Inspiring Inspiron from Dell

I purchased the Dell Inspiron 1545 laptop back in January for my daughter's birthday. I had a limited budget but wanted to get her something with decent enough spec for playing computer games should she wish to do this, and a large hard drive as she is a big fan of making videos on her digital camera and downloading music - two things which can eat up hard drive space.
I did a fair bit of research before purchasing and decided I wanted to get the best spec I possibly could for my money and the Inspiron ticked all the boxes. I paid £399 in January 2009 in Currys for the laptop which was the absolute limit on my budget.
The Dell I purchased has a dark blue coloured lid, however the rest of it is a shiny piano black which looks lovely. I would have preferred metal for the mousepad area - it feels sturdier and doesn't seem to attract the dust the way the piano black plastic does - however that's a small quibble. The screen is widescreen and measures 15.6 inches and overall it's pretty lightweight and easy to carry about if you wish to do so.
So - what came in the box?
As well as the laptop there was an instruction manual, mains lead, Dell restoration CD-ROMs and a CD-ROM for Works 9.
The laptop had Windows Vista Premium pre-installed - and I worried that this might be a challenge for me as it was my introduction to Vista - however setting the machine up was a piece of cake.
I merely switched it on and dealt with a few prompts as Vista set up and then the computer was up and running. It has wifi installed and this picked up my wireless connection without any problems - and once I entered the security details for my network we were home and dry and online in no time!
When I was researching laptops I learned that you really need a minimum of 2GB RAM to run Vista properly, so this was another factor to consider when deciding the spec I needed for her laptop.
The laptop had a trial version of MacAfee installed but I decided to ignore this and installed AVG instead as my daughter is more familiar with it. I also decided to install the Works program that came with the laptop rather than Office as she really only needs a word processing program at the moment. I was concerned she may find it hard to use at first but we had no such worries.
What I really noticed about this little beauty was the speed - it loads really quickly and smoothly. The processor is an Intel Core 2 Duo 2.00 Ghz and there is 3GB RAM. This combination makes the Inspiron easily the fastest computer in the house - making me green with envy!
So onto the litmus test - did my daughter like it? Well yes - she loved it! She was really pleased to have this compact little laptop in her bedroom instead of the old desktop computer she had had in the past. She loved how she didn't need a wireless adaptor, the speed, and everything about it! The laptop has a large hard drive of 250 GB but this is half full already - just over 3 months since she got it, so I can foresee me having to get an external hard drive for her in the future.
I had worried about her learning how to use Vista, but like all 12 year olds, she picked it up far quicker than I did, so my fears were unfounded.
There are three USB ports, which so far I have found sufficient. The laptop does have speakers but they are a bit on the tinny side and given my daughter listens to a lot of music on her computer, I got her some USB powered speakers which offer fantastic sound quality.
The laptop also has an integral SD card reader which is invaluable for my daughter as she can easily upload photos and videos from her camera and also copy music onto the SD card she uses in her new Nintendo DSi.
There is a CD/DVD RW drive which works a treat - my daughter thoroughly enjoys making music CDs up using it and has also burned the occasional DVD featuring some of her many video clips. She can also watch DVDs on the laptop but hasn't used the laptop this way - she prefers to watch her DVDs on TV. It also came with Windows Media Center already installed which was an extra bonus as my daughter was already familiar with this from her old desktop computer and was delighted to still be able to use it for her videos, photos and music.
The Inspiron I purchased does not have a built-in webcam but this feature is available on some models.
The one thing we haven't tested is the battery life - Dell claim it's 2 hours however. As my daughter hasn't removed it from her bedroom since she got it I cannot tell you for sure. As she just recently broke the screen on my Samsung laptop, resulting in a large repair bill, she is probably too scared to move this one!
I am really pleased with the Dell Inspiron 1545 and think it's a really good buy for children or students as it's easy to use, fast to load and has a large hard drive but is available at a good price for the spec offered.
I do advise getting some half decent speakers to use with it however and cleaning it regularly - the piano black doesn't half attract the dust and show up fingerprints.
Overall this is a good machine for the money and it can be found in various outlets right now, including Currys, Tesco and Dell online.
**Previously published on dooyoo by me under the same user name

For USA members who seeks to get Mortgage or refinance

Banks are there to make money and I would like educate you as how the Mortage market works. first of all Banks compound your interest rate daily .. that's bad..for example if you take out a loan or a Mortage 6% for 30 years, $300,000 you end up paying over $700,000 . What is the solution ? you can double payments that will reduce your 30 years to about 24 years. You can ask your Banker to have a simple interest loand which I will doubt it if they will give it to you.Also for member who are 60 years and older and they have equity on their house over $65,000 you can have a reverse Mortgage(refinance to this concept).What is a reverse Mortgage, simply you stop paying your mortgage bill until all your equity will become zero, nada, nothing left. At that time either you die or if you sell your house the Banker will get most of the preoceeds.With the new era and economic collapse, they Banks right now will give a 30 years mortgage 4%. If you can get that you will never be able to beat this rate any where and time . Good luck.

HSBC Mortgages

My partner has banked with HSBC since his student days and has had his fair share of run-ins with them (like over-extending the overdraft and maxing out the credit card etc!) but has mellowed out somewhat in the time we have been together. Following a period of what I fondly refer to as 'credit hell' we having been working our butts off ever since to try and improve our credit rating to get back to a clean slate. Circumstances came up (at not such a great time, which is normal)and we found ourselves in need of getting or having 12 months to find a lender who would offer us a mortgage. It seemed that every avenue we turned to ended in a closed door and so we went down to HSBC with not too many hopes. The mortgage advisor was fantastic. He told it to us straight, told us the things we needed to do and ultimately, he gave us a goal to work towards. We came out not feeling like we had been laughed, which, after a fair few declines, is no small feat, and began working towards the light at the end of the tunnel. Well, the year is almost up and boy, have we worked hard. We went back to our friendly mortgage advisor to check that we were on track and he congratulated us on our efforts, which made us feel very pleased with ourselves. Like he said, the only way for us to truly improve our credit is to get a mortgage and in order to do that, someone has to take a gamble on us so that we can prove ourselves... HSBC are taking that gamble and I believe that it would take a very big something to stop us from banking with them from now on. They have been the friendly face that you so rarely get from Banks and Building Societies these days and once we're on the ladder, we won't forget all the hard work we had to put in to get there.

Re-mortgaging with the Royal Bank of Scotland

I've been a home-owner now for about eleven years: bought my first house as the market hit rock bottom and and am still there. Naive as I was then about financial matters, I took advice from a professional and ended up with an endowment mortgage. I expect you can guess what happened next. Actually it wasn't that bad: I still had fifteen years to run on my mortgage and am young enough to get another 25-year mortgage. So that's what I decided to do.
I have banked with Royal Bank of Scotland ever since they took over Williams & Glynn's Bank nearly 20 years ago and while I've had other bank accounts as well, both personal and treasurers' accounts for some clubs I've been involved in, as well as building society accounts, RBS have always won hands down when it comes to customer service and helpfulness. Also, and this is VERY IMPORTANT, you can phone your branch up and speak to a real person instead of phoning a call centre and going through endless menus in order to talk to someone who can't or won't help you. So when it came time to re-mortgage, I looked at the available options with the intention to go with RBS unless something spectacularly better came up. It didn't - in fact the current account mortgage I decided on had one of the best rates I could find and in addition, the Bank paid all the legal fees and the valuation fee.
The actual process was simple. I filled out the application form and sent it off with the necessary copies of my payslip etc. The bank made an appointment to send their surveyor round and my partner stayed home that day. The bank's solicitors did all the legal work: they are based up north but there is no reason whatsover, with a routine transaction, why I should have needed to see them in person, and I didn't. I did speak to them a couple of times and they were friendly, helpful and phoned me back when they said they would. I had to do very little myself. The current account mortgage works like a huge overdraft secured on my house. I have my salary paid into it and all my direct debits etc. come out of it. The rate varies depending on how much you owe in relation to the value of your property – for me, fortunately, it’s in the lowest bracket. I am saving loads of money each month and actually paying the mortgage off, not merely paying the interest. I can use PC banking which was not available with the building society I had my previous mortgage with. There is no redemption penalty if I win the lottery and decide to pay the mortgage off. I could go on but you'd get bored.
The whole thing, from me deciding to re-mortgage to the money being in my new current account, took around six weeks. Whenever something cropped up, as things do, I simply rang my local branch (or they rang me) and talked to one of three ladies whose names I knew and who, despite being busy, took as much time as was necessary to sort out whatever needed sorting in the friendliest manner imaginable. There was one snag: the mortgage insurance. This is supposed to be free for the first six months and I expected the premium to start being taken out of my account at the beginning of this year, but this never happened. It seems that somewhere along the line, the application had gone astray: I've never established whether it was me, the bank or the insurance company who lost it. This is a minor problem - it had the potential to be major if anything had happened but I was lucky.
The Royal Bank of Scotland are only human, and do make mistakes from time to time. Little ones, in my experience, and not very often. They use their vast electronic machine to help, not to hide behind. I wish all banks were this nice!

How to Become a Forex Broker

It is a fact that you can make money with currency trading on Forex. Indeed, Forex investing is one of the most potentially rewarding types of investments available. Since individual traders and companies have equal chance to expand in Forex trading, we all have the option to becoming a forex trading broker in order to generate more revenue.
In order to help with your trading strategy and transactions, it is recommended that you must find a forex broker if you are new to the FOREX. The forex broker acts as a liaison of the client to the forex market, which provides technical analysis and research of the market situation and guides the client on the methods of trade as well. All of the information he provides is believed to increase the client's profit.
Before I will discuss on how to become a forex broker, here are some reasons why should you become one. As a forex trading broker you provide your customers access to the freedom that comes from actively trading their own money online on secure forex trading platforms. Since you offer your clients some money making opportunities and some investments, you are then greatly improving the scope and reputation of your own business leading to greater client retention levels. Aside from the fact that you are paid a commission you can also take advantage of the explosive growth in the demand for alternative investments by offering your high-net worth clients a managed forex account.
Becoming a forex broker is simple. A currency trading broker in the Forex trading market is like being a realtor in the property market. Here are steps to becoming one. Becoming Licensed and Registered. Sign on to a licensed business or seek appropriate securities license and fill out a registration form with the SEC in order to be a full service broker. Take note that licensing is different depending on which state you live in. If you move from state to state, license is not always acknowledged. You’re ready to start trading once registered.
However, if you want to become a business broker only and not a full service forex broker, you may work at a brokerage house. You may either go to school or try to learn forex trading by yourself in order to get license. Remember, knowledge is power for the successful broker! A successful forex broker is aware of what’s happening in the world. Forex brokers research heavily on all political and economic news from the countries for which they hold currency.
Forex brokers are much like any other broker that act as the middleman for the individual and the market itself. They key to a successful forex broker is to get licensed and educated about how the market works. With this article you now have information on how to become a forex broker. Get licensed and registered and start forex trading. Soon you will just be sitting up in your multi-million

Knowledge in Forex Trading

I read all the time about how important it is to learn lots of information to trade forex and how you continually need to learn, but this is NOT true. Succesful Forex trading is actually very simple and the knowledge is easy to acquire, yet 90% of traders lose - so why is this ?Because knowledge alone is not enough, furthermore you need to learn the right knowledge and most forex traders don't.There are plenty of very smart people who lose and plenty of small potato investors who make a lot. The fact you have a lot of knowledge or are clever does not ensure success and in most cases ensures you lose.Let's look at this in more detail.The right knowledge Is not hard to acquire and starts from learning yourself and not trying to get a short cut to success by buying it - if you think you can buy success you are going to lose.Trading means getting knowledge that works and you can have confidence in.Your aim is to make money, not be clever and you can build a simple system from free resources on the net.Simple systems beat complicated systems as they are easier to understand, easier to apply and make more money as they are more robust.Fact is most of the top traders in the world use simple systems.We have been traders for over 22 years and our system is simple:Trend lines, support and resistance to spot trends and 3 confirming indicators and that's it and it works.The right knowledge is easy to acquire but the trick is you MUST understand it, to have confidence and this gives you the trait that most traders lack. DisciplineIf you try and follow someone else you won't have confidence and you won't be able to follow a system with discipline. Unless your knowledge is acquired by you and you have confidence, you won't be able to follow your trading system through losing periods. You will simply throw in the towelDiscipline sounds easy to acquire but it isn't - it's extremely hard to hold your emotions in check.How do I get the RIGHT KnowledgeForget all the e-books, courses and other forex education sold on the net.Go to Amazon and get some books by top traders, who have walked the walk rather than simply talk the talk.Most sold info on the net is not worth the money and you can get far better knowledge cheaper at your local bookstore.Good books to start with are Jack Schwager - Market Wizards and New Market Wizards - the interviews here are all with legendary traders and is a great inspiring read.Then get some books on trader psychology.I am a big fan of Jake Bernstein who really shows how important and elusive getting the right trading psychology is and really hits it home.Another favourite of mine is Trader Vic by Victor Sperandeo, a fantastic book covering all you need to know from money management to system building.Done that?Then go on the net and build a simple system based around technical analysis, a breakout methodology find a few indicators you like to confirm trend momentum and you're all set to go. Sounds simple?Building the system is the easy part - getting the right mindset is the hard part - good luck.

Online Forex Broker Profile

MoneyForex Financial Ltd. is one of the world leading online currency trading broker offering low pips and commission-free online forex trading. Founded by Wall Street veterans, MoneyForex's vision is to service individual and corporate investors such as money managers, banks, and financial institutions in easing the complexity in dealing with forex trading. Our dealing software which specialized in forex dealing is rated second to none for it user friendly environment. Lightning speed and efficient execution is one of its many benefits.MoneyForex Financial Ltd. is incorporated in British Virgin Island (Registration Number 629302) under the provisions of the International Business Companies Act, 1984. MoneyForex is authorized to offer futures, securities, and foreign exchange as a forex broker and primary market maker.MoneyForex is founded by a group of Wall Street Veterans who has more than 30 years experience in the financial market. Other than the financial industry, the group operates various businesses including real estate development, media communication, advertising, internet technology and software application and development.In this complex forex market, a user friendly platform is a must in order to make fast and efficient trading decision and execution. Our trading platform is rated the most user friendly by professional traders. MoneyForex's clients consist of financial institutions, money managers as well as individual investors.

Foreign Exchange Education Centre

The Forex market is a non-stop cash market where currencies of nations are traded, typically via brokers. Foreign currencies are constantly and simultaneously bought and sold across local and global markets and traders' investments increase or decrease in value based upon currency movements. Foreign exchange market conditions can change at any time in response to real-time events.
The main enticements of currency dealing to private investors and attractions for short-term Forex trading are:
24-hour trading, 5 days a week with non-stop access to global Forex dealers.
An enormous liquid market making it easy to trade most currencies.
Volatile markets offering profit opportunities.
Standard instruments for controlling risk exposure.
The ability to profit in rising or falling markets.
Leveraged trading with low margin requirements.
Many options for zero commission trading.

Learn to Trade Forex
The GBPJPY is trading at an important long term resistance level around 159.45, in the short term charts it is trading in a tight range in between 159.79 and 158.23, so it first need to clear either support or resistance to start looking for trading opportunities, please take a look at the next chart:
If the market breaks the 159.79 short term resistance line, I will be looking for long opportunities. All take profit orders will be placed around 161.70
If the market breaks the 158.23 short term support level, I will be looking for short trading opportunities. All take profit orders will be placed around 157.00
If the market keeps trading in the short term range I will do nothing.
Good luck

Traits of Successful Forex Traders

Forex trading is an exiting way of earning a living or making some extra money on the side, but its not for everyone. There is always the risk of losing money on top of all the variables you have to take into account. Some people just cant make the cut into the realm of successful traders. If you are considering taking up Forex trading as something else than a hobby, you will want to read this article carefully. It contains the traits that set successful traders apart from the rest.If you can’t recognize these traits in yourself then maybe Forex trading isn’t for you.
Discipline. Successful traders always go by a strategy and don’t let their emotions get the better of them. They never ‘trade on the fly’.The ability to accept risk as part of the game. Despite what you may hear from shrewd sales pages, Forex trading is never without risk. Risk is the other side of the coin. There is big profits to be made but you have to be willing to accept the risk of losing.
Willingness to accept failure and learn from it. Even the best traders in the game lose trades. Its the natural order of things. But the difference between a successful trader and a losing trader is the ability to learn from failed trades and not dwell on the negative.
Confidence. Successful traders always keep confidence in their ability and knowledge. They don’t second guess themselves after making a trade.
The ability to accept being wrong. No one is perfect. You are going to make plenty of mistakes along the way. Don’[t be stubborn and stay in trades gone bad to save yourself from admitting you were wrong.
Patience. Smart traders stay with their system and wait patiently for the right spot to present itself. You don’t need to have positions open all the time. Don’t trade just to trade.
Know when to get out. There is more to trading than knowing when to get in, you need to know when to get out as well. Too many traders got greedy and stayed in a trade for too long, only to see their profits wiped out. Get out when your system tells you too. Don’t go chasing pips.
Know your financial limitations. Don’t over-leverage yourself and don’t trade with money you need to pay your bills or risk ending on the street. Only trade with money you can afford to lose even if this means starting out with only a few hundred dollars. There are many forex brokers where you can get started with that.

forex signal provider? which one?

So you decided to make full time leaving from foreign exchange market? Or you are going to supplement your income from here? You have set up yourself with proper broker available. I believe you spent hundred of hours in front of PC trying to put together all maths and physics involving currency market. Now you watching business news in the morning paper and following CNBC channel to be on the top with latest information from exchange market. You trading your demo account trying to figure out how to make it all work? So? Does it? No?Face the fact that in currency market all is possible and there is no golden rule to follow. There are so many aspects to consider that you will need at least another head to set this puzzle together.But do not worry there is a hope that can make it work.Signal solutions for forex trading. People who traded forex for a long time and developed their own systems to enter and exit with profit strategies. They will share this knowledge with you for varieties of prices from usd49 to usd499 a month for those precious information. Problem is which one will suit you best. Are they scams? How do I know?For medium advanced forex trader is almost impossible to choose proper forex signal system, which is not a scam, or at least not profitable. There is bulk of forex signals providers out there. They all offer their signal solution to trade currency with success.

Turkey Gold Market

Turkey has been an important regional gold market for many years; during the 1990s domestic jewellery fabrication averaged 125 tonnes (4.02 million oz). In addition, Turkey has been a key source of bullion for several neighbours countries. Turkish bullion imports, which normally exceed 100 tonnes (3.2 million oz) on an annual basis, came to 107 tonnes in 1999 but then rose significantly in 2000 to 205 tonnes (6.6 million oz). However, the following year bullion imports fell sharply. According to GFMS, this was partly due to the sharp devaluation of the Turkish currency and the associated economic and banking crises which affected the country. On a separate note, Turkey's position in the international market was enhanced by the full liberalisation of the local gold market in 1998 and the opening of the Istanbul Gold Exchange on 26 July 1995.

japan Gold Mraket

Japan has evolved as a major market for gold for fabrication and investment since trading was liberalised in 1974. But the gold business in Japan has much earlier origins. Gold mines in Japan in the 17th century exported through the Dutch East India Company to East Asian countries. Tokuriki Honten, still an important refiner and fabricator, traces its history back to 1727. Tanaka Kikinzoku Kogyo, the leading precious metal refiner and trader, was established in 1885.Actual mine production is limited. The only significant mine is Sumitomo Metal Mining's Hishikari on Kyushu island, opened in 1985, with output between seven and eight tonnes (0.25-0.26 million oz) annually. The Japanese market is supplied, therefore, both by imports of bullion and by-product gold from imported concentrates.Total gold demand in Japan ranges between 200 and 275 tonnes (6.4 – 8.8 million oz), embracing jewellery fabrication, electronic and industrial uses, dental applications and physical bar investment . Japan is the world's foremost user in electronics, using over 100 tonnes (3.21 million oz) in 2000 according to GFMS (although this fell sharply, to around 70 tonnes or 2.25 million oz, in 2001 on the back of the slowdown in global demand). Japan's use of dental gold in 2001 was around 21 tonnes (675,000 oz) according to GFMS. Physical bar hoarding is also much higher than in other industrial countries, and is an anonymous way of holding wealth outside of the banking sector. GFMS estimate that it averaged just under 60 tonnes (1.9 million oz) over the past decade and exceeding 100 tonnes (13.2 million oz) in 1999. The first few months of 2002 saw a surge in Japanese hoarding demand due to fears about the health of the banking system.It is also the custom in Japan for companies to give gifts of 24 carat ornaments such as teapots, saki cups, vases and chopsticks. The gold tea ceremony room at the Moa Art Museum in Shizuoka Province used 50 kilos (1,607 oz) for teapots and cups, plus gold leaf for its walls.

examples of multi unit smooth muscles arc in the (i) nictitating membrane, and (ii)

examples of multi unit smooth muscles arc in the (i) nictitating membrane, and (ii) pilomotor muscles in the hair follicle. [Because of complete absence of the spontaneous activity and because of the fact that it is very well developed the nictitating membrane of cat is a common experimental tool for the pharmacologists for studies of various drugs on autonomic nerves.smooth muscles]. However, some smooth muscles exist, which cannot properly fit into any one of these two types. Best example is arteriolar smooth muscles, which like the unitary, smooth muscles show autorhythmicity but shows some properties of multiunit muscles too. This type of overlapping of characteristics is seen in some other smooth muscles too Neuro effector junction As already stated earlier in this section, atypical motor end plate is absent in the junctional legion of the supplying autonomic nerve and the smooth muscle Instead, what is found is stated below: The smooth muscles are supplied by post ganglionic autonomic nerve fibers. As a rule both the sympathetic and parasympathetic fibers supply the muscle. The junctional region between the motor autonomic nerve and the smooth muscle may best be called, 'neuro effector junction'. [The term 'neuro muscular junction'should be reserved for the junctional region of the skeletal muscle and somatic nerve this ensures clarity]. The post ganghonic fiber (which is non myelinated) divides into many terminal branches. An individual branch supplies one muscle cell. Some smooth muscle fibers (cells) do not receive any nerve supply at all. In the smooth muscles of the eye (iris/ciliary muscles) each muscle cell is supplied by one nerve twig whereas many smooth cells of uterus are not directly connected with nerve fiber In such uterine cells the action potential (AP) spreads through the gap junctions That is the innervated cell gets a stimulus via its nerve supply develops an AP the AP enters (via gap junction) to a neighboring smooth cell which is not innervated the neighboring cell is stimulated. As the nerve teiminal approaches the smooth muscle cell to be supplied, it develops some swellings called Varicosities'. These swellings are due to the presence of vesicles -a-within the nerve terminal The vesicles are filled with the neurotransmitters. Between the nerve terminal and the muscle membrane, there exists a gap (cf. skeletal muscle neuromuscular junction). the width of the gap being between 20 nm to 100 nm. Throughout the vvhole surface of the sarcolemma of the smooth muscle numerous receptors are present. These receptors can combine with the chemical transmitter and act accordingly. When an AP develops in the supplying nerve the AP proceeds down the nerve towards its neuro effector junction (NEJ). As it passes over the zone of the varicosities, the vesicles rupture releasing the neurotransmittiter---->combination of the neurolransmitter with the receptor occurs -.-> AP on the sarcolemma of the smooth muscle develops -----> contraction of the muscle follows. Mechanism of contraction of the smooth muscles The major steps are same as those of skeletal muscle. There is development of cross bridge followed by sliding of the actin filaments over the myosin filaments and the muscle shortens. However, there are some differenc es too: (i) the amount of actin and myosin/gm of smooth muscle is only some 10% of that of the skeletal muscles. Because of this the smooth muscle can never contract violently and exert great force, as can be done by the skeletal muscles. (ii) the sarcoplasmic reticulum (L system of tubules) are very poorly developed in the smooth muscles During the excitation contraction coupling. Ca++ ions are provided by the L tubules in the skeletal muscle but here (because of the fact that the L tubules are practically not found at all). Ca++ have to be provided from the outside (i. e. the EOF) via the T tubules. So Ca++ must be present in the ECF and in sufficient quantity to ensure a satisfactory contraction of the smooth muscle. [This can be shovvn in the isolated organ bath experiments shovvn to the students If the bathing fluid (Tyrode/Ringer Lock) contains even a slightly lower concentration of Ca++ the contraction fails to develop in the smooth muscle] (iii) the speed of the smooth muscle contraction is much slower than that of the skeletal muscle. Pacemaker The student may, at this stage, recall properties of the heart muscles (chap.2. sec. V). Normally SA node (and abnormally other areas of the junctional tissues) acts as the pace maker. That is. in SA node an AP can develop spontaneously (the term spontaneous means, 'wthout stimulation') and this AP can spread to other cells. Such pace making cells exist also in the smooth muscles, and at rest, develop 'pace maker potential' a phenomenon which is same as thediastohc depolarization of the cardiac muscle (chap. 2, section V). In short during rest as is the case of all other cells, these pace maker cells are -ve inside and +ve outside and has a resting membrane potential (rmp) of about say. -70 mv. But during rest, spontaneous (and mild) depolarization, occurs in these cells, as a result of which the resting membrane potential (rmp) drops, (i. e. moves towards zero) and attains a value of say -50mv. When the rmp thus reaches -50 mv. which is the critical level firing begins and an AP develops General properties of the smooth muscles By now, it should be clear that smooth muscles (SM) are rather heterogenous tissues and there are different tvpes of the SMs, e.g. single unit multiple unit etc. having rather

The number of these cells is greatly increased in acute tubular necrosis. (vi) Casts - Red cell casts

syndrome, familial recurrent haematuria. 12. Renal embolization/infarction. 13. Analgesic nephropathy. 14. Unknown origin -Essential haematuria ("renal epistaxis"). Loin pain/haematuria syndrome. Ureter - (1) Trauma. (2) Calculi. (3) Infection. (4) Tumours - papilloma, carcinoma Prostate - Benign hypertrophy, carcinoma Bladder - (1) Diverticulum. (2) Trauma - following prostatectomy or other operations or instrumental. (3) Calculus or foreign body. (4) Tuberculosis. (5) Tumours - Simple, papilloma, carcinoma. (6) Ulcers. (7) Chemical cystitis - e. g. after cylophosphamide. (8) Parasitic - Schistosomiasis, Bancroftian filariasis. Urethra - (1) Malformations. (2) Injuries. (3) Calculus or foreign body. (4) Infections. (5) Tumours. (6) Naevus 2. Systemic causes - 1. Bleeding diathesis. 2. Collagen disorders - SLE, PAN. 3. Subacute infective endocarditis 4. Cryoglobulinemias. 5. Amyloidosis. 6. Acute fevers - Malignant malaria. 7. Tuberous sclerosis (associated angiomyolipomata). 8. Severe exertion (e. g. jogging). INVESTIGATION OF A CASE OF HAEMATURIA History - 1. Age - Newborn - haemorrhagic disease due to deficiency of vitamin K. Child - Acute nephritis, acute leukemia, acute infectious fevers, scurvy, haemophilia, bladder stone, meatal ulcer Young adults - Renal calculus or tuberculosis, gonococcal urethritis Middle or old age - Bladder tumours, congenital cystic kidneys, calculus, hypernephroma and other malignant tumours, hypertension, enlarged prostate 2 Sex - Bladder stone almost always in males. 3. Family history - of polycystic kidneys or urinary calculi. 4. Drugs - History of taking anticoagulants, sulphonamides or large doses of aspirin. 5. Previous history - of pulmonary or bone and joint tuberculosis. 6. Quantity of blood - Profuse in tumours of kidney or bladder injury with rupture of kidney. Rarely tuberculosis and enlarged prostate. 7. Precipitating cause - Trauma. Jolting or exercise in renal calculus. Instrumentation Intercourse. 8. Timing of bleeding in relation to urinary stream - Terminal haematuria preceded by clear urine suggests source in bladder, initial haematuria followed by clear urine is indicative usually of lesion in urethra. Haematuria equally distributed throughout the urinary flow is characteristic of renal and ureteric lesions, but may occur in bleeding from the bladder. 9. Pain - (i) Colicky in stone. (ii) Loin pain suggests renal cause. (iii) Pain at tip of penis especially after micturition indicates irritation of trigone. (iv) Pain in pen'neal area - malignant disease of bladder or prostate. (v) Hypogastric pain in cystitis. (vi) In Dietl's crisis, severe pain but haematuria rare. Haematuria precedes pain in tuberculosis and new growth of kidney, follows pain in renal stone. 10. Absence of pain - Enlarged congested prostate, early stage of malignant disease of bladder, renal neoplasms, congenital cystic kidneys, tuberculosis and systemic causes. Painless, periodic, progressive and profuse haematuria in simple papilloma. 11. Increased frequency of micturition - Local causes in bladder, tuberculosis or pyelitis. 12. Constitutional symptoms - Fever in pyelitis and cystitis Rash or eruption in acute fevers. 13. Haemorrhage elsewhere in the body - in purpura, haemophilia, fevers, hypertension Physical examination - (a) Local examination - 1. Palpation of kidneys - (i) Unilateral tumour - in tuberculosis, hypernephroma, hydro- or pyo-nephrosis (ii) Bilateral in polycystic disease. 2. Bladder tumour is occasionally palpable. 3. Inspection of external genitals and urinary meatus for local causes. 4. Examination of testis and epididymis for evidence of tuberculosis. 5. Rectal examination - Enlarged prostate, stone in bladder in children. 6. Vaginal examination - pelvic tumour, e. g. malignancy of uterus. (b) General examination -Examination of heart for SBE Blood pressure. Signs of anaemia Bruising or other evidence of haemostatic defect. Abdominal palpation for splenomegaly, enlarged kidneys or distended bladder Investigations - 1. Urine - (i) Excess of crystals of uric acid, oxalates, etc , may indicate presence of stones. (ii) Albuminuria and epithehal cells in acute nephritis. (iii) Pus cells in pyelitis and tuberculosis. (iv) Red cells - In glomerular bleeding there is great variation in size and many cells show loss of normal haemoglobin pigment. In non-glomerular bleeding the cells are uniform in appearance and usually have normal haemoglobin content (except in acid urine). (v) Renal tubular epithelial cells - A sharp rise in these cells may be produced by certain drugs The number of these cells is greatly increased in acute tubular necrosis. (vi) Casts - Red cell casts or casts containing red cells imply glomerular disease Granular casts, oval fat bodies and broad, waxy casts imply an underlying renal lesion. (vii) Culture - Pyuria with no growth on urine culture occurs with tuberculosis, tumours of urinary tract and analgesic nephropathy. (viii) Cytology -when urothelial neoplasm is suspected. 2. Blood examination - for evidence of hypoprothrombinemia, purpura or haemophilia. 3. Chest X-ray - for evidence of malignancy or tuberculosis. 4. IVU - may provide evidence of silent cysts or renal tumours Appearance suggesting papillary necrosis indicates analgesic nephropathy but may occur in diabetes, sickle-cell disease or obstructive uropathy. 5. Cystoscopy - If IVU and urine culture are normal Upper urinary tract bleeding is usually unilateral Bladder tumours and pre-malignant papillomata can be diagnosed by cystoscopy, with biopsy when necessary 6.

, formation, the subject can see to some extent, but as the cataract advances to its maturation, vision

limit already, he cannot see the closer objects also clearly. Correction is made by convex lens which causes convergence of the incident rays (fig. IOB2. 1. 9). Fig. IOB2 .1. 9 3. Presbyopia After the age of 40, presbyopia is commonly seen In this condition, the crystalline lens becomes rigid, so that, during accomodation, even though the ciliary muscles are contracting, the lens fails to become more globular, le, it fails to increase its diopteric power. Such persons cannot see printed words or small objects, when held at 'usual' distance for reading. But when he holds the book rather at a greater than usual distance, he may be able to see. Such eyes are corrected by the use of 'reading glasses', that is, convex glass (which he is to use during reading only). N B Although, the term 'infinite distance' normally means an immeasurably long distance, in optics, it means only 20 feet (about 6 meters) or more, because if the object Js at 6 meters away, the rays from it are parallel to the eye. Near Point The 'hardening' of lens begins early in life although the signs of presbyopia begins to become noticeable only after the age of 40 years (or in some people after about 50 years). Consequently, bulging of the anterior surface of the lens due to contraction of ciliary body, that is, accomodation, is maximum in childhood The nearest point that can be seen clearly is called the 'near point' At the age of 10 years, the near point usually is 9 cm away. Throughout adult life the near point recedes farther and farther At the age of 70 years the near point may be 100 cm away. In the myopic, some compensation of near point often occurs, that is, the near point is nearer than the emmetropics of his age. It is quite common to find a myope over 50 years, reading or threading the eye of the needle without the help of reading glass (the author of the current book, who is 54* years being one such example). 4. Astigmatism In some corneas, the curvature varies from meridian to meridian. Thus, in a given cornea, the curvature in a transverse direction (i. e. the direction which runs from nasal to the temporal side) may be less than that in the vertical meridian Such an eye is called an 'astigmatic' eye. As the power of a body acting as a fens depends upon its curvature, the refractive power of an astigmatic lens will be different in different meridians. As a result, images from all the portions of the object can not be simultaneously focussed on the retina and so the object can not be clearly seen If a person, suffering from astigmatism, is given a diagram consisting of radiating lines, he will fail to see all the lines simultaneously Correction of astigmatism is made by using a cylindrical lens. The errors of refractions described above are all examples of pathological conditions But even in normal persons, some errors may sometimes be seen Indeed no optical system is perfect and the optical system of our eyes is surprisingly free of imperfections, yet, it has a few, relatively minor, imperfections. These are: (i) spherical aberration, and (n) chromatic aberration. 5. Spherical aberrations Even in a normal person, the power of the lens at the extremes of its periphery, is not identical with the power in its central part Therefore, when the pupil is widely dilated (e.g. in darkness or after administration of atropine) some blurring of vision may occur and is called spherical aberration. * Written while the book was in its 1st edition. 6 Chromatic aberration Particularly at the periphery of the lens of the eye, rays of the different wave lengths are refracted differently, causing what is known as chromatic aberration. Red light is refracted least whereas the violet light the most and consequently on looking at a source of 'white light' (containing in full, the 'Vibgyor'), the red light falls posterior to and the blue or violet anterior to the retina. Cataract In advanced age, the lens may become opaque and fail tc transmit light, this is due to denaturation ultimately leading to coagulation, of lens protein Finally, in the coagulated protein, there may be calcium deposition, making, it still harder and more opaque. The whole process (from the onset of denaturation and coagulation to its complete opaci. ty) requires some time, (may be a few years). A matured cataract fie where the coagulation and opacity is complete) has to be removed surgically and to compensate for the loss of refraction, a convex lens (+ lens) of say around 1 D power has to be given In the initial phases of catarac, formation, the subject can see to some extent, but as the cataract advances to its maturation, vision becomes increasingly poor Exposure to strong sunlight or ultraviolet light probably favors cataract formation (by helping the process of denat uration and coagulation of the lens protein). It is advisa. ble, therefore, to use sunglass in the outdoors of a tropica country like India TESTING OF VISUAL ACUITY (fig. 10B2. 1. 11) To test the visual acuity for distant vision, visual char (Snellen's chart), is used Such a chart contains letters (o the alphabet) of different sizes For example, the letter I on the topmost row (fig. IOB2. 1. 11) has the biggest size and a normal man can see it early from a maximum distance o 60 meters Letters of the 2nd row can be seen learly with emmetropic eyes, from a maximal distances of 36 m and so on. The subject stands (or sits), 6 m away from such a charl If he can see, a letter of the top row, (which an emmetropic man can see from 60 m), but no more, then his vision is 6/60 This means he can see an object, only when he stands at 6 n distance which one should normally see from a distance o 60 m. Obviously a normal vision is 6/6. Physiological basis of visual acuity In fig 10B2 1 10, an object, mn is placed

MANAGEMENT OF END-STAGE RENAL DISEASE

depletion should be suspected if B P is not raised and postural hypotension tencte to occur. 4. Diuretics - Large doses of Frusemide 250 mg-2 g in 24 hours) may promote diuresis even in advanced CRF 5 Treatment of associated disorders - (a) ANEMIA - Some degree of anemia is well tolerated by most patients and it is best to leave it untreated except for correction of obvious iron deficiency. Anemia of CRF in dialysis patients as also pre-dialysis patients has greatly improved with use of recombinant human erythropoietin (r-HuEPo) Dose -25-50 g/kg I. M. 2-3 times a week. Maintenance dose, 10 g/kg 2-3 times a week Care must be taken to see that hypertension is not exacerbated in patients receiving this drug as it may lead to convulsions. (b) RENAL OSTEODYSTROPHY - results from combination of disturbed vitamin D metabolism and secondary hyperparathyroidism. A rise in serum alkaline phosphate and parathyroid hormone are the cardinal features Treatment - (i) Calcium carbonate is palatable and effective and also helps to correct metabolic acidosis. (ii) Synthetic vitamin D analogues, such as 1-hydroxycholecalciferol 0.25 g/day or vitamin D metabolite 1,25-dihydroxy-cholecalciferol 1-2 g/day Frequent monitoring of serum calcium is essential for early detection of hypercalcemia. which would further decrease renal function and cause pruritus, vomiting and occasionally, pancreatitis. (c) HYPERTENSION - Loop diuretics such as frusemide, -blockers, vasodilators such as nifedipine, ACE inhibitors (d) HYPERLIPIDEMIA - HMG and COA reductase inhibitors. (e) ALUMINIUM TOXICITY - Reverse osmosis to reduce aluminium level in the dialysate, and removal of aluminium by dialysis after infusion of desferriexamine. Oral calcium carbonate as phosphate binder. (f) SYSTEMIC ACIDOSIS -Most patients tolerate mild degree of acidosis, but when plasma bicarbonate falls to 15 mmol/litre or less, correction with sodium bicarbonate 6-12 gm b. d. or t ds is indicated - Domperidone 10 mg. t.d.s. Protein restriction. If no response dialysis should be considered. (h) PRURITUS - Correction of serum calcium and phosphate levels and use of antipruritic drugs such as chlorpheniramine maleate. (i) PERIPHERAL NEUROPATHY - If no obvious cause such as drugs (nitrofurantoin), or alcohol, dialysis is indicated CAPD is superior to hemodialysis in improving peripheral neuropathy MANAGEMENT OF END-STAGE RENAL DISEASE (ESRD) - Renal replacement therapy (RRT) -cab be provided by hemodialysis, peritoneal dialysis or kidney transplantation. Hemodialysis - Types of hemodialysis: HEMODIALYSIS - in its classical form is the most common treatment. The blood passes through an extracorporeal circulation where it is separated from the dialysis fluid by an artificial semipermeable membrane Solutes move across the membrane only by diffusion. The dialysis solution comprises water and electrolytes. By means of a controlled pressure gradient created between the blood and dialysis solution, it is possible to draw water corresponding to fluid overload Such ultrafiltration, is sometimes used alone, without diffusion to reduce fluid overload HEMOFILTRATION - Here a pump connected to the dialyser creates a negative pressure on the side of the dialyser opposite to the blood compartment This sucks the plasma fluid and the solutes dissolved in it across the dialysis membrane This process is called 'convection' No dialysis solution is used and high volumes of plasma fluid can be ultrafiltered (30-60 litres per session) HEMODIAFILTRATION - This method uses convection and diffusion Dialysis

The resulting solution complies with the limit test for chlorides, Appendix 3.10 (750

ml of saturated solution add 1. 5 ml of 0. 05M iodine, the solution remains clear. Add a few drops of dilute hydrochloric acid; a brown precipitate is formed which dissolves on neutralisation wilh sodium hydroxide solulion .E; Melts between 234° and 239°, determimed after drying at 100° for 1 hour, Appendix 8 8 Acidity or alkalinity Dissolve 0 .2 g in 10 ml of boiling water and cool. Add 0. 1 ml of bromothymol blue solution The solution is coloured green or yellow. Titrate with 0 .02M sodium hydroxide to a blue colour, not more than 0.1 ml is requiredClarity and colour of solution; A 1 0% w/v solution is clear, Appendix 6. 1, and colourless, Appendix 6 .2 Arsenic ;Mix 3 .3 g with 3 g of anhydrous sodium carbonate, add 10 ml of bromine solution and mix thoroughly Evaporate to dry ness on a water-bath, gently ignite and dissolve the cooled residue in 16 ml of bromimated hydrochloric acid and 45 ml of water. Remove the excess of bromine with 2 ml of stannous chloride solution AsT. The resulting solution complies with the limit test for arsenic, Appendix 3. 9 (3 ppm). Heavy metals Not more than 20 ppm, determined by Method A, Appendix 3. 12, on 25 ml of a solution prepared in the following manner. Mix 2.0 g with 5 ml of 0.1 M hydrochloric acid and 45 ml of water, warm gently until solution is complete and cool to room temperature. Related substances: Carry out the method for thin-layer chromatography, Appendix 4. 6, using silica gel GF254 as the coating substance and a mixture of 40 volumes of 1-butanol, 30 volumes of chloroform, 10 volumes of strong ammonia solution and 3 volumes of acetone as the mobile phase Apply separately to the plate 10 ul of each of the following solutions of the substance being examined in a mixture of 3 volumes of chloroform and 2 volumes of methanol containing (1) 2.0% w/v and (2) 0. 010% w/v. After removal of the plate, allow it to dry in air and examine under ultra-violet light [254 nm). Any secondary spot in the chromatogram obtained with solution (1) is not more intense than the spot in the chromatogram obtained with solution (2) Sulphated ash: Not more than 0.1 %, Appendix 3.22 Loss on drying Not more than 0.5% (for the anhydrous form) and 8.5% (for the monohydrate form), determined on 1 g by drying at 100° for 1 hour, Appendix 8.6 Assay: Weigh accurately about 0 18 g and dissolve with warming in 5 ml of anhydrous glacial acetic acid. For Caffeine Hydrate, use material previously dried at 100° to 105°. Cool, add 10 ml of acetic anhydride and 20 ml of toluene and carry out Method A for non-aqueous titration, Appendix 3.45, determining the end-point potentiometncally. Perform a blank determination and make any necessary correction Each ml 0 1 M perchloric acid is equivalent to 0.01942 g of C8H10N4O2CALAMINE Prepared Calamine Calamine is Zinc Oxide with a small proportion of ferric oxide Category: Topical protectant. Description: Fine, amorphous, impalpable, pink or reddish-brown powder. Solubility Insoluble in water. Practically completely soluble in mineral acids. Storage Store in well-closed containers. STANDARDSCalamine contains not less than 98.0 per cent and not more than 100. 5 per cent of ZnO, calculated with reference to the ignited substance. Identification A Shake 1 g with 10 ml of dilute hydrochloric acid and filter, the filtrate gives the reactions of zinc salts, Appendix 3.1.B:To 1 g add 10 ml of dilute hydrochloric acid, heat to boiling and filter To the filtrate add a few drops of ammonium thiocyanate solution, a reddish colour is produced Acid-insoluble substances: Not more than 1% w/w, determined by the following method Dissolve 1g in 25 ml of warm dilute hydrochloric acid. If any insoluble residue remains, filter, wash with water, dry to constant weight at 105°, cool and weigh Alkaline substances: Digest I g with 20 ml of warm water, filter and add 2 drops of phenolphthalem solution to the filtrate. If a red colour is produced, not more than 0 2 ml of 0 05M sulphuric acid is required to decolorise it. Water-soluble dyes: Shake 1 g with 10 ml of water and filter, the filtrate is colourless, Appendix 6.2 Ethanol-soluble dyes: Shake 1 g with 10 ml of ethanol (90%) and filter, the filtrate is colourless, Appendix 6.2 Arsenic: Dissolve 1.25 g in 15 ml of brominated hydrochloric acid AsT, add 45 ml of water and remove the excess ofbromme with a few drops of stannous chloride solution AsT The resulting solution complies with the limit test for arsenic, Appendix 3.9 (8 ppm). Lead Dissolve 2.0 g in a mixture of 20 ml of water and 5 ml of glacial acetic acid, filter and add 0 25 ml of potassium chromate solution, the solution remains clear for 5 minutes Calcium Dissolve 0.5 g in a mixture of 10 ml of water and 2 5 ml of glacial acetic acid by warming on a water-bath, if necessary and filter. To 0.5 ml of the filtrate, add 15 ml of dilute ammonia solution and 2 ml of a 2 5% w/v solution of ammonium oxalate and allow to stand for 2 minutes, the solution remains clear.Soluble barium salts: To the remainder of the filtrate obtained in the test for Calcium add 2 ml of IM sulphuric acid and allow to stand for 5 minutes, the solution remains clear. Chloride: Dissolve 0.33 g in water with the addition of 1 ml of nitric acid and dilute to 30 ml with water. The resulting solution complies with the limit test for chlorides, Appendix 3.10 (750 ppm). Sulphate: Dissolve 0 :1 g in water with the addition of 3 ml of 2M hydrochloric acid, filter and dilute to 60 ml with water The resulting solution complies with the limit test for sulphates, Appendix 3 15 (0 6%) Loss on ignition

CHOICE OF PSYCHOTHERAPY - would depend upon - (a) Factors related to the patient

psychotherapy - Unlike reconstructive psychotherapy, no insights are offered and therapy is directed towards correction of patient's maladaptive behavioural patterns. Behaviour therapy is a form of re-educative psychotherapy. 3. Supportive psychotherapy - Here attempts are made to strengthen a patient's existing defences by simple guidance and reassurance CHOICE OF PSYCHOTHERAPY - would depend upon - (a) Factors related to the patient - Age, intelligence, motivation for treatment, ability to express emotions, willingness to establish a relationship with the therapist, etc. (b) Factors related to the therapist - Training and skill of therapist to administer a particular type of therapy. (c) Psychiatric diagnosis - Circumscribed or stress-related psychiatric problems would require re-educative or supportive therapies, while neurotic disorders especially when associated with personality difficulties may benefit from re-constructive psychotherapy. ADDENDUM Chronic fatigue syndrome (CFS) Definition A condition of severe fatigue as a principal complaint associated with other somatic symptoms and considerable disability, but with no clear-cut biomedical diagnosis .Etiology; Uncertain. Some patients show immunological abnormalities. CFS can occur after infection. Risk factors are - (a) Previous psychiatric illness. (b) Encephalitis or other causes of nervous damage. (c) Lack of physical fitness. Cl. Fs. - Excessive physical and mental fatigue brought on by physical or mental effort, and with associated functional disability, for which a conventional biochemical cannot be found Symptoms may overlap with some psychiatric disorders such as depression .Tr. - None specific. Ant i depress ants in depressive illness .Rehabilitation is the mainstay of treatment. Cautious increases in physical activity. Factitious disorders These are characterised by physical or psychological complaints symptoms that are intentionally produced or feigned in order to assume the role of the sick patient Munchausen's syndrome is an uncommon, extreme and dangerous subtype of factitious disease, characterised by pathological lying, the deliberate use of self-induced symptoms to gain hospitalization, and wandering from hospital to hospital, even to the extent of undergoing numerous laparotomies for abdominal pain. Other more common factitious disorders are dermatitis artefacta, self-induced fevers and infections, haemorrhage and bleeding disorders, factitious diarrhoea and hypoglycemia 12.SKIN DISEASES A INFECTIONS. Ectoparasite Infections Scabies Definition: A contagious disease caused by a mite, Sarcoptes scabiei, disease is spread through contact with infected individuals, or rarely through contact with infected clothes, bed linen or towels. LIFE CYCLE -The fertilized female excavates a sloping tunnel (burrow) in the stratum corneum, depositing eggs and then dying in the burrow. The larvae emerge from the eggs after 3-7 days, wander to the skin surface and form shallow pockets in the horn of the original or a new host, and reach maturity 14-17 days after the eggs were laid. Copulation occurs in the pocket and the female excavates her burrow, while the male soon dies. Clinical features: Pruritus - The sole complaint is severe itching worse at night.The nocturnal pruritus may be regarded as suggestive of scabies but not pathognomonic Itching starts two to four weeks after the contagion, this time lag being required for the development of lesions other than the burrow. Scabies is suspected by the fact that several members of the family are itching at night. The burrow - is the diagnostic sign of scabies It is a slightly elevated grayish tortuous or dotted line in the skin. It represents a tunnel made by the female mite in the horny layer of the skin in which to lay her eggs.Burrows are best seen in the soft parts of the skin.Scratching destroys the roofs of the burrows.Other lesions such as follicular papules, papulopustules, and excoriation marks are more commonly seen.The sites of predilection for the lesions are the interdigital folds, flexor aspect of the wrists, the elbows, anterior axillary folds, around the nipples, umbilicus, lower abdomen, genitalia, buttocks, medial aspects of the thighs, legs and feet.The face and neck are spared except in children. If scabies is untreated for some period of time, various complications may arise Complications:1 Eczematization.2. Secondary infection.3. Id eruption. 4. Urticaria. 5. Contact dermatitis to antiscabetic drugs. Variants of Scabies: (a) Scabies in clean individuals. (b) Scabies incognito - occurs in persons treated with steroids. (c) Nodular scabies. (d) Animal scabies. (e) Norwegian scabies - Crusted form of severe scabies in persons with low immunological status Differential Diagnosis - Similar signs are found with papular rashes from fleas, including papular urticaria, also atopic skin lesions in young children with maximal lesions on extremities, generalised pruritus, delusions of parasitosis (parasitophobia), dermatitis herpetiformis, sarcoptic mange from pets Management : 1 All the family members should be treated at the same time.2.The clothes, bed linen andtowels should be boiled and ironed. 3. Secondary infection should be treated first. 4. Specific therapy - The patient must bathe and scrub the body with a brush to lay open the burrows. After the bath, the skin is dried and the scabicide applied from neck to toes. Avoid in

Milder than Rocky Mountain spotted fever. Primary cutaneous lesion or eschar at the site

BOUTONNEUSE FIEVRE - Milder than Rocky Mountain spotted fever. Primary cutaneous lesion or eschar at the site of tick bite Regional lymphadenopathy in glands draining the eschar. Maculopapular rash. Fever subsides by lysis in 2nd week RICKETTSIALPOX - caused by R akari, transmitted to man by blood-sucking mite. Fever, eschar and papulovesicular eruption Recovery in 1-2 weeks without sequelae. Diag. - Serology: MIF Rickettsia of the spotted fever group are antigenitically cross-reactive and the same antigen may be used to detect all species. A titre of 128 is diagnostic. Tr. - Doxycycline 200 mg/day, for 1-7 days depending on severity. Q-fever - Casual organism coxiella burnetti. Transmission - is directly from infected animals (goats, sheep or cats). Common route of human infection is inhalation of infected dust or aerosol, however consumption of contaminated milk products from sheep and goats and handling of meat are risk factors. Cl.Fs. - Infection may be asymptomatic, chronic or acute. Incubation period - 2-4 weeks Two major types of acute disease are pneumonia and purely febrile form Other presentations include meningitis, meningoencephalitis, exanthema, myocarditis, pericarditis and jaundice. Complete recovery may take months Chronic - Fever is characterised mainly by blood-culture negative endocarditis Diag - (a) MIF test. (b) Complement fixation - Single tit re of 1:64.Tr. - Doxycyline, rifampicin or ofloxacin for 3 weeks. Immunization - Vaccine consisting of a killed suspension of Rickettsia prowazeki cultured in yolk sac.Course of two injections of 1 ml. each at 7-10 day intervals Immunity relative, lasting for 6-8 months Booster injection of 0.5 ml.every year 10 RABIES Definition - Rabies is an infective disease caused by RNA-containing virus of the Rhabdoviridae family. It is primarily a zoonosis but is occasionally transmitted to man by animal bites, resulting in an encephalomyelitis which is nearly always fatal. Epidemiology - VIRUS - RNA neurotropic virus, genus Lyssavirus.TRANSMISSION -The virus can penetrate broken skin and intact mucous membranes (a) Animal bites - (i) Occurring in wild life and maintained by mammals such as wolves, mongooses, accoons, foxes and jackals, and by bats. (ii) Urban type - in which the dog mainly is responsible though during epidemics other domestic animals such as the cat and cattle may be infected. (b) Inhalation - extremely rare.Visiting caves inhabited by insectivorous bats, or following laboratory accidents with aerosols of fixed virus. (c) Person-to-person - transmission - by corneal grafts. Clinical features - Incubation period -varies from 20 days to 90 days in majority. Varies with - (i) Age - shorter in children (ii) Site of infection - Face about 30 days, hands 40 days, legs 60 days. (iii) Severity of wound. (iv) Animal - shorter period in order - wolf, cat, dog. Prodromal symptoms - Pain and irritation or discomfort at site of bite, fear and anxiety, depression, intolerance to loud sounds Periods of irritability Hoarseness of voice and sense of constriction in throat with difficulty in swallowing.Slight rise of temperature Duration 1 -2 days Subsequently, symptoms of either furious or paralytic rabies develop, depending on whether the spinal cord or brain are predominantly infected Furious rabies - (a) Hydrophobia - a combination of inspirator/ muscle spasm, with or without painful laryngopharyngeal spasm, associated with terror in response to attempts to drink water. Various other stimuli can excite the reaction, including a draught of cold air (aerophobia), and the sight, sound or mere mention of water. Hydrophobic spasms may end in opisthotonos and generalised convulsions with death from respiratory or cardiac arrest. (b) Periods of excitement - are common during which the patient becomes wild and hallucinated alternating with lucid intervals. (c) Other features - include meningism, cranial nerve lesions (especially III, VII, VIII), spasticity, involuntary movements, fluctuating body temperature and blood pressure, signs of autonomic overactivity such as salivation, sweating and tachycardia. Priapism Death may occur during hydrophobic spasm or patient, may lapse into coma and generalised flaccid paralysis. Paralytic rabies - is rare and seen especially in those bitten by vampire bats. Flaccid paralysis often begins in the bitten limb and ascends symmetrically or asymmetrically until it involves muscles of deglutition and respiration killing the patient in 2 or 3 days. Hydrophobia is unusual but a few spasms may occur late in the illness Laboratory Diagnosis - In the animal - responsible for the bite, rabies can be confirmed within a few hours by immunofluorescence of brain impression smears or histological examination for Negri bodies, and in about one week by intracerebral inoculation of mice with a suspension of the animal's brain tissue. In patients - Rabies can be confirmed early in the illness by immunofluorescence of skin biopsy, or corneal impression smear or brain biopsy and by virus isolation from saliva and other secretions. Fluorescent antibodies are not detectable in serum or CSF before the eight day. Management Aim is to neutralise the inoculated virus before it can enter the nervous system 1. Treatment of wound - (a) Scrub with soap (or detergent) and water under a running tap for atleast 5 minutes. (b) Remove foreign material. (c) Rinse with plain water (d) Irrigate with

A.C.A.C.I.A. POWDER. Acacia Powder is Acacia in powder form. Description

ACACIA Gum Anacia, Indian GumAcacia is the dried, gummy exudation from the stem and branches of Acacia nilotica (Linn. ) Del. subsp indica (Benth .) Brenan (syn. A arabica Willd var. indica Benth. ) (Fam Leguminosae), or other species of Acacia. Category; Pharmaceutical aid (emulsifying and suspending agent). Description; Irregular and broken pieces (tears) of varying size, yellow, sh-white, yellow or amber in colour, with numerous minute fissures, brittle fractured surface, glassy and occasionally iridescent, odourless Solubility; Almost entirely soluble in twice its weight of water yielding a very viscous, slightly acidic solution which is slightly glairy and, when diluted with more water and allowed to stand, yields a very small amount of gummy deposit, practically insoluble in ethanol (95%) and in ether. Storage; Store in tightly-closed containers, protected from moisture STANDARDS Identification ;A: An aqueous solution is gelatinised by the addition of lead subacetate solution. B: To 5 ml of a 10% w/v solution add gradually, while shaking, 10 ml of ethanol (95%) The cloudy liquid, on addition of 0 .5 ml of acetic acid, gives a white precipitate Filter and add to the clear filtrate 50 ml of ammonium oxalate solution, the filtrate becomes cloudy. C: A 10% wA/ solution is either dextro- rotatory or slightly Iaevo-rotatory. Sterculia gum and agar. To 50 mg of the powdered substance being examined add 0.2 ml of freshly prepared ruthenium red solution and examine microscopically, the particles do not'acquire a red colour after irrigation with water. Agar and tragacanth To 10 ml of a 10% w/v solution add 02 ml of lead acetate solution, no precipitate is produced Starch and dextrin; Boil 10 ml of a 1 0% w/v solution and cool, add 0 .1 ml of O. O5M iodine, no blue or brown colour is produced .Tannins; To 10 ml of a 10% w/v solution add 0.1 ml of ferric chloride test solution, a gelatinous precipitate is formed, but neither the precipitate nor the liquid "shows a dark blue colour. Sucrose and fructose; To 1 ml. of a 1 0% w/v solution add 4 ml of water, 0 .1 g of resorcinol and 2 ml of hydrochloric acid and heat on a water-bath, no yellow. or pink colour develops. Water-insoluble matter; Dissolve 5 g of a fine powder in about 100 ml of water in a 25Q-m1 Ehenmeyer flask, add 10 ml of dilute hydrochloric acid and boil gently for 15 minutes. Filter by suction while hot through a sintered-glass crucible,previously tared, wash thoroughly with hot water, dry at 105° and weigh, the residue does not exceed 50 mg. Sulphated ash; Not more than 5 0%, Appendix 3.22. Acid-insoluble ash; Not more than 1. 0%, determined on 1 g. Appendix 3; 39 Loss on drying; Not more than 15 .0%, determined on 1 g by drying in an oven at 105°, Appendix 8. 6. Microbial limits; 1. 0 g is free from Escherichia coli. Appendix 9.4.A.C.A.C.I.A. POWDER. Acacia Powder is Acacia in powder form. Description; White or yellowish-white powder, odourless, on treatment with water it dissolves to give a mucilaginous liquid which is colourless or yellowish, dense, viscous, adhesive and translucent .Solubility; As stated under Anacia Storage; Store in tightly-closed containers, protected from moisture . STANDARDS Identification, Sterculia gum and agar, Agar and tragacanth, Starch and dextrin, Tannins, Sucrose and fructose, Water-insoluble matter, Sulphated ash, Acid-insoluble ash,

Hemophilus influenzae meningitis - common in children under

leptomeninges caused by infectious agents, however infiltration of the, meninges by leukaemic or other malignant cells also produces inflammatory meningitis For bacterial meningitis, peak age of incidence is less than 5 years Neonates, particularly premature are at particular risk. Mechanism of infection - Pathogens usually gain access to the meninges through the blood stream. Most of the organisms causing bacterial meningitis are commonly carried in the upper respiratory tract, and there is evidence that invasion is triggered or facilitated by a coincident infection with a second pathogen (e g. influenza virus) causing mucosal damage or an immunosuppressive effect. Infectious causes of meningitis Bacterial Naegleria Aseptic meningitis - (a) Viral - e.g. HSV 2, polio. (b) Partially treated pyogenic meningitis (c) Non-infective causes - (1) Vasculitis (esp SLE) (ii) Meningeal carcinomatosis. (iii) Sarcoidosis. (iv) Bechet's/whipple's disease. VogtKoyanagi syndrome. (d) Specific infections in which causative agent may not be identified on ordinary microscopy or culture - TB or cryptococcal meningitis, neurosyphilis, leptospirosis, brucellosis.(e) Parameningeal suppuration. Clinical Features - In meningitis of any etiology the clinical features relate to three causes - 1. Infection - Fever, rigors, toxemia. 2. Increased intracranial pressure - Headache, nausea, vomiting, deterioration of consciousness and convulsions. 3. Meningeal irritation and inflammation - Neck rigidity, positive Kernig's sign, photophobia. ACUTE BACTERIAL MENINGITIS 1. Meningococcal- meningitis Etiology - Age - predominantly in children and young adults, more often during winter epidemics. Transmission - by way of nasopharynx. Carriers are the principal source of transmission. Acquisition is followed by meningitis and septicemia. Incubation period - 1 to 5 days. Clinical features -1. STAGE OF INVASION -Abrupt onset with severe headache, vomiting of cerebral type, fever, pains in neck and back, rigors or in children convulsions, restlessness, insomnia, delirium. 2. MENINGEAL STAGE - (a) More severe headache, intense lumbar pain. (b) Muscular rigidity - Neck rigidity, head retraction. Kernig's and Brudzinskis signs, sometimes muscular twitchings and tremors (c) Ocular symptoms - include optic neuritis, uveitis or purulent choroiditis usually unilateral. Optic atrophy may result particularly in association with hydrocephalus. Conjunctivitis and corneal ulcers. (d) Rash - Erythematous macules which soon become petechial (spotted fever). Petechiae in the conjunctivae. (e) Temperature variable, usually more than 30°C. (f) Exaggeration of deep jerks. (g) Retention of urine and constipation. (h) Herpes febrilis. (i) Pulse -slow in relation to temperature, may be irregular. (j) Rapid emaciation. DIAGNOSIS - (a) Leucocytosis - 20,000-30,000 per c. mm. (b) CSF - Turbid or purulent, under pressure, large number of pus cells mainly polymorphs , and presence of meningococci on smear or culture. (c) Polymerase chain reaction-(PCR)-based identification of bacterial pathogens in cellular CSF increases menigococcal diagnostic rates. Complications and sequelae - 1 Septicemia - Meningitis is associated with meningococcal septicemia and the organism may settle in lungs, bones, joints or eyes causing focal infection. 2. Arthritis - either purulent occurring early in the illness, or arthritis of later onset, possibly due to immune reaction. 3. Neurological - (a) Cerebral oedema of severe degree causing fluctuating neurological signs. (b) Focal neurological damage -e.g. deafness. (c) Psychiatric problems and mental retardation. (d) Hydrocephalus - rare 4 Cardiovascular - Myocarditis. 5. Waterhouse-Friderichsen syndrome - from haemorrhagic necrosis of both adrenals. Circulatory failure, cyanosis and widespread petechiae or purpura. Circulating steroid levels are usually high 6. DIC - often present Treatment - Benzylpenicillin 20-30 mg/kg 4-houhy for 5-7 days. If penicillin allergy. Cephalosporin (e.g. cefotaxime 1-2g i.v. 12 hrly). PROPHYLAXIS - Penicillin does not eradicate the organism from nasopharynx. Patient, and any close contacts should be given rifampicin 10 mg/kg b. d for 2 days. Ciprofloxacin 500 mg in a single dose, if rifampicin is contraindicated Menigococcal vaccine (A and C. and W 135) can be given. 2. Pneumococcal meningitis -associated with lobar pneumonia, rarely with chronic otitis media, sinusitis or head injury. Muscular spasms common More severe toxemia. CSF thick greenish fluid Gram positive diplococci in CSF and blood, or detection of pneumococcal antigen in CSF. Tr. - Penicillin or cefotaxime/ceftriaxone for atleast 7 days and continued till patient is apyrexial for 48 hrs. VACCINATION - Vaccine is effective and should be given to all patients in high-risk groups, other than neonates, in whom it is of limited efficacy. Patients undergoing splenectomy should be immunized before surgery. 3. Hemophilus influenzae meningitis - common in children under 5. Preceding or accompanying infection of respiratory or ear infection. The illness often develops insidiously with drowsiness and irritability. Subdural effusion is a common complication and may cause convulsions or become infected. CSF purulent with a high protein and polymorph count and low sugar. H. influenzae - Can be seen and grown on culture. Tr. - Benzylpenicillin parenterally, or if allergy to penicillin cefotaxime or

surface antigens. Pattern of infection - Major outbreaks can be caused by any of the three types or subtypes, but

organisms on culture. (d) Cryptococcal - caused by cryptococcus neoformans mainly in patients with depressed immunity e. g. corticosteroids, diabetes, lymphoproliferative disorders, AIDS and infection in immuno-compromised patient. Symptoms occur intermittently over weeks and meningism is less common than confusion and depressed consciousness. Diagnosis by presence of C. neoformans in CSF, or detection of cryptococcal antigen. Tr. - Amphotericin B 0. 6-1 mg/kg/day iv or combination of amphotericin B 0. 3 mg/kg/day plus flucytosine 150 mg/kg/day. Fluconazole for cryptococcal meningitis in AIDS. (e) Acute syphilitic meningitis - (a) Mostly young men, (b) history of primary infection 1 -2 years ago, (c) may follow inadequate treatment or occur during specific therapy, (d) CSF - 1,000 or 1,500 cells, 30% or more polymorphs. CSF and blood serological tests for syphilis positive. (f) Leptospiral meningitis - (a) History of occupational relationship to rats. (b) Liver may be enlarged. (c) Jaundice may appear. (d) Conjunctival injection. (e) Hemorrhages common. (f) CSF - Leptospira may be demonstrated by culture. (g) Brucellosis - Meningitis is an uncommon complication of acute brucellosis. CSF besides lymphocytosis shows elevated protein and reduced sugar leve.l (h) Lyme disease - due to infection with spirochetal bacterium - Borrelia burgdorferi. Meningitis may be associated with erythematous rash called erythema chronicum migrans. Tr. - Tetracycline or penicillin. (i) Carcinomatous meningitis - More common in leukemias and lymphomas. Combination of altered mental state (e.g. confusion), cranial nerve signs (commonly optic, facial and those supplying eye muscles). Papilloedema common Back and limb pain due to radiculopathy. Also depressed reflexes, muscle wasting and sensory loss. Defferential Diagnosis of meningitis A Meningism - Neck stiffness in presence of normal CSF. May be seen occasionally usually at onset, in typhoid fever, apical pneumonia, acute exanthema, acute pyogenic tonsilitis, pyelo-nephritis or cervical lymphadenopathy. Meningitis common and more extensive Lumbar puncture at once differentiates 2. Acute disseminated meningoencephalitis - due commonly to HSV. Begins with features of acute meningitis and progresses rapidly to irritability, confusion, focal fits, coma and death. 3. Post-infectious meningoencephalitis- Rare sequel of measles or influenza, or less frequently chicken pox, mumps or rubella, and vaccines. Reccurent meningitis: Predisposing causes - (a) CSF leakage from prior head injury or congenital malformation predispose to recurrent pneumococcal meningitis. (b) Immunological defects may predispose to meningococcal disease. (c) Patients with primary antibody deficiency have susceptibility to enterovirus infections of CMS. (d) Echovirus infection may cause a progressive chronic meningoencephalitis 4 INFLUENZA Etiology - Causative agent - There are three immunological types of influenza viruses - two subtypes of A, A (H3N2) and A(H1,N1), and type B. The type A subtypes can be distinguished from each other by differences in their haemagglutinin (H) and neuraminidase (N) surface antigens. Pattern of infection - Major outbreaks can be caused by any of the three types or subtypes, but type A(H3N2) cause large scale mortality Individuals of all ages may be affected by this subtypes, but type B viruses principally infect children, adults less frequently In each patient, characteristics of influenza caused by the different virus types overlap such an extent, that determination of the virus involved is possible only through laboratory studies or knowledge of the

corresponding to that due to barbalom in the chromatogram obtained with solution

A: The light absorption in the range 230 to 360 nm of the solution obtained in the Assay exhibits a maximum only at about 250 run, Appendix 5.5. B: Comply with the test D described under Allopunnol. Related substances: Compfy' with the test described under Allopunnol using as solution (1) a solution prepared by shaking a quantity of the powdered tablets equivalent to 0.25 g of Allopunnol with 10 ml of strong ammonia solution and filtering. Disintegration: Maximum time, 30 minutes, Appendix 7.1. Other requirements Comply with the requirements of tests stated under Tablets. Assay: Weigh and powder 20 tablets. Weigh accurately a quantity of the powder equivalent to about 0 1 g of Allopunnol and shake with 20 ml of 0 05M sodium hydroxide for 15 to 20 minutes, add 75 ml of 0 1 M hydrochloric acid shake for 1 0 minutes, add sufficient 0.1 M hydrochloric acid to produce 250.0 ml, filter and dilute 5 0 ml of the filtrate to 250.0 ml with 0.1 M hydrochloric acid. Measure the absorbance of the resulting solution at the maximum at about 250 nm, Appendix 5.5, using 0.1 M hydrochloric acid as theblank. Calculate the content of C5H4N4O, taking 563 as the value of A(1%, 1 cm) at the maximum at about 250 nm. ALOESAIoes is die dried juice of the leaves of Aloe barbadensis Miller (A. vera Linn), known in commerce as Curacao Aloes or Barbados Aloes, or of A ferox Miller and hybrids of this species with A. africana Miller and A. spicata Baker, known in commerce as Cape Aloes (Fam. Lihaceae). Indian Aloes of commerce is obtained from A barbadensis. Category: Laxative. Description: Unground Curacao Aloes - Brownish-black, opaque masses; fractured surface uneven, waxy and somewhat resinous; odour, strong and characteristic. Unground Cape Aloes - Dark-brown or greenish-brown to olive-brown masses; fractured surface shiny and conchoidal; odour, strong and characteristic. Solubility: Soluble in hot ethanol (95%); partly soluble in boiling water; practically insoluble in chloroform and in ether. Powdered Aloes is almost entirely soluble in ethanol (60%). Storage: Store in tightly-closed, light-resistant containers, protected from moisture Labelling: The label states whether it is Curacao Aloes or Cape Aloes. STANDARDSAIoes contains not less than 50.0 per cent of water-soluble extractive. Curacao Aloes contains not less than 18. 0 per cent and Cape Aloes not less than 28.0 per cent of hydroxyanthracene derivatives, calculated as anhydrous barbaloin. Identification Mix 0 5 g with 50 ml of water, boil until nearly dissolved, cool, add 0.5 g of silica gel and filter. On the filtrate carry out the following tests .A: Heat 5 ml with 0.2 g of borax until dissolved, add a few drops of this solution to a test-tube nearly filled with water, a green fluorescence is produced. B: Mix 2 ml with 2 ml of bromine water, a pale yellow precipitate is produced. The supernatant liquid is violet with Curacao Aloes; no such violet colour appears with Cape Aloes. C: Mix 5 ml with 2 -ml of nitric acid; with Cape Aloes a reddish-yellow colour is produced; with Socotrme Aloes a pale brownish-yellow colour is produced; with Cape Aloes a yellowish-brown colour passing rapidly to green is produced. D: Carry out the method for thin-layer chromatography, Appendix 4.6, using silica gel G as the coating substance and a mixture of 100 volumes of ethyl acetate, 17 volumes of methanol and 13 volumes of water as the mobile phase. Apply separately to the plate S µl of each of the following solutions, as bands 20 mm long and not more than 3 mm wide For solution (1) heat 0.5 g, in powder, with 20 ml methanol to boiling on a water-bath, shake well, decant the supernatant liquid, keep at 4° and use within 24 hours For solution (2) dissolve 50 mg of barbalom in 10 ml methanol. After removal of the plate, allow it to dry in air, spray with a 10% w/v solution of potassium hydroxide in methanol and examine under ultra-violet light (365 nm). The chromatogram obtained with solution (2) shows a yellow band with an Rf value of 0.4 to 0.5. In the case of Curacao Aloes, the chromatogram obtained with solution (1) shows a yellow flu orescent band corresponding to that due to barbalom in the chromatogram obtained with solution (2) and in the lower part a light blue fluorescent band (corresponding to aloesine). In the case of Cape Aloes, solution (1) shows a yellow fluorescent band corresponding to that due to barbalom in the chromatogram obtained with solution (2) and in the lower part two yellow fluorescent bands (due to alomosides A and B) as well as a blue fluorescent band (due to aloesine). Heat the plate at 110° for 5 minutes. In the case of Curacao Aloes, with solution (1) a violet fluorescent band appears just below the yellow band corresponding to barbalom while in the case of Cape Aloes no such violet band appears. Ethanol-msoluble substances: Weigh accurately about 1 g, in fine powder, and add to 50 ml of ethanol (95%) in a flask. Reflux the

Multiple sclerosis, neuromyelitis optica, acute disseminated encephalomyelitis. 4. Heredofamilial/Degenerative diseases

Delayed myelopathy may follow after some years. Other features include low hair line, short neck and restricted neck movements (Field's triad). Dysplastic face, associated congenital anomalies and absence of cranial nerve palsies. Diagnosis - is made from radiographs of neck in flexion and extension. Treatment - Surgical fusion of atlanto-axial joint. 2. Basilar invagination - Displacement of dense of axis into foramen magnum Usually presents as picture of posterior fossa lesion. Clinical features - LoSwer cranial nerve palsies, cerebellar signs, spinothalamic variety of sensory loss over the arms, and signs of increased intracranial pressure. Radiography - Dense of axis is seen to extend above a line drawn from the posterior end of hard palate to posterior tip of foramen magnum. 3. Occipitalization or fusion of other cervical vertebrae - (Klippel-Feil anomaly) - Usually asymptomatic. Signs due to other associated anomalies. 4. Arnold Chiari malformation - The medulla and cerebellum are elongated and extend down through the foramen magnum Usually presents with cerebellar signs and syringomyleia or syringobulbia-like clinical picture. Spina bifida frequent. Non-compressive spinal cord syndromes (Non-compressive myelopathy - NCM) Myelopathy is a generic name for specific disorders of the spinal cord by a heterogenous group of conditions in which there is acute, subacute or chronic involvement of the sp.cord with or without involvement of nerve roots (Myeloradiculopathy) or peripheral nerves (Myeloneuropathy). Causes 1. Infections (a) Viral - Poliomyelitis, rabies, herpes zoster/varicella, mumps, viral hepatitis, EV 70, AIDS (b) Bacterial/spirochetal - Bacterial meningitis, tuberculosis, typhoid, syphilis. (c) Parasitic - Malaria (falciparum), schitosomiasis. 2. Immuno-Allergic (post and parainfectious) - Influenza and other viral infections, post-exanthematous (measles, varicella), post-vaccinal (rabies, poliomyelitis) 3 Demyelinating diseases - Multiple sclerosis, neuromyelitis optica, acute disseminated encephalomyelitis. 4. Heredofamilial/Degenerative diseases - MND, heredo-familial spastic paraplegia, spino-cerebellar ataxia, syringomyelia. 5. Toxic myelopathy - Neurolathyrism, intrathecal injections (chemotherapeutic agents, penicillin, spinal anaesthetics), contrast media, TOCP, arsenic, SMON. 6. Vascular disorders - Anterior spinal artery infarction, dissecting aneurysm of aorta, angiography, SLE, PAN, vascular malformations (angiomas, AV malformations). Physical agents - Irradiation myelopathy, electrical injury to sp.cord. 8. Metabolic/Nutritional -Vitamin B12 deficiency, pellagra, myelopathy of Chronic liver disease, adrenomyeloneuropathy. 9 Tropical spastic paraplegia - HTLV-1 associated myelopathy. 10. Intramedullary tumours - Astrocytoma, ependymoma, lipoma, haemangioma, metastasis. 11. Carcinomatous myelopathy (Non-metastatic manifestation). Acute syndromes: 1. Post-infectious transverse myelitis - following infection of upper respiratory tract or post-varicella, measles, mumps, syphilic or post mycoplasma. Raely SLE 2 Multiple sclerosis - develops hours or days, usually with a partial cord syndrome. Partial or complete remission over several weeks. 3. Anterior spinal artery infarcts - develop over minutes to hours. There is paraplegia with dissociated anaesthesia. As a rule, there is little recovery. 4. Trauma - Sudden onset of weakness or complete paralysis following injury to sp cord 5. Epidural abscess- Suppurative process elsewhere in the body, fever, backache and vertebral tenderness. II: Chronic syndromes 1. Multiple sclerosis - 10% of patients present with slowly progressive neurological

protein helps generation of excess heat due to its SDA (specific dynamic action). For this, people living m cold

s of food values due lo cooking must get due consideration. In addition, digestibility of a food also should be considered. The water intake should be sufficient. However, in general, water is not considered as a food. Calorie need This must be satisfied. Question arises what is the calorie need of a given individual (whose diet is to be formulated) and how to calculate it ? General principles are described first. In an adult healthy man (= a man who is not gaming or losing body weight) the calorie intake = the calorie expenditure. Again, the calorie expenditure = BMR + extra calories expended during various works. BMR in a healthy adult person can be calculated, as stated before (chap. 7. 3) in short, BMR is 40 K cal or 37 K cal, per sq m per hour in males and females respectively. The determination of the body surface area has also been discussed in chap. 7. 3 How to calculate the extra calories expended ? Various methods are known although none is fully satisfactory for routine use. Most of them are applicable for a homogeneous community living, in, say, military or police barracks. Their work loads, ambient temp, etc. being known, the total calories can be calculated and from them, the extra calories needed per head can be found out. Another method is to compare with a so called 'reference man'. For example, for India, a hypothetical man, called the ICMR man (Indian Council of Medical Research) has been imagined who represents the 'average' Indian in an 'average' Indian ambient temperature The parameters of the particular person, whose diet is going to be formulated, can be compared with those of the ICMR man (the reference man), that is, his body surface area, ambient temp work routine are to be compared with the ICMR man and differences in those parameters found out. There are formulae which can now be applied to determine how much addition or subtraction of calories need be made for those differences. However, this cannot be a very practical method for routine use by a practising physician. One of the most universally applied practical method for the masses is to keep a weight chart of the person concerned. The person (who is, say, healthy adult) is allowed to eat as much as he likes (i.e. 'his appetite governs the amount of food'). Subsequently if he begins to develop obesity, the calories are cut down. Or if there is loss of body weight, calories are added However, in case of growing children this should lead to normal growth .In this connecton, it is important to have a gross idea about the calorie requirement at the beginning. Heavy manual workers (wood choppers, earth diggers, rickshaw pullers, sportsmen undergoing training for the tournament for every hour of their heavy1 muscular work, expend around 570 Kcallhr (= 2,400 Kmr) or more. Values for light and moderate works are also available. Examples of light works are shaving, dressing and light domestic works. Examples of moderate works are walking at brisk pace, soil tilling in agriculture and so on The interested reader can consult special books*. Like the ICMR man there is a FAO' (Food and Agricultural Organization, under the United Nations) man, who is an international man, or 'British reference man' (and indeed various other reference man and woman for different countries). On an 'average', moderately working healthy adult male Indians require about 2200 Kcallday. Excess intake of calories will lead to as stated earlier, obesity, whereas the reverse produces starvation; both the conditions have been discussed towards the end. The principle of'appetite governing the amount of food to be taken'works excellently with the animals. The animals, when given a free access to food, will eat only that much food required by it, not more not less. However, some human beings are prone to eat excess and develop obesity when they have free access to food (see Obesity, later, this chap). However, there is no easy and practical method (which can be used by the masses), to determine the exact number of calories needed in a given individual. The best method for him is to follow appetite governing the amount of food and watch his own weight (A rough guide for daily calorie requirement in the Western climate, provided the person is healthy adult and only moderate^ working, is between 31 to 35 Kcallkg body wt/day ] Protein Cause of indispensability: Protein of satisfactory quality must be present in the diet, m sufficient quantity. Causes of the md is pens ability of the protein are given below: Protein is required for (i) replenishment of the lost tissues, lost due to wear and tear, (ii) for accretion of new tissue during growth, convalescence and pregnancy, (iii) for synthesis of enzymes (all enzymes are protein m nature), protein hormones (e.g. insulin, parathormone, ADH etc.) and breast milk, (iv) for maintenance of concentration of plasma proteins. These are the reasons, which make food protein, an essential (N.B. essential = indispensable) article of diet Besides these reasons, there are other reasons why protein is needed by the body. (i) Extra heat: protein helps generation of excess heat due to its SDA (specific dynamic action). For this, people living m cold environment like to take extra protein m their diet By the same token, persons living in hot and tropical climates do not like to have excess protein (ii) many persons have a great fascination for such proteins like meat or fish which whets up their appetite. Quality of protein First class and second class proteins: Essential ammo acids Of the 20 ammo acids found m our body, some can be synthesized by the body whereas others cannot be synthe Davidson. S, Passmore. R, Brock. J.F, and Truswell. A: Human Nutrition and Dietetics. 6th edition, Churchill, Livingstone, 1975. sized Those ammo acids which cannot be synthesized, obviously have to be supplied from outside in the form of food Such amino acids, which must be supplied from outside are called essential (i.e., indispensable) amino acids The students of Sir A. V. Hill devised a simple way to remember the names of essential ammo acids, thus, A. V. HILL, M.P. TT where, A= Arginine, V = Valine, H = Histidine, I = Isoleucme, L = Leucine, L = Lysine M = Methionine, P = Phenylalanine, T = Tryptophan, T = Threonme (total, ten m number). [Sir AN. HILL was a great British physiologist who received a Nobel Prize for his works on muscular contraction. He, in his later part of life, entered politics and became a Member of Parliament (M.P.) from the Tory (today called Conservative) team (T.T.)1. Rose and his colleagues in the 1930s found that, at least for adult human beings, eight (not ten) ammoacids are really essential. They are isoleucme, leucme, lysme, methiomne, phenylalanine, threonine.

add this solution to the prepared silamsed diatomaceous support and evaporate the solvent under reduced pressure

mixture. Dissolve over a 5-hourperiod 0.4 g of low-vapour pressure hydrocarbons (type L) (such as Apiezon L) in 60 ml of toluene, add this solution to the prepared silamsed diatomaceous support and evaporate the solvent under reduced pressure while slowly rotating the mixture. Allow the temperature of the column to increase from 100° to 200° at a constant rate of 6' per minute with the inlet port at 220° and the detector at 300° .Use a flow rate of 30 ml per minute for the carrier gas. Record the chromatogram for at least 2 5 times the retention time of the principal peak The area of any secondary peak is not greater than 0.3% and the sum of the areas of any secondary peaks is not greater than 1 % by normalisation. Sulphated ash: Not more than 0.1 % Appendix 3.22. Water. Not more than 0 5% w/w, determined on 2 g, Appendix 3.24. Assay: Weigh accurately about 0.15 g, dissolve in a mixture of 5.0 ml of 0.01 M hydrochloric acid and 50 ml of ethanol (95%) and titrate with 0.1 M sodium hydroxide determining the end-point potentiometrically. Record the volume used between the two inflections. Each ml of 0.1M sodium hydroxide is equivalent to 0.01S77 g of C10H17,HCI AMANTADINE HYDROCHLORIDE CAPSULESUsual strength : 100 mg. Storage: Store in tightly-closed containers in a cool place. STANDARDSAmantadme Hydrochlonde Capsules contain not less than 95.0 per cent and not more than 105.0 per cent of the stated amount of amantadme hydrochlonde, C10H17N,HCI. Identification: To the contents of one capsule add 2 ml of pentane and shake well. Collect the undissolved solids on a smtered-glass filter, wash with two portions, each of 1 ml, of pentane and dry in air, the residue so obtained complies with the tests described under Amantadme Hydrochlonde. Other requirements Comply with the requirements of tests stated under Capsules Assay Weigh accurately a quantity of the mixed contents of 20 capsules equivalent to about 0.12 g of Amantadme Hydrochlonde and warm in a mixture of 30 ml of anhydrous glacial acetic acid and 10 ml of mercuric acetate solution. Carry out Method B for non-aqueous titration, Appendix 3. 45, using crystal violet solution as indicator. Perform a blank determination and make any necessary correction . Each ml of 0 1M perchloric acid is equivalent to 0.01877 g of C10H17N,HCI. Amikacm is (S)-O-3-amino-3-deoxy- α -D-glucopyranosyl(6)-O-[6-amino-6-deoxy-α-D-glucopyranosyl(1 D4)]N"-(4-amino-2-ydroxy-l-oxobutyl)-2-deoxy-D-streptamine. Category: Antibacterial Dose By intramuscular or slow intravenous injection or by infusion, upto 1.5 g daily, in two divided doses. Description: White crystalline powder, almost odourless. Solubility Sparingly soluble in water. Storage: Store in tightly-closed containers. STANDARDSAmikacm contains not less than 9001µg of C22H43N5O13 per mg, calculated with reference to the anhydrous substance. Identification: A: Carry out the method for thin-layer chromatography, Appendix 4. 6, using silica gel G as the coating substance and a mixture of 60 volumes of methanol, 30 volumes of strong ammonia solution and 25 volumes of chloroform as the mobile phase. Apply separately to the plate 3 µl of each of the following solutions. Solution (1) is a 0.6% w/v solution of the substance being examined. Solution (2) is a 0.6% w/v solution of amikacm RS. Solution (3) is a mixture of equal volumes of solutions (1) and (2). After removal of the plate, allow it to dry in air, heat it at 110° for 15 minutes and immediately spray it with a 1 % w/v solution of mnhydrm in a mixture of 100 volumes of l-butanol and 1 volume of pyndine. The principal pink-coloured spot in the chromatogram obtained with solution (1) corresponds to those in the chromatograms obtained with solutions (2) and (3). B: To 1 ml of a 1 % w/v solution add 1 ml of 2M sodium hydroxide, mix and add 2 ml of a 1 % w/v solution of cobalt nitrate; a violet colour is produced. C: To a solution of 50 mg in 5 ml of water add 4 ml of a 0.035% w/v solution of anthrone in sulphuric acid; a bluish-violet colour is produced. pH: Between 9.5 and 11.5, determined in a 1 % w/v solution in carbon dioxide free water, Appendix 8.11. . Specific optical rotation: Between +97° and +105°, determined in a 2.0% w/v solution, Appendix 8.9. Sulphated ash: Not more than 1.0%, the charred residue being moistened with 2 ml of nitric acid and 5 drops of sulphuric acid, Appendix 3.22. Water: Not more than 8.5% w/w, determined on 0.2 g, Appendix 3.24 Assay Carry out the microbiological assay of antibiotics, Method B, Appendix 9.1, and express the result in µg of Amikacin, C22H43N5O13, per mg. (S)-O-3-amino-3-deoxy-a-D-glucopyranosyl-(1 □6)-O-[6-ammo-6-deoxy- -gluco-pyranosylN'-(4-amino-2-hydroxyoxobutyl)-2-deoxy-D-streptamine sulphate (1:2 or 1:1. 8)(salt). Category: Antibacterial. Dose: By intramuscular or slow intravenous injection or by infusion, upto 1.5 g daily, in two divided doses. Description: White