, Critical Care Pharmacy, Nuclear Pharmacy, Nutrition Support Pharmacy, Oncology Pharmacy, Pediatric Pharmacy, Pharmacotherapy and Psychiatric Pharmacy. Over 24,000 pharmacists are certified in the eight specialities areas of pharmacy worldwide to date.

Why should you take a board certification?

As of 2015, Singapore is ranked number 5 in the number of international pharmacists certified by the BPS, after Egypt, Canada and Saudi Arabia. A total of 215 pharmacists were certified by BPS1. There are a few reasons to take a board certification. The BPS board certification is a well-validated examination administered to multiple candidates in many countries worldwide. Obtaining a board certification is one way to obtain an official validation that you possess a certain level of expertise in pharmacy.

Another reason is to update your knowledge. As the healthcare field constantly advances, what you learned in school many years ago might become obsolete faster than you thought. Board certification by BPS allows you to be updated on the changes in your field of practice.

Finally, board certification gives you a competitive edge in the job market. Many pharmacy departments in Singapore recognize BPS certification as a measuring stick to determine if a pharmacist is competent in the practice of their speciality. Some pharmacy department in Singapore even provides salary increment as a bonus for pharmacist with additional board certification.

What should you consider before taking the board certification?

With eight different specialities areas of Pharmacy to choose from, do consider which speciality is most suitable for your needs. Most pharmacists will take the Board Certification for Pharmacotherapy (BCPS), as it is a universal certification – topics covered in this certification are extensive and is relevant to most cases seen on a daily basis, such as geriatrics to fluids and nutrition, gastrointestinal diseases to infectious disease. Pharmacists who desire to specialise in pharmacist-related services, such as nutrition support, can consider the Board Certification for Nutrition Support Pharmacy, while those who love critical care should consider the Board Certificate for Critical Care Pharmacy.

Another thing to consider is how to prepare for the exam. Different board specialisation has different test sites and test dates annually. Most of them will have examinations conducted twice yearly, with one each usually in spring and winter. Registration is usually open three months ahead of the exam date. While BCP exam questions are not easy, neither are they out of this world. Most questions are case-based, which require analytical skills rather than a mere regurgitation of facts. Some individuals take up to a year to prepare for it, while others take only one week. Sample test questions, handouts as well as tutorial lessons are available at a cost online from either BPS website itself or the American College of Pharmacy (ACCP) website2.

As a pharmacist, it is vital to keep yourself updated on the latest happenings in your field, and taking a board certification is one way to enhance your knowledge and skills as a pharmacist. Further, the board certification would also be an official recognition of your abilities and give you a competitive edge in the job market. As such, pharmacists should definitely consider taking a board certification. MIMS

Sources:
1. BCP Annual Report 2015. Available at: http://board-of-pharmacy-specialties.epaperflip.com/v/2015-Annual-Report#?page=10. Last accessed on 21 November 2016.
2. Pharmacotherapy self-assessment program (PSAP), American College of Pharmacy (ACCP). Available at: http://www.accp.com/bookstore/psap2016.aspx. Last accessed on 21 November 2016.

3. http://today.mims.com/topic/pharmacists--should-you-take-a-board-certification-?country=Malaysia&channel=GN-Career&elq_mid=9173&elq_cid=6062

High cholesterol 'does not cause heart disease' new research finds, so treating with statins a 'waste of time'

*Cholesterol* is finally officially removed from Naughty List

The US government has finally accepted that *cholesterol* is not a _nutrient of concern_. doing a U-turn on their warnings to us to stay away from high-cholesterol foods since the 1970s to avoid heart disease and clogged arteries.

This means eggs, butter, full-fat dairy products, nuts, coconut oil and meat have now been classified as *safe* and have been officially removed from the _nutrients of concern_ list.
The US Department of Agriculture, which is responsible for updating the guidelines every five years, stated in its findings for 2015: "Previously, the Dietary Guidelines for Americans recommended that cholesterol intake be limited to no more than 300 mg/day.

"The 2015 DGAC will not bring forward this recommendation because available evidence shows no appreciable relationship between consumption of dietary cholesterol and serum (blood) cholesterol, consistent with the AHA/ACC (American Heart Association / American College of Cardiology)
The Dietary Guidelines Advisory Committee will, in response, no longer warn people against eating high-cholesterol foods and will instead focus on sugar as the main substance of dietary concern.

US cardiologist Dr Steven Nissen said: _It's the right decision_. _We got the dietary guidelines wrong. They've been wrong for decades_."
"When we eat more foods rich in this compound, our bodies make less. If we deprive ourselves of foods high in cholesterol - such as eggs, butter, and liver - our body revs up .
The Real Truth about Cholesterol
The majority of the cholesterol in you is produced by your liver. Your brain is primarily made up from cholesterol. It is essential for nerve cells to function. Cholesterol is the basis for the creation of all the steroid hormones, including estrogen, testosterone, and corticosteroids. High cholesterol in the body is a clear indication which shows the liver of the individual is in good health.

Dr. George V. Mann M.D. associate director of the Framingham study for the incidence and prevalence of cardiovascular disease (CVD) and its risk factors states: _Saturated fats and cholesterol in the diet are not the cause of coronary heart disease_. _That myth is the greatest deception of the century, perhaps of any century_
*Cholesterol is the biggest medical scam of all time*
There is no such thing as *bad Cholesterol*
So you can stop trying to change your Cholesterol level. Studies prove beyond a doubt, cholesterol doesn't cause heart disease and it won't stop a heart attack. The majority of people that have heart attacks have normal cholesterol levels.

OUR BODY NEEDS 950 mg OF CHOLESTEROL FOR DAILY METABOLISM AND THE LIVER IS THE MAIN PRODUCER.
ONLY 15% OF CHOLESTEROL IS BEING DONATED BY THE FOOD WE EAT. If the fat content is less in our food we eat, our liver
Got to work more to maintain the level at 950 mg. If the cholesterol level is high in our body, it shows the liver is working perfect.
Experts say that there is nothing like LDL or HDL.
…………..
….. *Cholesterol is not found to create block any where in human body*.
Please post the recent facts about CHOLESTEROL

Source: http://www.telegraph.co.uk/science/2016/06/12/high-cholesterol-does-not-cause-heart-disease-new-research-finds/

By Henry Bodkin

13 June 2016

___________________

Time to halt the overprescribing of proton pump inhibitors

Inappropriate use of proton pump inhibitors can cause a range of side effects and even harm to patients.

Proton pump inhibitors (PPIs) are among the most frequently prescribed drugs globally. Although they are cost effective when used appropriately, studies show they are prescribed without a clear indication in up to 70% of cases. Although the absolute risk of harm to individuals from PPIs is low, their widespread, long-term use can cause adverse effects that contribute to significant negative impacts at a population level. Action is required to limit inappropriate prescribing of PPIs and support deprescribing in patients on long-term therapy for whom the original indications no longer apply. 

The rise of PPIs

PPIs were introduced in the 1980s and rapidly became some of the bestselling medicines of all time. They inhibit gastric acid secretion through blockade of H⁺/K⁺-ATPases in parietal cells, and are highly effective for treating peptic ulceration, oesophagitis and gastro-oesophageal reflux^[1],[2]. They are also important components of Helicobacter pylori eradication regimens^[3], and useful for prophylaxis against non-steroidal anti-inflammatory drug (NSAID) induced upper gastrointestinal injury^[4]. For most of these presentations, they are only intended for short-term use and are rarely required beyond four to eight weeks. In a minority of conditions (for example, severe Barrett’s oesophagus, gastrinoma and eosinophilic oesophagitis), protracted courses may be required^[5]. 

PPIs combine high efficacy with low toxicity, and are perceived to be safe and cost effective^[6]. Consequently, they are widely prescribed. The total cost of PPIs to the UK NHS is more than £100m each year^[6] and global spend is in excess of £2bn. Five PPIs are currently licensed in the UK: omeprazole, lansoprazole, pantoprazole, esomeprazole and rabeprazole. In most cases, there is no clear evidence to support use of one over another, and class effects can be assumed^[7].

Overprescribing is the norm

Studies consistently find that PPIs are overprescribed globally in both primary and secondary care. Their prevalence continues to increase: in Australia, prescriptions rose by 1,318% over one decade (1996–2006)^[8]. Most of this growth occurs in primary care, with increasing numbers of patients treated for longer durations^[9]. This is partly related to substitution of histamine-2 receptor antagonists, but the bulk represents expanded use of acid suppression therapy. A proportion of this increase is legitimate, on account of rising groups of patients treated with dual antiplatelet therapy for coronary artery or cerebrovascular disease, or bisphosphonates (for which PPIs partially mitigate risk of oesophagitis^[10]). There is also a small cohort of patients with chronic cough in whom gastro-oesophageal reflux is believed to be a contributor^[11]. The recent approvals of esomeprazole for general sale, and pantoprazole as an over-the-counter medicine, may further drive consumer use in the UK.

Some studies have examined the appropriateness of PPI prescriptions. In one study of older patients in Italy, 30% were taking a PPI with no clear indication, although a further 11% of this cohort possessed a recognised indication and were not on treatment (that is, PPIs were underprescribed)^[12]. A study of 124,133 first-time adult users from Denmark found that only one third met criteria for potential long-term use^[13]. In the same catchment population, only 4% of pre-existing long-term users (defined as more than 60 daily doses over a six-month period) had a diagnosis that merited long-term management^[14].

Within hospitals, a retrospective study of surgical inpatients from the Netherlands identified non-compliance with guidelines in 46.6% of cases; 93.1% of these represented overprescribing^[15]. Audits of medical inpatients in the UK show inappropriate prescribing rates of 40.7–54.0%, of which 86.0% are cases of overprescribing^[16],[17]. 

Other studies have probed the underlying rationale for PPI prescriptions and their continued use^{[18],[19],[20]}. The reasons are often questionable, and adherence to guidelines is poor despite educational and stewardship strategies^[21]. The most common explanations for long-term PPI use were inappropriate treatment of dyspepsia, prophylaxis for low-risk patients on NSAIDs or corticosteroids, and stress ulcer prophylaxis (in secondary care).

Communication is often poor. In one UK centre, suggested duration of treatment was specified in fewer than 20% of hospital discharge letters, less than one third indicated that prescriptions needed to be reviewed, and only half contained information explaining why the drug was started^[22].

Overprescribing is more common in patients with comorbidities and polypharmacy who are likely to see several specialists, increasing the chance of a drug being prescribed and making it less likely that one clinician will take overall responsibility for the patient’s medicines.

Another problem is that once a patient has taken a PPI for longer than a few weeks, acid hypersecretion can occur on discontinuation. This causes rebound symptoms, and frequently establishes a vicious cycle of drug reinitiation and long-term continuation^[23].

Possible harms

Over the past decade, many adverse effects of PPI therapy have been identified.

The most widely studied of these is Clostridium difficile infection. A meta analysis of 23 cohort and case-control studies, involving almost 300,000 patients, identified a 65% increase in the relative risk of C. difficile-associated diarrhoea^[24]. The mechanism remains unproven, but it may be that acid suppression permits viability of the C. difficile vegetative state, leading to clinically symptomatic infection. There are suggestions that PPIs also increase risks of Campylobacter and Salmonella gastroenteritis^[25], and two studies demonstrate alterations in the gut microbiome^[26].

Increased fracture risk has been reported with PPI use, most notably in the Nurses Health Study, which followed 79,899 female participants for eight years^[27]. The age-adjusted hazard ratio of hip fracture was 1.35 with more than two years of PPI use, and even higher in smokers. Possible explanations include reduced calcium absorption^[28], or competition with osteoblast and osteoclast proton pumps that impedes bone remodelling^[29]. Deficiencies have also been reported in both iron^[30] and vitamin B₁₂^[31] absorption, and a major issue in a small subset of patients is severe hypomagnesaemia^[32]. If the latter occurs, it is typically a drug class effect, likely caused by inhibition of cation transport in the colon.

PPIs are now well recognised as a cause of acute interstitial nephritis, which, in a nested case control study of 572,661 patients, occurred with an odds ratio of 5.16 (translating into an incidence of 11.98 per 100,000 person-years)^[33]. Early recognition and drug discontinuation are crucial for maximising renal recovery. There have also been reports of PPIs triggering subacute cutaneous lupus erythematosus^[34]. 

Finally, increased rates of chronic kidney disease and myocardial infarction have been reported among PPI users. In one study of 173,321 patients, the hazard ratio of developing chronic renal impairment was 1.22, rising with increasing duration of exposure^[35]. In a further data-mining exercise examining records from 2.9 million patients, PPIs were associated with a 1.16-fold risk of myocardial infarction, and a 2-fold increased risk of cardiovascular mortality^[36]. The cause was not ascertained, and although the authors speculated about interference with nitric oxide signalling, an alternative explanation would be confounding because of increased use of acid suppression in patients with comorbidities and polypharmacy, and hence overall cardiovascular risk.

Drug interactions

Patients with multiple comorbidities and polypharmacy who take PPIs on a long-term basis are at high risk of drug-drug interactions. Specifically, an alteration of pH in the gastrointestinal tract can impact on drug absorption, and PPIs inhibit (to varying degrees) cytochrome (CYP) p450 and the p-glycoprotein pathway^[37]. This may be a particular issue for omeprazole, which has high affinity for CYP2C19 and moderate affinity for CYP3A4^[38].

Drug interactions were raised as a major concern in the case of clopidogrel, which requires CYP2C19 for conversion to its active metabolite. An initial randomised controlled trial of 140 patients found a reduction in the platelet reactivity index after one week in patients receiving clopidogrel with omeprazole^[39], and on this basis several regulatory agencies counselled that both omeprazole and esomeprazole should be avoided in this context. The clinical relevance of the interaction has, however, been called into question, with the prospective COGENT trial reporting no increase in cardiovascular events in 3,761 patients on omeprazole and dual antiplatelet therapy^[40]. The trial was terminated prematurely because of a lack of funding but a subsequent review concluded that, despite evidence of an ex vivo interaction, the case for adverse impact in patients in vivo had not been made^[41]. 

Other research has highlighted a significant risk of bias in many retrospective studies that report harmful interactions between PPIs and clopidogrel^[42], and showed that concomitant use halves the risk of gastrointestinal bleeding^[43]. Consequently, some authorities advocate preferential use of alternative PPIs with lower CYP2C19 affinity (such as pantoprazole or rabeprazole) in this patient cohort, although the effectiveness of this strategy has not been proven. 

Although studies on drug interactions have been dominated by those focusing on antiplatelet therapies, PPIs can also decrease plasma concentrations of several antiretroviral agents, dabigatran, mycophenolate mofetil, and targeted oncological signal pathway inhibitors, as well as increase the concentrations of calcineurin inhibitors, methotrexate and metformin^[44]. As with clopidogrel, little evidence has emerged to date that these can cause clinically meaningful harm, although it would still be prudent to take care when prescribing PPIs with drugs that have potential for an interaction to occur. 

Minimising overprescribing

The steps required to curb and subsequently reduce inappropriate prescribing include: recognition of the problem; use of alternative approaches to manage conditions currently treated “by default” with PPIs; education regarding appropriate indications and durations for their use; and enhanced drug stewardship akin to that employed widely for antimicrobials, mandating better documentation around PPI prescriptions and regular review. Patient involvement and shared decision-making are also essential^[45].

One of the most frequent reasons for long-term PPI use is dyspepsia. This condition can often be ameliorated by medication rationalisation and lifestyle modification, such as weight loss or smoking cessation^[2]. Possible drug contributors to dyspepsia include calcium channel blockers, nitrates, theophyllines, bisphosphonates, antiplatelet agents and NSAIDs. A review should be conducted to consider whether these are still indicated or could be substituted. Where PPIs are prescribed, the lowest effective dose should be used for the shortest possible duration. The indications and intended durations should be clearly documented and communicated to the primary care provider and pharmacy.

Patients on long-term therapy should be reviewed at least annually. Substitution of PPIs with antacid or alginate therapy, or H₂ receptor antagonists, can also be considered. Patients should be counselled on rebound acid secretion on drug discontinuation and on strategies to manage this (preferably without re-escalating PPI dose) and it should be explained that this does not necessarily represent recurrence of disease^[23].

The other common rationale for long-term PPI prescribing is prophylaxis when receiving antiplatelet agents or NSAIDs. Most guidelines suggest this is only required for high-risk patients, specifically those aged over 65 years, with a history of peptic ulcer disease or upper gastrointestinal haemorrhage, or taking multiple medicines that augment gastrointestinal adverse effects^[46],[47].

Time to deprescribe

Prescribing of PPIs has skyrocketed over the past decade. These drugs can be effective, but are principally intended for short-term use and yet are often not discontinued. There is clear and consistent evidence of overprescribing as clinicians overestimate benefits and underestimate harms, associated with substantial costs to healthcare providers. Measures should be put in place to educate prescribers on appropriate indications and durations for PPI use, provide a degree of stewardship, and facilitate long-term users in de-escalating therapy.

Daniel J B Marks is a clinical pharmacologist at University College London Hospital and a postdoctoral research fellow at the Centre for Molecular Medicine, University College London.

References:

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^[2] Ford AC & Moayyedi P. Dyspepsia. The BMJ 2013;347:f5059. doi: 10.1136/bmj.f5059
^[3] Graham DY & Fischbach L. Helicobacter pylori treatment in the era of increasing antibiotic resistance. Gut 2010;59:1143–1153. doi: 10.1136/gut.2009.192757
^[4] Laine L. GI risk and risk factors of NSAIDs. J Cardiovasc Pharmacol 2006;47:S60–66. PMID: 16785831
^[5] Fitzgerald RC, di Pietro M, Ragunath K et al. British Society of Gastroenterology guidelines on the diagnosis and management of Barrett’s oesophagus. Gut 2014;63:7–42. doi: 10.1136/gutjnl-2013-305372
^[6] Forgacs I & Loganayagam A. Overprescribing proton pump inhibitors. The BMJ 2008;336:2–3. doi: 10.1136/bmj.39406.449456.BE
^[7] Neumann I, Letelier LM, Rada G et al. Comparison of different regimens of proton pump inhibitors for acute peptic ulcer bleeding. Cochrane Database Syst Rev 2013;(6):CD007999. doi: 10.1002/14651858.CD007999
^[8] Hollingworth S, Duncan EL & Martin JH. Marked increase in proton pump inhibitors use in Australia. Pharmacoepidemiol Drug Saf 2010;19:1019–1024. doi: 10.1002/pds.1969
^[9] Haastrup P, Paulsen MS, Zwisler JE et al. Rapidly increasing prescribing of proton pump inhibitors in primary care despite interventions: a nationwide observational study. Eur J Gen Pract 2014;20:290–293. doi: 10.3109/13814788.2014.905535
^[10] McGowan B, Bennett K, Barry M et al. The utilisation and expenditure of medicines for the prophylaxis and treatment of osteoporosis. Ir Med J 2008;101:38–41. PMID: 18450246
^[11] Ribolsi M, Savarino E, De Bortoli N et al. Reflux pattern and role of impedance-pH variables in predicting PPI response in patients with suspected GERD-related chronic cough. Aliment Pharmacol Ther 2014;40:966–973. doi: 10.1111/apt.12919
^[12] Schepisi R, Fusco S, Sganga F et al. Inappropriate use of proton pump inhibitors in elderly patients discharged from acute care hospitals. J Nutr Health Aging 2016;20:665–670. doi: 10.1007/s12603-015-0642-5
^[13] Haastrup PF, Rasmussen S, Hansen JM et al. General practice variation when initiating long-term prescribing of proton pump inhibitors: a nationwide cohort study. BMC Fam Pract 2016;17:57. doi: 10.1186/s12875-016-0460-9
^[14] Haastrup PF, Paulsen MS, Christensen RD et al. Medical and non-medical predictors of initiating long-term use of proton pump inhibitors: a nationwide cohort study of first-time users during a 10-year period. Aliment Pharmacol Ther 2016;44:78–87. doi: 10.1111/apt.13649
^[15] van den Bemt PM, Chaaouit N, van Lieshout EM et al. Noncompliance with guidelines on proton pump inhibitor prescription as gastroprotection in hospitalized surgical patients who are prescribed NSAIDs. Eur J Gastroenterol Hepatol 2016. doi: 10.1097/MEG.0000000000000634
^[16] Batuwitage BT, Kingham JG, Morgan NE et al. Inappropriate prescribing of proton pump inhibitors in primary care. Postgrad Med J 2007;83:66–68. doi: 10.1136/pgmj.2006.051151
^[17] Jarchow-Macdonald AA & Mangoni AA. Prescribing patterns of proton pump inhibitors in older hospitalized patients in a Scottish health board. Geriatr Gerontol Int 2013;13:1002–1009. doi: 10.1111/ggi.12047
^[18] Van Soest EM, Siersema PD, Dieleman JP et al. Persistence and adherence to proton pump inhibitors in daily clinical practice. Aliment Pharmacol Ther 2006;24:377–385. doi: 10.1111/j.1365-2036.2006.02982.x
^[19] van Vliet EP, Otten HJ, Rudolphus A et al. Inappropriate prescription of proton pump inhibitors on two pulmonary medicine wards. Eur J Gastroenterol Hepatol 2008;20:608–612. doi: 10.1097/MEG.0b013e3282f52f95
^[20] Heidelbaugh JJ, Goldberg KL & Inadomi JM. Magnitude and economic effect of overuse of antisecretory therapy in the ambulatory care setting. Am J Manag Care 2010;16:e228–234. PMID: 21250399
^[21] van Vliet EP, Steyerberg EW, Otten HJ et al. The effects of guideline implementation for proton pump inhibitor prescription on two pulmonary medicine wards. Aliment Pharmacol Ther 2009;29:213–221. doi: 10.1111/j.1365-2036.2008.03875.x
^[22] Walker NM & McDonald J. An evaluation of the use of proton pump inhibitors. Pharm World Sci 2001;23:116–117. PMID: 11468876
^[23] Reimer C, Sondergaard B, Hilsted L et al. Proton-pump inhibitor therapy induces acid-related symptoms in healthy volunteers after withdrawal of therapy. Gastroenterology 2009;137:80–87. doi: 10.1053/j.gastro.2009.03.058
^[24] Janarthanan S, Ditah I, Adler DG et al. Clostridium difficile-associated diarrhea and proton pump inhibitor therapy: a meta-analysis. Am J Gastroenterol 2012;107:1001–1010. doi: 10.1038/ajg.2012.179
^[25] Leonard J, Marshall JK & Moayyedi P. Systematic review of the risk of enteric infection in patients taking acid suppression. Am J Gastroenterol 2007;102:2047–2056. doi: 10.1111/j.1572-0241.2007.01275.x
^[26] Imhann F, Bonder MJ, Vich Vila A et al. Proton pump inhibitors affect the gut microbiome. Gut 2016;65:740–748. doi: 10.1136/gutjnl-2015-310376
^[27] Khalili H, Huang ES, Jacobson BC et al. Use of proton pump inhibitors and risk of hip fracture in relation to dietary and lifestyle factors: a prospective cohort study. The BMJ 2012;344:e372. doi: 10.1136/bmj.e372
^[28] Graziani G, Como G, Badalamenti S et al. Effect of gastric acid secretion on intestinal phosphate and calcium absorption in normal subjects. Nephrol Dial Transplant 1995;10:1376–1380. PMID: 8538929
^[29] Costa-Rodrigues J, Reis S, Teixeira S et al. Dose-dependent inhibitory effects of proton pump inhibitors on human osteoclastic and osteoblastic cell activity. FEBS J 2013;280:5052–5064. doi: 10.1111/febs.12478
^[30] McColl KE. Effect of proton pump inhibitors on vitamins and iron. Am J Gastroenterol 2009;104:S5–9. doi: 10.1038/ajg.2009.45
^[31] Lam JR, Schneider JL, Zhao W et al. Proton pump inhibitor and histamine 2 receptor antagonist use and vitamin B12 deficiency. JAMA 2013;310:2435–2442. doi: 10.1001/jama.2013.280490
^[32] Hess MW, Hoenderop JG, Bindels RJ et al. Systematic review: hypomagnesaemia induced by proton pump inhibition. Aliment Pharmacol Ther 2012;36:405–413. doi: 10.1111/j.1365-2036.2012.05201.x
^[33] Blank ML, Parkin L, Paul C et al. A nationwide nested case-control study indicates an increased risk of acute interstitial nephritis with proton pump inhibitor use. Kidney Int 2014;86:837–844. doi: 10.1038/ki.2014.74
^[34] Sandholdt LH, Laurinaviciene R & Bygum A. Proton pump inhibitor-induced subacute cutaneous lupus erythematosus. Br J Dermatol 2014;170:342–351. doi: 10.1111/bjd.12699
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Citation: Clinical Pharmacist, Vol 8, No 8, online | DOI: 10.1211/CP.2016.20201548

PHARMACEUTICAL CARE AND THE SCOPE OF PHARMACY PRACTICE

I. Introduction

     The Practice of Pharmacy embraces a variety of settings, patient populations, and specialist as well as generalist pharmacists. Central to the practice of pharmacy, however, is the provision of clinical services directly to, and for the benefit of patients.

     Definition. The term Pharmaceutical care describes specific activities and services through which an individual pharmacist “ cooperates with a  patient and other professionals in designing, implementing and monitoring a therapeutic plan that will produce specific therapeutic outcomes for the patient.”

II. Scope of Practice within Pharmaceutical Care

\    Role. Pharmaceutical care has evolved from an emphasis on prevention of drug- related problems (basically drug management) to extend roles of pharmacists in the Triage of patients, treatment of routine acute illnesses, management of chronic diseases, and primary disease prevention.

    
     Function. The provision of pharmaceutical care does not imply that the pharmacist is no longer responsible for dispensing functions. In many instances, however, implementation of pharmaceutical care services necessitates a redesign of the professional work flow, with assignment of technical functions to technical personnel under the direct supervision and responsibility of the pharmacist.

III. Uniqueness of Pharmaceutical care

Provision of pharmaceutical care overlaps somewhat with other aspects of pharmacy practice (Table 1). However, pharmaceutical care is not the same as these other areas, which include:

1st.       Clinical Pharmacy

2nd.         Patient counseling

3rd.         Pharmaceutical services; when the activities of a pharmacy or pharmacy department are performed for “ faceless” patients or charts, the activity is one of pharmacy service, not pharmaceutical care (e.g., chart or drug profile reviews without input from the patient or care giver is not pharmaceutical care).

Table 1 – Uniqueness of Pharmaceutical Care

	Traditional Pharmacy	Clinical Pharmacy	Pharmaceutical Care
Primary Focus	Prescription order or OTC request	Physicians or other health professionals	Patient
Continuity	Upon Demand	Discontinuous	Continuous
Strategy	Obey	Find fault or prevention	Anticipate or improve
Orientation	Drug product	Process	Outcomes

IV. Essential Components of Pharmaceutical Care

A. Pharmacist – patient relationship

B. Pharmacist’s workup of drug therapy (PWDT)

• Data collection. Collect, synthesize, and interpret relevant information.
• Develop or identify the CORE (Condition, Outcomes, Regimen) Pharmacotherapy Plan.
• Identify the PRIME( Pharmaceutical, Risk, Interactions, Mismatch, Efficacy) pharmacotherapy problems or indications for pharmacist intervention.
• Formulate a FARM (Finding, Assessment, Resolution, Monitoring) process note to describe and document the interventions intended or provided by pharmacist.

V. Clinical Skills and Pharmacists roles in Pharmaceutical

       care

1. Patient assessment
2. Patient education and counseling
3. Patient-specific pharmacist care plans
4. Drug treatment protocols
5. Dosage adjustment
6. Selection of therapeutic alternatives
7. Prescriptive authority

VI. Pharmaceutical Care as the Model for Pharmacy      

        Practice

The concepts, activities,, and services of pharmaceutical care form the  basis for provision of clinical services directly to, and for the benefit of patient in all pharmacy practice settings. These settings include home health, hospital, ambulatory care, primary care, consultation, long term care, and community pharmacy practice. Workflow, staffing patterns, processes, and pharmacy programs might differ, but the core approach to patient care remains pharmaceutical care in all settings.

VII. Documentation of Pharmaceutical Care

Documentation of pharmaceutical care is integral to continuity of care, demonstration of clinician competence, communication among health care providers, evidence of contributions to patient care, and reimbursement of professional services.

VIII. Pharmaceutical Care : An ongoing process

The patient profile is revised and re-assessed each time a new drug is added to or deleted from the medication regimen, a new disease or condition is diagnosed, or the patient undergoes other clinical intervention, such as surgery

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Key Points

                                                                                  

1. Focus on outcomes, not interventions.

2. Daily pharmacy rounds are important  – Pharmacists can make rounds without medical team.

3. Use this approach with all clinical programs, such as pharmacokinetic  dosing, disease management clinics, clinical pathways, etc

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