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Monday 14 September 2009

How appetite is regulated


Appetite (the desire to eat) is regulated by many internal and external factors.

Internal factors:
(1) Appetite regulation centres in the brain stem and the hypothalamus play a central role in appetite regulation. There are two main pathways through which appetite related signals are transmitted between brain and periphery: appetite stimulating (orexogenic) pathway and central appetite suppressing (anorexogenic) pathway. Appetite stimulating pathway releases chemicals that encourage eating. The central appetite suppressing pathway, on the other hand, releases chemicals that inhibit eating

(2) Gastrointestinal tract: GI hormones (such as peptide YY and Insulin) can influence appetite

(3) Adipose tissue hormones: Adipose tissues (or body fat’s main role is to store fat as a form of energy) can secrete hormones (eg adipokines) that can influence appetite.

(4) Others: serotonin and cannabinoids can have an effect on appetite

External factors:
(1) Emotional and psychological factors: factors such as depression, stress, guilt and low self-esteem usually stimulate, but sometimes inhibit appetite. Factors such as cultural attitudes and peer influence can be important, too.

(2) Environmental factors: factors such as the taste, texture and presentation of food could affect appetite

(4) Drugs: Some drug act on central appetite centre. Appetite suppressant agents either stimulate brain catecholamic pathways (e.g. amphetamine can reduce signal to start eating), or effecting serotonin pathways (e.g. sibutramine which enhances the signals to stop eating). Some drugs (e.g. corticosteroids and tricyclic antidepressants) increase appetite.
Some drugs (eg metformine, levodopa, digoxin) can reduce appetite as a side effect of their main action. A large number of drugs can cause adverse GI side effects that can cause poor appetite.

Loss of appetite
Generally, appetite links to the amount of energy that body needs. It increases, for example during puberty and decreases in old age. Under-nutrition and weight loss are the risks of poor appetite.

Poor appetite could be due to many factors:
- Mental and emotional issues (e.g. depression, tiredness)
- Pain, minor ailments (e.g. cold), or some diseases (e.g. cancer, gastrointestinal conditions such as Crohn’s disease)
- Some medicines, drug and alcohol misuse
- Unappealing food (e.g. culturally inappropriate)
- It may also be signs and symptoms of eating disorders

Management of poor appetite usually depends on the underlying cause; however, paying attention to some points may help.
- Reduce portion sizes and increase the frequency of meals
- If appropriate, use more high energy foods (e.g. cream, sugar) and when people feel hungry or at their best
- Limit liquid intake during meals as it can be filling
- Vary the colour and texture of foods to make it more appealing
- Consider using a multivitamin and mineral supplement.
- Liquid oral nutritional supplements (e.g. Ensure) may also be beneficial.

Children appetites vary and they may go through phases of dislike particular foods, but generally if they have a normal BMI and continue to grow, there is little to worry about. But in these cases there are some ways to help:
- Some children may like to eat small snacks rather than a proper meal.
- Healthy snacks between meals are acceptable.
- Their involvement with choosing what to eat or preparing it may help
- Not giving food too much attention

In cases highlighted below it is important that the patient is referred to:
- People who are acutely ill and have not eaten or unlikely to eat for more than five days
- People with a BMI < 18.5 kg/m2
- People with unintended weight loss (more than 10 per cent of body weight in three to six months)
- People with a BMI or 18.5-20 and unintended weight loss of 5-10 percent of body weight over three to six months.
- Infant and children who are failing to eat and failing to grow appropriately

Extracted from:
Mason P. (2008). Dealing with loss of appetite. The Pharmacy Journal, 281, pp: 395-398.

Tuesday 9 June 2009

درمان دارویی آکنه


درمان آکنه (التهاب مزمن غدد چربی) بستگی به شدت و همچنین عفونی بودن آن دارد. دوره درمان ممکن است که تا چند ماه ادامه داشته باشد. هر چه که در جهت درمان این بیماری سریعتر اقدام شود از شدت ضایعات پوستی حاصل از آکنه (برجستگی و فرورفتگیهایی که بر روی پوست باقی میماند) کاسته میگردد. برای درمان اکنه خفیف و متوسط معمولا از داروهای موضعی استفاده میشود. داروهای خوراکی را برای درمان نوع شدیدتر این بیماری یا در مواردی که امکان استفاده از درمانهای سطحی نباشد به کار میبرند. برای درمان این بیماری در خانمها گاهی از قرصهای هورمونی هم استفاده میشود

داروهای موضعی
_____________________
(ا)
benzoyl peroxide
و گاهی ترجیحا
Azelaic acid

(2)
کرمهای آنتیبیوتیک
erythromycin
clindamycin
Topicycline

(3)
کرم و ژلهای رتینوید
استفاده از این نوع داروها ممکن است که باعث قرمزی و پوسته پوسته شدن موقت پوست بشود که با مرور زمان متوقف میشود. مداوا با این نوع داروها چند ماه به طول خواهد انجامید و درمان تا زمانی که هیچ جای جوش جدیدی به وجود نیاید ادامه خواهد داشت. بیمارانی که از این دارو ها استفاده میکنند باید ار اشعه خورشید دوری بجویند
به عنوان مثال میشود از داروهای زیر نام برد
adapalene (a retinoid like drug, brand name Differin)
isotretinoin (Isotrex)
tretinoin (Retin-A)
Isotrexin (ترکیبی از آنتی بیوتیک و ایسو تریتینویین میباشد )

(4)
داروهای موضعی دیگر چون
Salicylic acid


داروهای خوراکی
__________________
چنانچه درمان موضعی اکنه نتیجه نداد از داروهای خوراکی استفاده میشود

(1)
آنتی بیوتیکها
oxytetracycline
tetracycline (or alternatively Doxycline 100mg daily and Minocycline 100mg daily in one or two divided dose)
Erythromycin (500mg twice daily)
Trimethoprim (300mg twice daily)

(2)
داروهای هورمونی
Co-cyprinidiol (cyproterone acetate with ethinylestradiol, brand name Dianette)
که شامل داروی ضد اندروژن است. به خصوص برای خانمهایی که مایل به استفاده از قرصهای ضدحاملگی هستند مناسب است. اما به دلیل اینکه احتمال ایجاد شدن لخته خون در سیاهرگها پس از استفاده از این قرص بیشتر از کسانی است که دوز پایین قرصهای ضد حاملگی را استفاده میکنند این دارو فقط در خانمهایی استفاده میشود که درمان با آتنی بیوتیکهای خوراکی برایشان نتیجه ای نداشته

(3)
داروهای خوراکی رتینوید
isotretinoin
Roaccutane
این دارو میزان تولید چربی غدد پوستی را کاهش میدهد. از آنجا که دارویی است سمی استفاده از آن باید تحت نظر متخصص پوست باشد. این دارو معمولا به مدت 16 هفته تجویز میشود و مصرف آن درخانمهایی که امکان باردار شدنشان موجود است (به استثنای شرایط خاص) مجاز نمیباشد


References:
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Tuesday 12 May 2009

[Influenza A (H1N1)] آنفولانزای خوکی

آنفولانزای خوکی بیماری ویروسی است که عامل بیماری آن دارای برخی از ساختمان ویروسی شناخته شده در خوک میباشد. این بیماری معمولا ازطریق انسان به انسان و با ذرات کوچکی که در اثر سرفه یا عطسه از بینی یا دهان شخص مبتلا خارج شده، به دیگران منتقل میشود. ویروس این بیماری نوعی ویروس جدید است و هیچ یک از واکسنهای موجود برای آنفولانزای فصلی از بروز این بیماری نمیتوانند جلوگیری کنند. در حال حاضرشرکتهای داروسازی مشغول تحقیق وساخت واکسنی مناسب هستند، امری که دست کم چندین ماه به طول خواهد کشید. طبق آخرین اخبارتاکنون در30 کشورجهان این بیماری رسما شناسایی شده، 5251 نفر به این بیماری دچار شده اند و 61 نفر (56 نفر در مکزیک) جان خود را بر اثراین بیماری از دست داده اند.

علائم بیماری عبارتند از بروزناگهانی تب، سرفه و نفس تنگی. علائمی مثل سردرد، گلودرد، خستگی، درد ماهیچه ها، لرز، عطسه، آبریزش بینی و از دست دادن اشتها نیز میتواند جز علائم این بیماری باشد.

دولت انگلستان که یکی از کشورهایی است که توسط سازمان جهانی بهداشت به عنوان یکی از آماده ترین کشورها جهان برای مقابله با این بیماری شناخته شده، داروهایی از قبیل
Tamiflu & Relenza
را ذخیره دارد. این داروها درمان مستقیم بیماری نیستند، بلکه به بهبودی کمک میکنند. در صورتی که به موقع ( در48 ساعت اولیه بروز بیماری) مصرف شوند، در بهبودی برخی از عوارض بیماری چون کوتاه تر کردن دوران بیماری و کاهش احتمال وقوع بیماریهای ثانوی چون ذات الریه موثرند.

برای جلوگیری از بروز بیماری رعایت نکات بهداشتی ضروری است.از تماس با افراد بیمار باید دوری کرد. پوشاندن دهان و بینی با دستمالی تمیزدرهنگام سرفه یا عطسه کردن، دورانداختن دستمال استفاده شده در سطل زباله و شستن دستها با صابون و آب گرم و یا استفاده از مواد ضدعفونی کننده مخصوص دست از موارد مهمی است که میتوانند ازهمه گیر شدن این بیماری پیشگیری کند. شواهدی در دست نیست که نشان دهد که استفاده از ماسکهای ابتدائی به مبتلا نشدن به این بیماری کمک می کند.

آدرس اینتزنتی زیر برای اطلاع رسانی به مردم انگلستان توسط دولت این کشور باز شده
www.direct.gov.uk/swineflu

References:
- Directgov
http://www.direct.gov.uk/en/Swineflu/DG_177831 accessed on 12 May 2009
- Swine Flue information leaflet
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© All rights reserved

Tuesday 5 May 2009

Hyperuricemia

Uric acid (an antioxidane) is a metabolite of purines (in food products as well as body cells going through their natural breakdown). Its continual supply is important for preventing damage to blood vessel linings. Uric acid is mostly excreted by the kidneys. But if too much uric acid is being produced or if the kidneys are not able to remove it, its level in the blood increases. Excessive uric acid is deposited in the tissues of the body. An increase in the level of Uric acid is referred to as hyperuricemia.

Because uric acid is formed from the breakdown of purines, low-purine diets are often considered in managing hyperuricemia. High-purine foods include: organ meats like kidney; fish like mackerel, herring, sardines and mussels; and yeast.
More information on the list of foods that contain high purines level [http://www.acumedico.com/purine.htm]

Drug treatment of hyperuricemia
There are two types of hyperuricemia, asymptomatic & symptomatic. Treatment for asymptomatic hyperuricemia is not considered cost-effective and generally, is not recommended. Treatment for symptomatic hyperuricemia is discussed under the treatment for gout, nephrolithiasis and uric acid nephropathy.

1) Drug treatment for gout: Drugs used for the treatment of acute attacks of gout are different from those used in long-term control of the disease.

Acute attacks of gout:
The main goal is to provide symptomatic relief from pain.
- The usual treatment is with high dose of NSAIDs (e.g. diclofenac, etorcoxib, indometacin and naproxen).
- Colchicine can be used alternatively (it has the risk of toxicity in higher dose, but as unlike NSAIDs it does not induce fluid retention, it can be used in patients with heart failure. It can also be given to patients on anticoagulants).
- Intra-articular injection of a corticosteroid may be used in acute monoarticular gout

Long term control of gout:
The main goal is to prevent further attacks of gout. The treatment for this phase is usually given 2-3 weeks after the acute attack has settled. The initiation of treatment may precipitate an attack of acute gout, hence prophylactic use of an anti-inflammatory analgesic or colchicine is recommended and it is continued for about three months.

The formation of uric acid can be reduced by
- uricosuric drugs (which promote uric acid excretion), probenecid, which is a uricosuric drug, inhibits the tubular reabsorption of filtered and secreted urate, thereby increasing urate excretion. But crystallisation of urate in the urine may occur, so adequate urine output must be ensured.
- xantine-oxidase inhibitors (which inhibit uric acid production).
Allopurinol is the most widely used antihyperuricemic agent. The major metabolite of allopurinol is oxypurinol, and both allopurinol and oxypurinol are competitive inhibitors of the enzyme xanthine oxidase.
Sulfinpyraone, can be used instead of allopurinol, or in conjunction with it.

2) Drug treatment for Uric acid nephrolithiasis (the process of forming a stone in the kidney or in the urinary tract).
Adequate hydration is recommended to maintain a high urine output, unless volume overload may be a concern. Allopurinol is the drug of choice in patients with hyperuricemia who develop uric acid stones. Patients with calcium stones who are hyperuricosuric may also benefit from allopurinol because urate crystals in the urine may act as a base for other stones to form.
Potassium citrate and occasionally sodium bicarbonate or acetazolamide may be required to alkalinize the urine and to decrease the solubility of uric acid.

3) Uric acid nephropathy (causing damaged to the kidney)
Xanthine is not very soluble in water; therefore, an increase in xanthine (could be induced by allopurinol) result in damage of the kidney.

Intravenous hydration with saline and the administration of furosemide or mannitol (to dilute the urine), and alkalinizing the urine with sodium bicarbonate or acetazolamide may be necessary.

If acute renal failure develops, then early hemodialysis is indicated.

Sourses:
In writing this piece the following articles were used:
- British National Formulary, March 2005
- WebMD, http://www.webmd.com/a-to-z-guides/uric-acid-in-blood, accessed on 5 May 2009
- emedicine, http://emedicine.medscape.com/article/241767-treatment, accessed on 5 May 2009
- The word’s healthiest foods, http://www.whfoods.com/genpage.php?tname=george&dbid=51, accessed on 5 May 2009



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Disclaimer: the main purpose of this blog is to assemble my notes for my Continuing Professional Development (CPD). The topic discussed here should not be referred to as the only source of information on the given topic. If there is anything with respect to this article that concerns you, please contact your doctor or pharmacist.
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Sunday 8 February 2009

Rizatriptan



Thanks to Mohammad Gashmardi for his kind premission for using his photograph


Rizatriptan (a 5-HT receptor agonist) is the active ingredient in Maxalat Melt (wafer). The usual dose for adult over 18 is one 10mg wafer at the first sign of a migraine attack. Not more than two doses in a 24-hour period. (the second dose for the treatment of the same migraine should not be taken). If works faster if taken on empty stomach

It helps the headache phase of migraine.
- Reduces swelling of blood vessels surrounding the brain
- Blocks the release of chemicals causing symptoms of migraine
- It interrupts the pathway of pain signals to the brain

Most common side-effects: dizziness, sleepiness and tiredness
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Disclaimer: the main purpose of this blog is to assemble my notes for my Continuing Professional Development (CPD). The topic discussed here should not be referred to as the only source of information. If there is anything with respect to this article that concerns you, please contact your doctor or pharmacist.
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ریزاتریپتن داروی فعال قرص ماکسیلات میباشد که برای درمان سردردهای میگرنی به کار میرود. این قرص روی زبان گذاشته میشود تا حل شود، مقدار مصرف معمول این دارو برای افرادی که هجده سال به بالا دارند، ده میلیگرم_یعنی یک قرص به محض بروز اولین نشانه های حمله میگرنی است. چنانچه با مصرف یک قرص علائم میگرن از بین نرفت، نباید مجددا از این دارو برای درمان همان حمله میگرنی استفاده شود. این قرص روی معده خالی سریعتر عمل خواهد کرد
ریزاتریپتن به چند طریق با علائم میگرن مبارزه میکند: (1) کاهش میزان تورم رگهای اطراف مغز(2) جلوگیری از ترشح مواد شیمیایی که موجب بروز علائم میگرن میشوند (3) ایجاد اختلال درمسیرعبور پیامهای درد به مغز
متداولترین عوارض جانبی ریزاتریپتن: سرگیجه، بیخوابی و خستگی است

Wednesday 4 February 2009

Promogran

Promogran is a topical wound treatment. Growth factors and protease (protein-digesting enzyme) levels are often inbalanced during the inflammatory phase of healing. Promogran inactivates protease, whilst enhancing the release of natural endogenous growth factors back into the wound, hence modifys the wound environment to optimise healing.

Promogran is indicated for the management of all types of chronic wounds that are free of necrotic tissue and infection (e.g. leg ulcers and pressure sores). The wound must be completely debrided before application of Promogran. The dressing is applied directly to the wound.

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Disclaimer: the main purpose of this blog is to assemble my notes for my Continuing Professional Development (CPD). The topic discussed here should not be referred to as the only source of information. If there is anything with respect to this article that concerns you, please contact your doctor or pharmacist.
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Tuesday 3 February 2009

Banana peel

Apparently, banana skin has some unique properties. These include analgesic; treatment of wart, psoriasis, constipation, diarrhoea, gastric ulcer, hangover, morning sickness and swelling of insect bites; can even be used as a repellent to prevent insect bites. Banana peel is also rich in serotonin and hence can be helpful in depression.

I must admit that I have not tried these for myself. But I have heard of the effectiveness of banana (the fruit rather than the skin) for treatment of diarrhoea. Banana also is a good source of fibre, which its regular intake can help to maintain a healthier digestive system. Of course, this only applies to a moderate intake.

But for me the most intriguing part is the effect of banana peel as an analgesic for headache. Apparently high potassium content of banana skin can re-connect the broken circuits of electrical signals between cells across the forehead and the back of the neck. Now, I must try this for myself.

For skin condition banana peel can be rubbed against the effected skin areas (with inner side touching the skin). Brewed or mashed up banana peel can be used for other conditions.


Reference:
That bananna peel appeal, Pharmaceutical Journal, 282 (7537) :116


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Disclaimer: the main purpose of this blog is to assemble my notes for my Continuing Professional Development (CPD). The topic discussed here should not be referred to as the only source of information. If there is anything with respect to this article that concerns you, please contact your doctor or pharmacist.
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پوست موز خواص دارویی زیادی دارد. از درمان حساسیتهای پوستی، خارش و تورم بر اثر نیش حشرات و برخی از گیاهان گرفته تا
درمان ناراحتی های گوارشی چون اسهال، یبوست و حالت تهوع و حتی کمک به بهبود افسردگی _ به جهت سروتنین موجود در پوست این میوه
با نقش موز در کمک به بهبودی بیماریهای گوارشی (به شرط آنکه در مصرف آن زیاده روی نشود) کم و بیش آشنا هستیم. ولی شاید جالبترین نکته در مورد پوست موز نقش آن در بهبود سر درد باشد. گفته میشود که برخی از سر دردها بی ارتباط به اختلال در مدارهای الکترونیکی بین سلولی در ناحیه پیشانی و پشت گردن نیستند. از آنجا که میران بالای پتاسیم در پوست موز به برقراری این ارتباطات کمک میکند، قرار دادن پوست موز مستقیما در محل درد میتواند در کاهش سریع درد موثر باشد

،برای بیماریهای پوستی یا درمان گزش گیاهان، قسمت داخلی پوست موز باید در تماس با بخش آسیب دیده پوست بدن نگه داشته شود مثلا توسط استفاده از چسب زخم. دم کرده یا پوره (له شده در مخلوط کن) پوست موز را میتوان در بقیه موارد استفاده کرد

مرجع اطلاعات
That bananna peel appeal, Pharmaceutical Journal, 282 (7537) :116

Monday 2 February 2009

Levodopa (L-dopa): a treatment for Parkinson's disease

Parkinson’s disease is a degenerative disorder of the central nervous system. It is characterized by tremor, muscle rigidity, a slowing of physical movement (bradykinesia) and a loss of physical movement (akinesia). It also associates with non-motor symptoms, such as thinking or behaviour disorders.

Dopamine depletion is typical in people with Parkinson, so dopamine was tried as a treatment for Parkinson’s disease. It was first synthesized in 1910, but as it does not cross blood-brain barrier, it could not reach its site of action.

Levodopa (a precursor or dopamine) was then used instead. L-dopa decarboxylase (which converts levodopa to dopamine) was used clinically in combination with levodopa. But much of levodopa was broken down to dopamine before reaching the brain and hence there were still problems with the amount of dopamine reaching its target. At the same time, dopamine released outside its target area caused major side effects. Hence, decarboxylase inhibitors were used to delay the conversion to dopamine until it reaches the brain.

To improve the efficacy of levodopa without the symptom fluctuationsand dyskinesias, dopamine agonists were developed. At first dopamine agonists were combined with levodopa; with a growing trend to use dopamine agonists at the early stage of treatment. Patients on dopamine agonists are less likely to develop dystonia and motor fluctuations than those on levodopa. But non-motor side effects (e.g. oedema, constipation, dizziness, and hallucinations) are more common on dopamine agonists.

Dopamine is converted to 3-O-methyldopa by catechol-O-methyl transferase (COMT). Hence, COMT inhibitors can improve the levodopa availability by improving the half life of dopamine. Entacapone (a COMT inhibitor) combined with levodopa and carbidopa (a decarboxylatase inhibitor) is considered as an effective combination.

Overall the choice of treatment should be individualized to each patient on the basis of clinical & lifestyle characteristics and patient preference.


Extracted from:
Jenny Bryan (2009). Levodopa_still the gold standard after 40 years of successful treatment. Pharmaceutical Journal, 282 (7537): 113-114



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Disclaimer: the main purpose of this blog is to assemble my notes for my Continuing Professional Development (CPD). The topic discussed here should not be referred to as the only source of information. If there is anything with respect to this article that concerns you, please contact your doctor or pharmacist.
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Friday 30 January 2009

Hypertension

Blood pressure depends on the amount of blood pumped out of the heart each minute and the resistance to the blood flow in the blood vessels. It is quoted as two values (in mmHg unit), systolic (maximum pressure per heart beat) and diastolic (minimum pressure per heart beat).

In general, in most people hypertension can remain untreated for a number of years. However, symptoms such as headache, blurred vision, anxiety, coma, nausea and vomiting may be experienced, although some are very rare. Therefore, hypertension is usually diagnosed by routine blood pressure measurement (on a number of occasions) or as a result of other complications.

Hyper tension can be divided into two types:

- primary (aetiology or essential)

- secondary (secondary to a disease such as renal artery stenosis)

Why does hypertension need treatment?
With hypertension structural and functional changes to the blood vessels occur over time. This changed blood flow, capillary permeability and vessel wall shear streees, which in turn affects cardiac workload, which may result in myocardial ischemia or even cardiac failure. Hypertension can also result in stroke or transient ischemic attacks. Damaged to other organs (renal failure or hypertensive retinopathy) can also occur.

The cardiovascular risks due to hypertension depends on other risk factors, such as age, family history, lifestyle, other illnesses (e.g. diabetes and high cholesterol)


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Disclaimer: the main purpose of this blog is to assemble my notes for my Continuing Professional Development (CPD). The topic discussed here should not be referred to as the only source of information. If there is anything with respect to this article that concerns you, please contact your doctor or pharmacist.
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