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Monday, July 20, 2009

Theory: Trading With Little To No Margin

Theory: Trading With Little To No Margin
As I often do, especially when the markets are excruciatingly slow in determining when to make the next significant move, I've been thinking about Forex.Take a mental walk with me...The DOW falls from 10,000 to 5,0000 and loses 50% of it's value. It returns from 5,000 to 10,000 and gains 100% of it's value.Wait, think about that for a minute. In the normal world having the ability to gain double digit gains, per year, is considered excellent.If you are confident that an upward cycle will eventually happen, in a suitable time frame of course, then movement is valuable. If you aren't trading on margin, and you don't have the associated risk, then you can afford to look at each dip in price as an opportunity.While this may be applicable to the DOW, it is ever more applicable to the Forex markets. If you are trading with little or no margin it's simply a matter of scaling your entry and exit based on price moves. This is very similar to the gridding concept that I posted recently.However, when the margin is gone the risk is gone. You choose the price range you expect and scale your entry and exit points within it. If you must, you leave some positions in place while you recapitalize to attack another range. In fact, perhaps you simply allocate a set number of dollars per thousand pip trading range. If the price falls into a lower range you simple ante up and play within a lower range -- while your higher range positions provide interest income.However, keep in mind, it's possible that currency pairs adjust interest rate differential. This could erode or reverse the suitability of holding a pair over a long period of time.

While I don't have any pictures to show, yet, I am working on an EA that trades AUDJPY based on the market price relative to the average price of positions held.The first few passes at this type of system were pitiful. My testing starts from September of last year to now while only opening long positions. As you can imagine this is a difficult period of time for a long only system!However, late last night I was able to complete a test that showed profits.The strategy behind this EA is basically as follows:
If you've just seen a recent downward movement open an initial position.
If the price is high enough above or below your average order open price, open another.
If the current price is above your average price close your lowest and most profitable position.
Try not to open any position while in a downward movement regardless of the above rules.
Obviously, the last item mentioned is not simple, but it is the key to account survival. If you open too many positions and the market falls too far you will get a margin call.As ever, I'm basically using the AUDJPY for this. I am interested in strategies that can accumulate a safe quantity of long positions such that they pay me to wait for the eventual upturn.

Microtrading: Decent Returns?

I blogged about this idea not too long ago. The concept is to use very small trades relative to your available margin and net asset value (NAV). I'm doing this with the AUDJPY pair so that when I accumulate positions I am earning a positive carry trade return.My trade size over the last week has been such that the margin involved in each trade is 0.2% of my NAV. That's tiny. Twenty five trades in and you are looking at using 5% of your available margin.However, the carry trade interest would represent approximately a 3.65% return if annualized. At the same time my unrealized profits had me up almost 4% earlier this morning. This 4% unrealized profit is due to only the last 10 days of trading. We've had a downturn, I've accumulated positions, and the AUDJPY has jumped just recently.Anyway, I hope this demonstrates that short term scalping is not the only way to earn money using forex. While this concept won't make you rich overnight the risk is very low and the returns can be good compared to currently available financial instruments.

FX Trading And Analysis

I've become a little frustrated with most of news sources out there. If you've been an active forex trader for any length of time you'll notice that talking heads are always trying to tell you why something happened.That's really nice, and might possibly help you learn about various financial interactions, but it's absolutely useless from a trading point of view. If you are trading you need to figure out what's going to happen -- not what just happened. Check out this video (complete with atrociously low audio levels).
This type of analysis is unlikely to help you with your fx trading tomorrow. Generally, how the markets will move tomorrow, based on tomorrow's news, is not something you'll get from any of the gurus and talking heads.On the other hand useful analysis will be too slow to be meaningful. For example, I'm very confident the world economy will eventually recover. When that happens we'll have a period of high interest rates as rising commodity prices drive inflation. Guess what? This will mean that carry trades pairs will end up at much higher prices. Unfortunately, I can't tell you when the world is going to focus on this. Generally, not before the money moves from wherever it is to wherever it is finally going to end up.The closest thing to predictive analysis, or something you can really use to drive your forex trades, is technical analysis. Charting. Something which gets very little respect in some circles. Many people don't understand it and many others discount it because it isn't able to make perfectly accurate predictions. Technical analysis does not have to be a perfect tool for prediction. It merely has to increase the odds that your fx positions end up earning you a profit.

Forex Tips - Microtrading

The AUDJPY currency pair is currently trading around the 76.00 mark.Over the last twenty days, from May 7 through May 27, I've been experimenting with a concept I've been calling microtrading.I don't intend to close all of my positions at the moment, but if I did my account NAV would increase by more than 10% over that period.While I realize that active trading can return spectacular results compared to a paltry 10% it does require a lot more effort and time. Personally, my full time job and other issues have my complete attention. I don't have the luxury of time or the mindset to take larger risks at the moment.Anyway, open up your trading platform and I'll walk you through the process of trading this strategy.1) On May 10 we topped out around 76.00 on the AUDJPY pair.2) Based on my account size I could safely open long positions for every fall of 20 pips. This isn't the goal but it is the maximum density of trades I'd allow.3) As the price of this currency pair dropped to around 70.50 on May 15 I would accumulate positions based on the previous point. Basically, when you see what looks like a support point or if the price moved down a lot while you were at work or sleeping, then you open another micro trade.4) When any one trade has more than 200% profit with respect to margin committed and you believe you are at a resistance point, consider unloading it.5) Be patient when the market moves sideways. In terms of serious monetary strategies a week or a month is not a long period of time. Keep in mind that you are trading a carry trade pair so you will be paid to wait.6) I firmly believe that eventually the AUDJPY pair will recover strongly. I'm willing to hold positions for long periods of time as I wait for this. If you don't believe this or you aren't willing to wait, then this strategy may not be useful for you.Using the above method, with almost zero stress except for impatience during several weeks of sluggish movements, my trading account never committed more than 6% of it's NAV (using 50:1 leverage which is the maximum at my fx broker -- Oanda). However, this morning, as I've stated above, I could close out all my positions at a 10% NAV gain.This is a simple trading system, though purists may balk at calling it a "system" due to its loose definition. Wait for a drop and buy tiny positions. Capture large profits when they present themselves. Be patient and don't accumulate too large a portion of your NAV. I'd definitely recommend using Oanda due to the ability to trade any size positions and the fact that you can't trade with extreme leverage.

Monster Scalps With AUDJPY

I've been shamelessly scalping the AUDJPY this week (via Oanda). It may be hard to fathom, at least when you see the numbers, but I'm not entirely happy with my results.Jun 28: 00.28% NAV+Jun 29: 06.65% NAV+Jun 30: 11.66% NAV+So far this week, if I can hang onto it, I'm up over 19% on my trading account.Now, you may be wondering why I'm not satisfied with my trading. Basically, I've made too many mistakes. From time to time my discipline is lacking and I jump into a position at what is realistically an unwise entry point.This keeps me from capitalizing on later opportunities until I've extracted myself from the position foolishly entered. It also subjects me to a lot more stress while I wait out moves on a larger timeframe.Anyhow, I've decided to quit fooling around, scalp myself a decent stake, and get serious about trading. Now, if I can just work out my discipline issues I'll be set.

Twitter Forex Tweet Strategy
Have you been following people involved in fx trading on twitter?Have you noticed how many people are happy to tell you what happened? While macroeconomic news and previous day post analysis can be useful, it certainly doesn't help you make a trading decision based on current charts. I have a little proposal to make.Instead of tweeting that you've opened a long or short position provide some information that other people can use to apply their own strategies. Frankly, I don't care what crappy decisions others are making. I care what the charts are saying. I'll do my own technical analysis and decide on my own trades.So, tell me that a pattern is forming on a named pair's chart in a certain timeframe. For example, right now the AUDJPY is retesting May highs of 76.00 and obviously this is true on any chart -- though you may need a longer chart to actually see it.Then, I can whip open my chart, draw some lines, figure out a strategy, and trade on the opportunity.To summarize, we need to tweet about opportunities that are shaping up. We need to just drop each other a note that something is happening. Anybody who has traded for any length of time can figure out what to do -- but unless we have the luxury of trading full time we just can't spot all the opportunities.In short. Smarten up and stop trying to show the world how damned smart you are. We don't care!How about we call this the Useful Forex Tweet Agreement (UFTA).UPDATE: I've tweeted the AUDJPY information (again) using the #ufta tag...

Recent Forex Efforts

Since the recent yen cross meltdown started I've been trying to keep from getting caught on the wrong side of any massive downward moves.As I generally trade only the AUDJPY, mostly on the long side, things have been pretty quiet!However, we are now facing some resistance at 74.50 on the 1hr -- which should be illustrative. We have done what might be a triple bounce off of support in the vicinity of 70.90 or so too. I'm thinking we may have another downturn to confirm support but we could certainly get right back to business without it.In any case, as the market is starting to act rational, I'm just about ready to start trading according to my own particular style.

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.We take pride in our professional staff that is thoroughly trained to look after the best interests of our clients. Our professional staff is available twenty-four hours a day (Monday to Friday) to answer your inquiry. Try out our service by open a free demo forex account.

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

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.

forex signal provider? which one?

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.

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.

Saturday, July 11, 2009

DIFFERENCE BETWEEN ENDOGENOUS AND NEUROTIC DEPRESSION

Recurring episodes of depression only. (The term unipolar mania is not used because nearly all patients who have mania eventually experience a depressive disorder). These two disorders ware earlier referred to as manic depressive disorder. The depressive or manic symptoms should be of atleast 15 days duration. Types of depressive disorders. 1. Endogenous depression - is characterised by the classical triad of depressive symptoms, sadness of mood, poverty of ideation and psychomotor retardation. The onset of this type of depression can occur even in the absence of a significant stressor. 2. Reactive (or neurotic) depression - The onset of this disorder is usually precipitated by an environmental stressor. In addition to the depressive symptoms, concurrent symptoms of anxiety may be present. 3. Dysthymic disorder - This type of depression is characterised by chronic depressive signs and symptoms which are not as severe as those in major depressive disorder. Depressive symptoms should be present for atleast two years during which time symptom-free periods, if any, should be less than two months at a time. DIFFERENCE BETWEEN ENDOGENOUS AND NEUROTIC DEPRESSION: Endogenous depression Neurotic depression 1. Significant stress situation preceeding the 1. Significant stress situation preceding 1. Hypomania - Milder form of manic disorder characterised by euphoria and over-estimation of personal abilities and importance. If the symptoms are not disruptive, the patient's work efficiency may be relatively unimpaired and he may be socially acceptable. 2. Delirious mania - A severe form of mania with concurrent symptoms suggestive of delirium i.e. Clouding of consciousness, disorientation, illusions, hallucinations, incoherence. This form of mania is usually precipitated by emotional or physical stress and frequently results in deterioration of physical health. 3. Chronic mania - Continuous occurrence of manic symptoms in an attenuated form for a prolonged period of time Prognosis of mood disorders: Suicidal tendencies and attempts are unpredictable, hence caution is always needed while determining the prognosis. 1. Duration of illness - Shorter duration carries better prognosis. 2. Type of depression - Reactive depression has better long-term prognosis than endogenous depression. 3. Personality - Well adjusted personality carries better prognosis than maladjusted, neurotic (i.e. obsessive, inadequate or anxious) personality. 4. Type of onset - Acute onset carries better prognosis than gradual onset. 5. Precipitating factors - Presence of precipitating factors carries better prognosis than absence of precipitating factors. 6. Number of attacks - Repeatedepisodes couldresult in chronicity Management of depressive episodes - 1. Hospitalization - Indicated in (a) severe attack of depression, (b) suicidal and homicidal tendencies, and (c) stuporose condition of the patient. 2. ECT - About G to 8 convulsions spread out over a period of 2 to 3 weeks give excellent results in endogenous depression (90 to 95% success rate). Indications: (a) Severe attack, (b) Suicidal and homicidal tendencies, (c) Stupor and (d) Poor response to the other treatments. (e) Patients non-compliant with drug treatment. 3. Drug therapy - (a) Ant i depress ants I Anxiety disorder II Phobic disorder. III. Obsessive compulsive disorder IV Hysteria (a) Conversion disorder. (b) Dissociation disorder. V. Somatisation Disorder VI. Psychogenic Pain Disorder VII. Hypochondriasis. I. Anxiety disorder Definition: Anxiety disorder is characterised by an anxious and apprehensive overconcern often extending to panic and frequently associated with somatic symptoms. Etiology. 1. Genetic factors - Role of genetic factors in anxiety disorder is controversial and higher incidence in relatives of patients with the disorder could be the result of upbringing rather than inheritance. 2. (Biochemical and endocrine factors) - In anxious patients there is increased secretion of adrenaline and noradrenaline. Also post-exercise serum lactate levels are higher in patients with anxiety states than in normal subjects. But these disturbances have been shown to be accompaniments of anxiety rather than its cause. 3. Psychological theories -regard anxiety to be the result of a failure of an individual to successfully repress unwanted thoughts, ideas and feelings into the subconscious mind. Anxiety is also regarded as a fear response to another stimulus through the process of conditioning. 4. Age -Although the disorder can occur any age, it is most common in young adults. 5. Sex - Equal incidence in both sexes. 6. Personality - Persons with anxious, dependent and obsessive traits are more likely to suffer from anxiety states. Clinical manifestations: These are broadly grouped into: 1. PHYSICAL - They are referable to autonomic nervous system imbalance and commonly include palpitations, shortness of breath, tremulousness, unsteadiness, dryness of mouth, headache or heaviness of head, giddiness, blurring of vision, frequency of micturition, diarrhoea, and excessive sweating particularly in palms and soles, etc. On examination, one finds tachycardia, elevation of blood pressure, increase in depth and frequency of respiration, exaggerated deep reflexes 2 PSYCHOLOGICAL - Worries, nervousness, apprehension, irritability and a morbid fear as ifRecurring episodes of depression only. (The term unipolar mania is not used because nearly all patients who have mania eventually experience a depressive disorder). These two disorders ware earlier referred to as manic depressive disorder. The depressive or manic symptoms should be of atleast 15 days duration. Types of depressive disorders. 1. Endogenous depression - is characterised by the classical triad of depressive symptoms, sadness of mood, poverty of ideation and psychomotor retardation. The onset of this type of depression can occur even in the absence of a significant stressor. 2. Reactive (or neurotic) depression - The onset of this disorder is usually precipitated by an environmental stressor. In addition to the depressive symptoms, concurrent symptoms of anxiety may be present. 3. Dysthymic disorder - This type of depression is characterised by chronic depressive signs and symptoms which are not as severe as those in major depressive disorder. Depressive symptoms should be present for atleast two years during which time symptom-free periods, if any, should be less than two months at a time. DIFFERENCE BETWEEN ENDOGENOUS AND NEUROTIC DEPRESSION: Endogenous depression Neurotic depression 1. Significant stress situation preceeding the 1. Significant stress situation preceding 1. Hypomania - Milder form of manic disorder characterised by euphoria and over-estimation of personal abilities and importance. If the symptoms are not disruptive, the patient's work efficiency may be relatively unimpaired and he may be socially acceptable. 2. Delirious mania - A severe form of mania with concurrent symptoms suggestive of delirium i.e. Clouding of consciousness, disorientation, illusions, hallucinations, incoherence. This form of mania is usually precipitated by emotional or physical stress and frequently results in deterioration of physical health. 3. Chronic mania - Continuous occurrence of manic symptoms in an attenuated form for a prolonged period of time Prognosis of mood disorders: Suicidal tendencies and attempts are unpredictable, hence caution is always needed while determining the prognosis. 1. Duration of illness - Shorter duration carries better prognosis. 2. Type of depression - Reactive depression has better long-term prognosis than endogenous depression. 3. Personality - Well adjusted personality carries better prognosis than maladjusted, neurotic (i.e. obsessive, inadequate or anxious) personality. 4. Type of onset - Acute onset carries better prognosis than gradual onset. 5. Precipitating factors - Presence of precipitating factors carries better prognosis than absence of precipitating factors. 6. Number of attacks - Repeatedepisodes couldresult in chronicity Management of depressive episodes - 1. Hospitalization - Indicated in (a) severe attack of depression, (b) suicidal and homicidal tendencies, and (c) stuporose condition of the patient. 2. ECT - About G to 8 convulsions spread out over a period of 2 to 3 weeks give excellent results in endogenous depression (90 to 95% success rate). Indications: (a) Severe attack, (b) Suicidal and homicidal tendencies, (c) Stupor and (d) Poor response to the other treatments. (e) Patients non-compliant with drug treatment. 3. Drug therapy - (a) Ant i depress ants I Anxiety disorder II Phobic disorder. III. Obsessive compulsive disorder IV Hysteria (a) Conversion disorder. (b) Dissociation disorder. V. Somatisation Disorder VI. Psychogenic Pain Disorder VII. Hypochondriasis. I. Anxiety disorder Definition: Anxiety disorder is characterised by an anxious and apprehensive overconcern often extending to panic and frequently associated with somatic symptoms. Etiology. 1. Genetic factors - Role of genetic factors in anxiety disorder is controversial and higher incidence in relatives of patients with the disorder could be the result of upbringing rather than inheritance. 2. (Biochemical and endocrine factors) - In anxious patients there is increased secretion of adrenaline and noradrenaline. Also post-exercise serum lactate levels are higher in patients with anxiety states than in normal subjects. But these disturbances have been shown to be accompaniments of anxiety rather than its cause. 3. Psychological theories -regard anxiety to be the result of a failure of an individual to successfully repress unwanted thoughts, ideas and feelings into the subconscious mind. Anxiety is also regarded as a fear response to another stimulus through the process of conditioning. 4. Age -Although the disorder can occur any age, it is most common in young adults. 5. Sex - Equal incidence in both sexes. 6. Personality - Persons with anxious, dependent and obsessive traits are more likely to suffer from anxiety states. Clinical manifestations: These are broadly grouped into: 1. PHYSICAL - They are referable to autonomic nervous system imbalance and commonly include palpitations, shortness of breath, tremulousness, unsteadiness, dryness of mouth, headache or heaviness of head, giddiness, blurring of vision, frequency of micturition, diarrhoea, and excessive sweating particularly in palms and soles, etc. On examination, one finds tachycardia, elevation of blood pressure, increase in depth and frequency of respiration, exaggerated deep reflexes 2 PSYCHOLOGICAL - Worries, nervousness, apprehension, irritability and a morbid fear as if

- Chemotherapeutic drugs exert a direct. inhibitory effect on the rapidly proliferating cells of the hair matrix and lead to hair loss.

involved (alopecia totalis). Hair loss may occur at other sites such as eyebrows, eye lashes, beard and body hair. Tr. - In majority, lesions regress spontaneously. Regrowth usually occurs within 3 months and only those patches that persist beyond this period require treatment. Topical corticosteroids may hasten recovery. Systemic corticosteroids (20-30 mg prednisolone) daily can produce regrowth of hair. 100 mg prednisolone once a week is equally effective. 2. Tinea capitis - Irregular patch of alopecia with scaling and broken off stubs of hair within the patch. Multiple patches may develop. Occasionally the patch may be inflamed (kerion). Tr. - Topical antifungal therapy is ineffective. Griseofulvin 10 mg/kg/day for 6 weeks or ketoconazole, itraconazole and terbinafine. 3. Lichen planopilaris - Lichen planus affecting hair follicles produces a patchy, scarring alopecia. Mimute, purple papules may be seen around hair follicles at the edges of the patches. Tr. - Clobetasol topically. If not controlled 20-30 mg prednisolone p. o. for 6-8 weeks. 4. Folliculitis Decalvans - rare cause with pustules around follicles which heal with scarring and destruction of hair follicles. T.r - Anti-staphylococcal antibiotics. 5. Skin diseases - that produce alopcia are discoid lupus erythematosus and morphoea. 6. Trichotillomania - produced by pt with psychiatric illness plucking her hair. 7. Traction alopecia - produced by tying a tight pony tail. This is most prominent along hair margins because distant hair is subject to most traction. Diffuse alopecia 1. Androgenetic alopecia - Loss of hair as result of androgenic hormones, hence the hair follicles that normally produce coarse terminal hair give rise instead, to vellus hair. The male type of alopecia has a typical pattern showing frontal recession of the hairline and thinning of the vertex. This may progress to involve the entire scalp except the occipto-temporal region. In women, the condition presents with diffuse alopecia with considerable thinning on the vertex. Tr. - Minoxidil lotion applied to scalp b. d. is of benefit in some who have thinning of the vertex, but require continued application. In women, anti-androgens can also be used and may be effective in some. 2. Telogen effluvium - Postpartum and postfebrile alopecia are not uncommon. There is diffuse loss of hair from entire scalp 2-3 months after pregnancy. This occurs because, following child birth, all the hair enter the resting phase (telogen) at the same time. All the hair are thus lost at the end of telogen which lasts 3 months. A similar mechanism underlies hair loss following fevers especially typhoid. Since there is no abnormality of the follicles, they begin to grow new hair immediately after the old hair are lost. 3. Drug-induced alopecia - Chemotherapeutic drugs exert a direct. inhibitory effect on the rapidly proliferating cells of the hair matrix and lead to hair loss. Recovery is usually complete after withdrawal of the drug. Other drugs include thiouracil, carbimazole, heparin, lithium, pyridostigmine and etretinate. 4. Alopecia of SLE - With subsidence of activity of the disease, hair regrow completely. 5. Alopecia of severe chronic illness - Diffuse hair loss may be a feature of a number of long-standing illnesses that cause constitu tional upset. 6. Idiopathic diffuse hair loss - mostly in women. Note: Surgery for alopecia is useful in diseases where there is a clear distinction between areas affected by disease and areas that are spared, e. g. androgenic alopecia, where the occipito-temporal fringe is never affected. Transplantation of hair from this area to bald areas is effective. G. URTICARIA Definition: Urticaria is a vascular reaction pattern characterized by transient, evanascent, pruritic wheals on the skin occurring on any site of the body. This, is a type I hypersensitivity reaction (IgE mediated immediate hypersensitivity) of the skin to a variety of exogenous and endogenous antigens. Vascular dilatation, the resultant dermal oedema and pruritus are caused by the release of histamine and other mediators from mast cells consequent upon binding of IgE antibodies to the antigen over cell surfaces. It is characterised by evanascent, pruritic wheals which last for 4-8 hours. When the subcutaneous tissue is involved it is termed angioedema. Provoking causes. A. Exogenous: 1. Ingestants: (a) Drugs e.g. penicillins, sulphonamides, aspirin, chloromphenicol, phenytoin. NSAIDs. (b) Foods e.g. seafoods, coloring agents (tartrazine), eggs, meat, spices, some vegetables, some dais, peas, etc. 2. Inhalants: pollens, plant, animal dander, dust, spores. 3 Injectants : Penicillins, insulin, antisera, vaccines. 4. Contactants : Bee stings, bug bites, animal dander, plants. B. Endogenous: 1. Infections: Chronic septic focus, UTI, virus infection (particularly hepatitis and respiratory tract infection), Candida infection. 2. Infestations: Helminths, amoebiasis, giardiasis. 3. Systemic diseases: SLE, lymphomas, malignant mastocytosis. 4. Psychogenic : Emotional stress. Types of Urticaria : 1. Ordinary urticaria - (a) Acute urticaria - lasts for a few hoursordays. It is characterized by the presence of small circumscribed areas of oedema, pink in colour, with central pallor. The number varies, and it occurs anywhere on the body asymmetrically. It is seen in patients with anaphylaxis, atopy, serum sickness or as a reaction to insect-bites, foods and drugs. (b) Chronic urticaria - Recurrent lesions for 3 months with or without arthralgias, adenopathy.

Genetic factors - are thought to act through a delayed maturation of parts of the nervous system. (b)

of any physical disorder Etiology - (a) Genetic factors - are thought to act through a delayed maturation of parts of the nervous system. (b) Smaller capacity of urinary bladder. (c) Environmental stresses - Enuresis sometimes starts after stressful event, such as birth of a younger sibling, conflict between parents, problems in school, etc. (d) Poor toilet training. Clinical features -Enuresis may be nocturnal, diurnal or both. It is termed primary if there has been no preceding period of urinary continence for at least one year, or secondary if there has been a preceding period of urinary continence for this duration. Treatment - (a) Counselling of parents about nature of the disorder, and about toilet training. (b) Bladder training by which the child is encouraged to increase the interval between successive acts of micturition (c) Imipramine or amitryptiline 25-50 mg at night, may be effective. FUNCTIONAL ENCOPRESIS - is defined as the involuntary passing of faeces into clothing after the age of which bowel control is usual and in absence of a known organic cause. Etiology - (a) Poor toilet training. (b) Mental retardation. (c) Environmental stress - Involuntary voiding follows stressful situation, such as birth of a younger sibling, confict between parents, illness of a parent. Clinical features - Involuntary passing of stools of normal or near-normal consistency into clothing, or in places not appropriate for that purpose in the child's socio-cultural setting. Encopresis like enuresis could be present from birth (primary), or could appear after a sustained period of continence (secondary). Treatment - (a) Counselling regarding faulty toilet training. (b) Behaviour therapy by which the child is encouraged to remain continent. 10. DRUG INDUCED PSYCHIATRIC DISORDERS Classification: 1. Behavioural toxicity (a) Drowsiness - Benzodiazepines, neuroleptics, antihistaminics, antidepress ants, antihypertensives. (b) Behavioural changes - consisting of irritability, aggressive outbursts and a generalised hostile attitude Benzodiazapines, barbiturates, levodopa, neuroleptic drugs, alcohol, drug-withdrawal states. Some tricyclic ant i depress ants, selective serotonin uptake inhibitors. 2. Delirium (Acute organic psychosis) (a) Cardiovascular drugs - Digitalis, diuretics, propranolol, pindolol, oxprenolol. (b) Anticholinergic drugs - atropine, homatropine, scopolamine, antiparkinsonian drugs, tricyclic ant i depress ants. (c) Tranquillizers and hypnotics - barbiturates, benzodiazepines, ant i depress ants, phenothiazines, bromides. (d) Antituberculous drugs - Isoniazid, rifampicin, cycloserine. (e) Anticonvulsants - Phenytoin, sodium valproate. (f) Miscellaneous drugs - Corticosteroids, insulin, disulfiram, cimetidine, chloroquine, aminophylline, oral hypoglycemic agents. (h) Drug withdrawal -Barbiturates, benzdiazepines, chlormethiazole, dextropropoxyphene, alcohol, opiates, phencyclidine. 3. Affective states - (i) Depression - (a) Ant i hypertensive agents - reserpine, alpha methyl dopa, clonidine, propranolol, pindolol (b) Corticosteroids (c) Psycho-active drugs - phenothiazines, neuroleptics, benzodiazepines. (d) Anti-parkinsonian agents - Levodopa. (e) Analgesics -Indomethacin, pentazocine. (f) Hormones - Oestrogens, oral contraceptives. (g) After withdrawal of CNS stimulants -amphetamines, cocaine. (h) Miscellaneous drugs - Ethanol, antineoplastic agents, disulfiram, tetrabonazine, phenytoin, phenobarbitone, theophylline, digoxin, danazol, cimetidine, chloroquine, cycloserine. (ii) Elation - (a) Ant i depress ants. (b) Corticosteroids. (c) Anti-parkinsonian agents - benzhexol, procyclidine, levodopa, bromocriptine (d) CNS stimulants -amphetamines, cocaine, methylphenidate. (e) Miscellaneous - Isoniazid, aminophylline, cyclizine, yohimbine, salbutamol, clonidine withdrawal. 4. Psychotic states - (a) Hallucinogens - LSD, cannabis, phencyclidine. (b) CNS stimulants - Cocaine, amphetamines. (c) Appetite suppressants - Phenmetrazine. (d) Sympathomimetics - Ephedrine, pseudoephedrine, phenylephrine. (e) Alpha-adrenergic agonists - phenylpropanaloamine. (f) Beta-adrenergic agonists - Salbutamol. (g) Beta-adrenergic antagonists - Propranolol, oxprenolol. (h) Dopaminergic drugs - Levodopa, dopamine, bromocriptine. (i) Narcotic analgesics - Pentazocine. (j) Corticosteroids (k) Nonsteroidal ant i-inflammatory agents - Indomethacin. (1) Ant i-de press ant drugs (m) Anticholinergic drugs (n) Miscellaneous - Disulfiram, anti-tuberculosis drugs, cimetidine, ant i-hist ami nics, digoxin. methyldopa, phenytoin. 5. Pseudodementia - Benzodiazapines and barbiturates, major tranquillizers, anti- hypertensive, diuretics, antiparkinsonian drugs and digoxin in the elderly, and overdose of antiepileptic drugs in some epileptics. Chronic hypoglycemia due to oral hypoglycemic drugs or insulin. 6. Neuropsychiatric states - Combinations of psychiatric and neurological symptoms and signs. Phenytoin can -induce a paranoid hallucinatory psychosis or delirium with cerebellar signs and symptoms. Neuroleptics can produce extra-pyramidal reactions like akathisia, pseudo-parkinsonism, acute dystonias and tardive dyskinesia. 11. TREATMENT METHODS IN PSYCHIATRY Broadly these can be divided into two main groups: A. Physical methods of treatment - (I) Drug therapy -Psychotropic drugs can be classified as follows - (1) ANTIPSYCHOTIC DRUGS - (a) Mechanism of action - is postulated to be

characterised by presence of obsessions and compulsions. Obsessions are recurrent or persistent ideas

manifestations: are characterised by presence of obsessions and compulsions. Obsessions are recurrent or persistent ideas, thoughts, images or impulses. Compulsions are urges or impulses to action that, when put into operation lead to compulsive acts which are performed either according to certain rules or in a stereotyped manner. Obsessions and compulsions have certain features in common - (a) An idea or impulse intrudes impellingly into an individual's conscious awareness. (b) A feeling of intense anxiety accompanies the central manifestation and leads the individual to take counter measures against the initial idea or impulse. (c) The obsession or compulsion is ego-alien, i. e. is experienced as being foreign to and not a part of one's experience of oneself ; it is undesirable and unacceptable. (d) The individual recognises the obsession or compulsion as being absurd or irrational. (e) The suffering individual feels a strong need to resist those obsessions or compulsions. When the symptoms become severe, the patient may develop additional symptoms of anxiety anchor depression. PROGNOSIS - Natural remissions of symptoms are known; hence the prognosis is not always gloomy. Prognosis is bad when the personality is obsessional and symptoms are severe and of long-standing. Management: 1. Drugs - Fluoxetine (20-60 mg/day) or sertraline (50-300 mg/day) or clomipramine (75-200 mg/day) Trazodone (50^1-00 mg/day) is also effective in some cases. 2. Psychotherapy- Supportive as well as analytical gives satisfactory results in some cases. 3. Behaviour therapy - Satisfactory results are seen in some cases. IV. Hysteria Types of hysterical disorders -1. Conversion disorder - (Hysterical neurosis, conversion type). Here the special senses or voluntary nervous system are affected causing symptoms such as blindness, deafness, paralysis, akinesias, etc. for which there is no organic basis. Often the patient shows an inappropriate lack of concern ("la-belle" indifference) about those symptoms which may actually provide secondary gains by winning sympathy. 2. Dissociative disorder - (Hysterical neurosis, dissociative type). Here alterations may occur in the patient's state of consciousness or in his identity to produce such symptoms as amnesia. somnambulism, fugue and multiple personality. Etiology: There is sufficient evidence to suggest that the symptoms are psychogenic and that the environmental factors are the important etiological factors. 1. Age - The peak incidence is between the ages of 20 to 35 years. 2. Sex - Incidence is higher in females. 3. Intelligence - People with low intelligence more likely. 4. Personality - Commonest is histrionic personality (characteristics - dramatizing and exhibitionistic, attention seeking, immature, having shallow and superficial emotional relationships). 5. Marital status - More common in unmarried, widowed and divorcees. 6. Socio-cultural factors - More common in primitive, developing and less sophisticated or cultured societies. 7. Psychoanalytical theories - Hysterical symptoms are viewed as symbolic representations and distorted expressions of unresolved intrapsychic conflicts about one's sexual drive (libido). When the libidinal energy manifests itself as somatic symptoms through the ego-defence mechanism of conversion, the resulting disorder is known as conversion disorder. When the libidinal energy manifests as psychological symptoms through the defense mechanism of dissociation, the resulting disorder is labelled dissociative disorder. Clinical manifestations: 1. SYMPTOMS OF CONVERSION DISORDER - These arise because of the involvement of voluntary neuromuscular system. (a) Motor symptoms - These are of two types: (i) Akinesia e.g. paresis or paralysis involving a part of the body like monoplegia, hemiplegia, paraplegia, etc. (ii) Hyperkinesia and dyskinesia e. g. tremors, torticollis, convulsons or fits (b) Sensory symptoms: These can be in the form of anaesthesia, hypoaesthesia, hyperaesthesia and paraesthesia. This disturbance can affect all the general sensations. Special organs of sense, like those for sight, hearing, smell and taste can also be disturbed resulting in blindness, deafness, etc. (c) Visceral symptoms - Common ones are hiccoughs, vomiting, dyspnoea, dysphagia, aphonia, etc. 2. SYMPTOMS OF DISSOCIATION DISORDER - (a) Somnambulism and somniloquy. (b) Amnesia -usually circumscribed and covers up the psychologically traumatic event. (c) Trance - An altered state of consciousness lasting for a few minutes to a few hours, during which the patient appears to be oblivious of the surroundings. (d) Fugue - An altered state of consiousness wherein the patient travels long distances over a period of days and subsequently has amnesia for the entire episode. (e) Multiple personalities like those of Dr. Jekyl and Mr. Hyde. (f) Ganser's syndrome, a rare disordercharacterised by giving of "approximate answers", somatic or psychological hysterical symptoms, hallucinations and an apparent clouding of consciousness. Characteristics of hysterical symptoms - 1. Absence of organic basis for symptoms. 2. They serve both primary gain (resolution of intrapsychic conflicts) and secondary gain (obtaining sympathy and attention). 3. In conversion disorder - (a) Symptoms seldom occur when patient is alone, on the other hand, symptoms are exaggerated in presence of other persons. (b)

multilocularis, the ^malignant1 hydatid is transmitted between foxes and rodents, but is very rare in humans

widespread in dogs and livestock (sheep, goats, cattle and camels) and in man (b) Alveolar E multilocularis, the ^malignant1 hydatid is transmitted between foxes and rodents, but is very rare in humans LIFE CYCLE OF ECHINOCOCCUS - The adult worm lives in the small intestine of the dog. Eggs are shed in the faeces and ingested by sheep, usually from contaminated pasture. The eggs hatch in the duodenum and larvae migrate through the gut wall. Blood stream dissemination follows usually to the liver, but any tissue or organ can become infected. The larva develops into a hydatid cyst containing many scolices/ When infected organs of the sheep are ingested by the dog, the scolices attach themselves to the small bowel mucosa and develop into adult worms/ Man becomes infected after ingestion of eggs after contact with dogs faeces or via contaminated food stuffs. Clinical features - Hydatid cysts especially if calcified may be asymptomatic and first noted incidentally during routine physical examination. Symptoms and signs depend on the organ affected. 1. LIVER - Hydatid cyst may present as - (a) Painless hepatomegaly. (b) Pyrexia of unknown origin following secondary pyogenic infection. (c) Jaundice due to pressure on the bile ducts. (d) Severe systemic reaction following rupture into peritoneal cavity, gut itself or pleural cavity. (e) Cholangitis from rupture into biliary tree. 2. LUNG - Pulmonary hydatid cyst can present as - (a) Solitary or at times multiple cysts, on plain radiograph. (b) Shortness of breath or chest pain if cyst is large. (c) Haemoptysis following ulceration into a bronchus. (d) Expectoration of watery fluid and daughter cysts fgrape skin' expectoration) following rupture into the bronchial tree. Respiratory distress may follow due to aspiration of fluid elsewhere in the lungs, and may be associated with urticaria and anaphylactic shock. (e) Fever, cough and purulent sputum, if secondary pyogenic infection occurs. 3. OTHER ORGANS - Presence of cysts in - (a) Brain -Epilepsy or hemiplegia. (b) Long bones - Pathological fractures. (c) Spleen - Splenomegaly. (d) Kidneys - Hematuria. (e) Spinal cord - Seizures or signs of increased intracranial pressure of subacute onset and progressive course. Root pains- and motor or sensory deficits. (f) Thyroid - Goitre. (g) Behind the eye - Exophthalmos. (h) Abdomen - Pseudocycesis from rapidly growing cysts. Diagnosis - 1. DEMONSTRATION OF HYDATID CYSTS - (a) Chest radiograph - various signs are - (a) Classical appearance of a circular shadow sharply defined with no reaction in surrounding lung parenchyma. The cyst may change shape on maximum inspiration an expiration (Escudero nimerove sign). (b) Crescent sign or pulmonary meniscus sign - If the cyst communicates with a bronchus, a cap of air may be seen above the cyst (also seen in lung abscess partially filled with ins pisated pus or blood clot, tuberculous cavity containing a Rasmussen aneurysm, and in intracavitary fungal ball). (c) Double arch (Gumbo's) sign - As more sir enters between pericyst and endocyst, the shrinking cyst ruptures with resultant air fluid level within the endocyst capped with crescent of air between pericyst and endocyst. (d) Water lilly sign - With further separation of endocyst and evacuation of fluid, a wavy endocyst membrane floats on top of remaining TREATMENT - Praziquantel in three equal doses of 20 mg/kg at 4h intervals with meals. Apart from mild side-effects of drowsiness, headache, dizziness, etc. , a syndrome of severe abdominal pain followed by bloody diarrhoea may occur. PREVENTION - 1. Protection of snail habitats from infection by provision of clean water and toilet facilities, and health education. 2. Mass therapy with oxamniquine, metriphonate or praziquantel to reduce amount of egg excretion. 3. Snail destruction by improved irrigation methods and use of molluscicides. 4. Prevention of infection by wearing protective clothing. 18. HYDATID DISEASE : Definition - Hydatid disease of man is zoonosis caused by infection with tapeworm larvae of the genus Echinococcus. There are two forms - (a) Cystic: The much more common E. granulasus causes unilocular hydatid cysts and is widespread in dogs and livestock (sheep, goats, cattle and camels) and in man (b) Alveolar E. multilocularis, the `malignant' hydatid is transmitted between foxes and rodents, but is very rare in humans. LIFE CYCLE OF ECHINOCOCCUS - The adult worm lives in the small intestine of the dog. Eggs are shed in the faeces and ingested by sheep, usually from contaminated pasture. The eggs hatch in the duodenum and larvae migrate through the gut wall. Blood stream dissemination follows usually to the liver, but any tissue or organ can become infected The larva develops into a hydatid cyst containing many scolices. When infected organs of the sheep are ingested by the dog, the scolices attach themselves to the small bowel mucosa and develop into adult worms. Man becomes infected after ingestion of eggs after contact with dogs faeces or via contaminated food stuffs. Clinical features - Hydatid cysts especially if calcified may be asymptomatic and first noted incidentally during routine physical examination. Symptoms and signs depend on the organ affected. 1. LIVER -Hydatid cyst may present as - (a) Painless hepatomegaly. (b) Pyrexia of unknown origin following secondary pyogenic infection.

loss of elasticity of skin and sunken abdomen Fever, restlessness, tachycardia and oliguria. Later symptoms of toxemia

depressed anterior fontanelle, loss of elasticity of skin and sunken abdomen Fever, restlessness, tachycardia and oliguria. Later symptoms of toxemia - apathy, staring sunken eyes, shallow respirations, uncountable pulse, cyanosis, acidotic breathing. Temperature high or sub-normal "Cholera infantum" or acute toxic diarrhoea - In a very severe case rice water stools and symptoms of toxemia. Abrupt onset with high fever and extreme prostration, vomiting, irritability, restlessness and often convulsions, collapse, suppression of urine and finally stupor and coma. Copious watery stool suggestive of toxigenic diarrhoea, small, frequent with tenesmus, blood and mucus in invasive infections - EEC, Salmonella, Shigella, amoebiasis. III. Parenteral diarrhoea - At onset of any acute infection e. g. acute otitis media and mastoiditis, infection of respiratory tract, acute pyelitis and meningitis. Probably same virus involves both systems as in measles. Management: I FLUIDS - (a) Solution used - (i) Ringer lactate - Full strength 1 ampoule with 5% glucose or 1/2 strength. (ii) Isolyte M is suitable rehydrating fluid in infants. (iii) Glucose-saline IV - 1/5th in newborns, 1/3 in older children use after initial rapid rehydration. (iv) Potassium chloride (1 ml =2mEq), add 1 ml of solution to 100 ml IV solution (maximum 2 ml) after patient starts passing urine. (b) Quantity - (i) Assessment of fluid loss -According to grade of dehydration: (a) Mild - Irritability, pallor, pink lips - <5%>

- Minimal change disease, mesangial proliferate GN, focal and segmental

Primary glomerular disease - Minimal change disease, mesangial proliferate GN, focal and segmental GN, membranous GN, megangiocapillary GN, crescentic GN (ii) Secondary glomerular disease - Diabetes, collagen vascular disease, amyloidosis, drugs (gold, penicillamine, mercury). (b) Overflow proteinuria - Multiple myeloma, amyloidosis, myoglobinuria, haemoglobinuria. (c) Tissue proteinuria - Acute inflammation of urinary tract. QUANTITATIVE ANALYSIS OF PROTEINURIA - Less than 0.5 g/day - (a) Normal, after prolonged exercise, orthostatic. (b) Abnormal - Orthostatic proteinuria can occur in mild or resolving glomerular disease. 0.5-2 g/day- (a) Benign - Usually fixed1 i.e. present at all times. (b) Abnormal - Glomerular disease or proximal tubular lesion, congenital or acquired. More than 2 g/day - (a) Glomerular disease. (b) Overproduction of proteins small enough to escape the glomerular barrier e. g. free immunoglobulin light chains produced by a B cell monoclone. Proteinuria more than 5 glday - (with hypoalbuminemia and oedema) - Nephrotic syndrome, specific glomerular disease, accelerated hypertension, unilateral renal artery stenosis, renal venous thrombosis, severe congestive heart failure. Systemic diseases that may present as asymptomatic albuminuria - Diabetes mellitus, amyloidosis, hypertension, gout, SLE. TESTS FOR PROTEIN - (a) Boiling test - For this purpose the urine must be clear, if opalascent it must be filtered. A test-tube is filled with two-thirds urine and the top portion gently heated over a flame, 2 or 3 drops of acetic acid should be added and the urine boiled If turbidity appears in the urine on boiling and it persists after the addition of acetic acid it indicates presence of albumin and the amount of precipitate indicates the amount of albumin. If the turbidity disappears on addition of acetic acid the turbidity is due to phosphates. (b) Dipstick - Test with fresh specimen and ensure that dipsticks are not out of date. (c) Salicylsulphonic acid - The precipitated proteins form a suspension. Mucin - Traces in normal urine. Increased amounts in irritation and inflammation of urinary tract or vagina Sulphonamides - Crystal forms of certain derivatives of sulphonamide may precipitate out from the urine. Fat globules -After ingestion of large quantities of cod liver oil or other fats, phosphorus poisoning and chronic parenchymatous nephritis. In alkaline urine - Phosphates - in osteitis fibrosa cystica, administration of parathyroid hormone, alkalosis, compensatory measure in acidosis to help maintain acid base balance. Calcium carbonate - as amorphous granules, or rarely as colourless spheres and dumb-bells. Ammonium biurate - "Thorn apple" crystals. 2 ERYTHROCYTES -The excretion of erythrocytes should not exceed 1 X 105/ hour. (a) Dysmorphic pattern - Profusion of erythrocytes of bizarre and dissimilar size with variable haemoglobin concentration (Normal upto 8000 urinary erythrocytes). (b) Isomorphic pattern - Non-glomerular bleeding associated with urinary calculi, tumours and papillary necrosis. Erythrocytes which are uniform in size and shape with normal haemoglobin concentration are not a normal component of urine and thus a count as low as 4000/ml may be a sensitive and specific indicator of non-glomerular bleeding. The number of red cells present provides information on the probable type of underlying glomerulonephritis, particularly if haematuria is associated with other urinary abnormalities, such as the presence of protein, fat and casts. Thus a patient with membranous glomerulonephritis has an erythrocyte count of 20,000-50,QQQ/ml accompanied by marked proteinuria, oval fat bodies and many casts containing fat. Mesangial IgA nephropathy is associated with a count of 100,000/ml or more and there may be no fat, casts or protein in urine. An erythrocyte count of more than 1,000,000/ml is likely to reflect the presence of underlying crescents whatever the nature of the glomerular lesion. The dipstick method detects <>

caused directly by the virus. No secondary bacterial infection. 1. Arthralgia and polyarthritis

Complications - are caused directly by the virus. No secondary bacterial infection. 1. Arthralgia and polyarthritis - usually in young women with involvement of small joints of hands or feet, at times larger joints. Arthritis may be accompanied by tenosynovitis and peripheral neuritis. 2. Encephalitis - Rare, affects adults more frequently and develops usually within a day or two of the appearance of rash. 3. Guillain-Barre syndrome. 4. Thrombocytopenic purpura - appears after about a week and may occasionally persist for several months. 5. Hepatitis. Diagnosis - 1. Virus isolation - Virus may be recovered from nasopharynx, blood, urine and stools. Inoculated into tissue cultures. 2. Serological tests - (a) Haemagglutination-inhtibition test - HAI antibody level rises within 24-18 hours, reaches a peak in 6-12 days and persists for a long time. (b) Complement fixation test -Determination of rubella-specific IgM or IgA antibody if there is delay in obtaining blood sample. Treatment - Bed rest and analgesics suffice for the uncomplicated attack. Rubella proven by antibody estimation in first 4 months of pregnancy is a strong indication for termination. PREVENTION - Rubella immunization: (a) Combined measles, mumps and rubella (MMR) vaccine is given routinely to all children in second year of life. (b) All female adults are screened when they reach child-bearing age and are immunized if non-immune with monovalent rubella vaccine. (c) Routine screening and immunization in immediate postnatal period. Immunized mothers excrete the vaccine virus in breast milk, but this is not a contraindication to vaccination or breast-feeding. Congenital rubella syndrome Pathogenesis - The foetus is infected during maternal viremia and the virus gains access to foetal tissues, causing a cytopathic effect or merely promoting an immune response. Defects - The consequences of rubella in pregnancy are varied and unpredictable, ranging from foetal death to birth of an infected but otherwise normal child. 1. TEMPORARY DEFECT - if cytopathic damage to non-organ tissue: (a) Thrombocytopenic purpura. - at birth or shortly after. (b) Hepatosplenomegaly. (c) Hepatitis. (d) Low birth weight. 2. PERMANENT DAMAGE - (Triad of Gregg) if cytopathic effect early in organogenesis: (a) Cataracts and retinopathy. (b) Microcephaly. (c) Congenital heart defects (PDA with or without PS most common) LATE CONGENITAL RUBELLA In some infants, particularly those infected after the first trimester, there is no obvious congenital defect, but the infant sheds the virus. In this group, late congenital rubella features include: 1. Growth retardation. 2: Behaviour disorders. 3. Psychiatric manifestations. 4. High-tone deafness. 5. Insulin-dependent diabetes mellitus PROCEDURES TO BE ADOPTED IN A PREGNANT WOMAN - (a) Suspicion of having rubella-Accurate diagnosis should be established by serological tests. If HAI antibody is present, explain the degree of risk to the patient and decide about termination of pregnancy. (b) Suspicion of having been in contact with rubella - (i) If possible, confirm the diagnosis by serological studies on the original case. (ii) If contact is close and the pregnant woman has decided to continue with pregnancy give 1500 mg. of immunoglobulin IM as soon as primary sample of serum is obtained. If there is no detectable antibody, give further 1500 mg. immunoglobulin within 3-4 days (iii) If she does not want to continue with pregnancy, or if the contact is not close, do not give immunoglobulin. (iv) In either case, take a second sample of blood after 3-4 weeks to see if there has been sera-conversion. The risk to the foetus when the mother has a subclinical attack is not known with certainty but appears to be slight. Should the mother develop an illness with serological evidence of rubella, the risks should be explained and decision taken about termination of pregnancy. 7. CHICKEN POX Epidemiology- Age - Primarily children, uncommon in adults in whom the disease tends to be more severe. Causative agent - Virus is identical to virus of herpes zoster and hence designated varicella zoster virus (V-Z virus). Transmission - Droplet discharges from air passages. May be direct skin contact or by recently contaminated utensils. Incubation period - 14 to 15 days. Period of infectivity - From 7 days before onset of rash until 6 days after development of last vesicle. Clinical features - Stage of invasion or pradramata - not constant. Headache, sore throat and fever for 24 hours. Prodromal rashes - Erythmatous, scahatiniform, morbilliform or urticarial. Rarely hemorrhagic. Stage of eruption -1 ENANTHEM - Earliest lesions on buccal and pharyngeal mucosa 2. EXANTHEM - (a) Evolution - in crops; at first back, then chest, abdomen, face, and lastly limbs. (b) Character - At first macule, in few hours dark pink papule which soon turns into vesicle - (i) superficial i e 'on' rather than 'In' the skin (glass pox), (ii) elliptical or oval ("tear drop" vesicles) with axis parallel to ribs, (iii) unilocular, hence collapse if pierced with needle. Vesicles turn into pustules in 24 hours. Scabs in 2 to 5 days. (c) Distribution-centripetal, i.e. more on upper arms and thighs and upper part of face, and in concavities and flexures. Less commonly lesions on genital mucous membranes, conjunctivae and cornea. (d) Crapping - Rash matures very quickly and most spots dry up within 48 hours of

Arthralgia and polyarthritis - usually in young women with involvement of small joints of hands or feet, at times larger joints

Complications - are caused directly by the virus. No secondary bacterial infection. 1. Arthralgia and polyarthritis - usually in young women with involvement of small joints of hands or feet, at times larger joints. Arthritis may be accompanied by tenosynovitis and peripheral neuritis. 2. Encephalitis - Rare, affects adults more frequently and develops usually within a day or two of the appearance of rash. 3. Guillain-Barre syndrome. 4. Thrombocytopenic purpura - appears after about a week and may occasionally persist for several months. 5. Hepatitis. Diagnosis - 1. Virus isolation - Virus may be recovered from nasopharynx, blood, urine and stools. Inoculated into tissue cultures. 2. Serological tests - (a) Haemagglutination-inhtibition test - HAI antibody level rises within 24-18 hours, reaches a peak in 6-12 days and persists for a long time. (b) Complement fixation test -Determination of rubella-specific IgM or IgA antibody if there is delay in obtaining blood sample. Treatment - Bed rest and analgesics suffice for the uncomplicated attack. Rubella proven by antibody estimation in first 4 months of pregnancy is a strong indication for termination. PREVENTION - Rubella immunization: (a) Combined measles, mumps and rubella (MMR) vaccine is given routinely to all children in second year of life. (b) All female adults are screened when they reach child-bearing age and are immunized if non-immune with monovalent rubella vaccine. (c) Routine screening and immunization in immediate postnatal period. Immunized mothers excrete the vaccine virus in breast milk, but this is not a contraindication to vaccination or breast-feeding. Congenital rubella syndrome Pathogenesis - The foetus is infected during maternal viremia and the virus gains access to foetal tissues, causing a cytopathic effect or merely promoting an immune response. Defects - The consequences of rubella in pregnancy are varied and unpredictable, ranging from foetal death to birth of an infected but otherwise normal child. 1. TEMPORARY DEFECT - if cytopathic damage to non-organ tissue: (a) Thrombocytopenic purpura. - at birth or shortly after. (b) Hepatosplenomegaly. (c) Hepatitis. (d) Low birth weight. 2. PERMANENT DAMAGE - (Triad of Gregg) if cytopathic effect early in organogenesis: (a) Cataracts and retinopathy. (b) Microcephaly. (c) Congenital heart defects (PDA with or without PS most common) LATE CONGENITAL RUBELLA In some infants, particularly those infected after the first trimester, there is no obvious congenital defect, but the infant sheds the virus. In this group, late congenital rubella features include: 1. Growth retardation. 2: Behaviour disorders. 3. Psychiatric manifestations. 4. High-tone deafness. 5. Insulin-dependent diabetes mellitus PROCEDURES TO BE ADOPTED IN A PREGNANT WOMAN - (a) Suspicion of having rubella-Accurate diagnosis should be established by serological tests. If HAI antibody is present, explain the degree of risk to the patient and decide about termination of pregnancy. (b) Suspicion of having been in contact with rubella - (i) If possible, confirm the diagnosis by serological studies on the original case. (ii) If contact is close and the pregnant woman has decided to continue with pregnancy give 1500 mg. of immunoglobulin IM as soon as primary sample of serum is obtained. If there is no detectable antibody, give further 1500 mg. immunoglobulin within 3-4 days (iii) If she does not want to continue with pregnancy, or if the contact is not close, do not give immunoglobulin. (iv) In either case, take a second sample of blood after 3-4 weeks to see if there has been sera-conversion. The risk to the foetus when the mother has a subclinical attack is not known with certainty but appears to be slight. Should the mother develop an illness with serological evidence of rubella, the risks should be explained and decision taken about termination of pregnancy. 7. CHICKEN POX Epidemiology- Age - Primarily children, uncommon in adults in whom the disease tends to be more severe. Causative agent - Virus is identical to virus of herpes zoster and hence designated varicella zoster virus (V-Z virus). Transmission - Droplet discharges from air passages. May be direct skin contact or by recently contaminated utensils. Incubation period - 14 to 15 days. Period of infectivity - From 7 days before onset of rash until 6 days after development of last vesicle. Clinical features - Stage of invasion or pradramata - not constant. Headache, sore throat and fever for 24 hours. Prodromal rashes - Erythmatous, scahatiniform, morbilliform or urticarial. Rarely hemorrhagic. Stage of eruption -1 ENANTHEM - Earliest lesions on buccal and pharyngeal mucosa 2. EXANTHEM - (a) Evolution - in crops; at first back, then chest, abdomen, face, and lastly limbs. (b) Character - At first macule, in few hours dark pink papule which soon turns into vesicle - (i) superficial i e 'on' rather than 'In' the skin (glass pox), (ii) elliptical or oval ("tear drop" vesicles) with axis parallel to ribs, (iii) unilocular, hence collapse if pierced with needle. Vesicles turn into pustules in 24 hours. Scabs in 2 to 5 days. (c) Distribution-centripetal, i.e. more on upper arms and thighs and upper part of face, and in concavities and flexures. Less commonly lesions on genital mucous membranes, conjunctivae and cornea. (d) Crapping - Rash matures very quickly and most spots dry up within 48 hours of

Either sex. Onset usually in third decade. (i) Pelvifemoral form - Weakness begins in pelvic girdle musculat

dystrophy - Either sex. Onset usually in third decade. (i) Pelvifemoral form - Weakness begins in pelvic girdle musculature (psoas, glutei and quadriceps) and results in waddling lordotic gait with difficulty in climbing stairs. Winging of scapulae. (ii) Scapulohumeral form- Weakness confined initially to shoulder girdle and upper arm muscles. Deltoids are usually spared and may appear enlarged due to severe atrophy of upper arm muscles. Pelvic girdle musculature usually becomes affected at a later stage. The disease runs a variable course leading to severe disability in fourth or fifth decade. CPK is elevated and muscle biopsy shows non-specific dystrophic changes. (b) Scapuloperoneal muscular dystrophy - Presents in early adult life with foot drop due to weakness of anterior tibial and peroneal groups. Extensor digitorum muscle is characteristically spared and may be hypertrophied. The disease runs a benign course. Wasting and weakness in upper limbs is initially confined to scapular muscles but later spreacte to involve biceps, triceps, forearm extensors and sometimes small muscles of hand. (c) Congenital muscular dystrophy - One of the causes of the floppy infant. Myopathy manifests at birth or early life. Small, weak, hypotonic muscles, proximal usually more affected than distal. Both sexes (3) Autosomal dominant muscular dystrophy - (a) Facioscapulohumeral dystrophy - Either sex. Onset usually in adolescence. Initial involvement, sometimes symmetrical, of facial and shoulder-girdle muscles, soon followed by weakness of anterior tibial and peroneal muscles, usually with spread within 20 or 30 years to pelvic muscles. Profound facial weakness produces pouting of the lips and a transverse smile. Slow insidious progression with periods of long arrest of the disease. (b) Distal muscular dystrophy of Welander - Very rare Presents with slowly progressive, predominantly distal wasting and weakness. Muscle biopsy similar to myotonic dystrophy. (c) Ocular and oculopharyngeal muscular dystrophy - Presents in adult life with ptosis and extraocular weakness, usually without significant diplopia. Dysphagia is prominent in some families. Face and sternomastoicte are commonly affected and most patients develop weakness in the legs. Relatively benign course. Muscle biopsy shows vacuolar changes. Management - None specific. Principles are to treat complications such as respiratory and urinary infection if and when they occur, to avoid trauma which may easily result in fracture of limb bones and to keep the patient active as long as possible. II. Myotonic disorders -Failure of voluntary muscles to relax immediately innervation ceases. 1. MYOTONIC DYSTROPHY (Dystrophia myotonica) - (i) Onset - Most patients present in adult life with distal weakness and wasting in upper or lower limbs. (ii) Muscle weakness/wasting - (a) Myopathic facies - Ptosis, hanging jaw, haggard ap­pearance, temporal wasting. (b) Weakness of neck flexion, wasting of sternomastoicte. (c) Distal limb weakness with wasted brachioradialis. 3. Frontal baldness. Hyperostosis frontalis interna. 4. Cataracts (post. subcapsular) 5. Cardiac conduction defects (Heart block, at rial arrhythmias). Cardiomyopathy. 6. Hypoventilation, post-an aesthetic respiratory failure. 7. Hypersomnolence, mental retardation. 8. Hypogammaglobulinemia. 9. End-organ resistance to insulin (Impaired glucose tolerance). 10. Dysphagia, oesophageal dilatation. Investigations - (a) CPK - Normal or slightly elevated. (b) EMG - Characteristic myopathic picture with myotonic discharges. (c) Muscle biopsy - Chains of central nuclei, marked variation of

- Frusemide 1g/day may be needed to produce naturesis and reduce oe

insignificant. (b) Diuretics - Frusemide 1g/day may be needed to produce naturesis and reduce oedema. If diuresis is too vigorous, it may precipitate circulatory collapse and acute renal failure. The possibility can be anticipitated by infusion of 'salt-poor1 albumin to maintain plasma volume. (c) Hypehipidemia - There is increased incidence of cardio-vascular disease when proteinuria is heavy and prolonged Hydroxymethyl glutaryl co-enzyme A (HMG CoA) reductase inhibitors may be helpful. (d) Antibiotics - Prophylactic antibiotics should be given against possible pneumococcal peritonitis andsepticemia MANAGEMENT OF RFLAPSE - Relapses may be associated with bacterial or viral infection especially of upper respiratory tract. Treatment consists of - (a) Corticosteroids - for infrequent relapses and if the disease remains sensitive to steroid therapy. The drug may be given as a continuous low dosage regime, each patient should be 'titrated' for the lowest effective dose (usually 5-15 mg/day). This may eliminate the need for giving ACTH, or alternate day steroid schedule to prevent the most important side effect of steroids in children namely growth failure. (b) Cytotoxic drugs - in those who suffer frequent relapses Cyclophosphamide 1.5-2.5 mg/kg/day for 8 weeks induces stable remission averaging about 3 years. Leucocyte count should be checked weekly. Immediate toxicity of the drug is negligible but there may be long-term effects. II. With diffuse membranous glomerulonephritis -Long term outlook is poor. Prednisolone 120 mg on alternate days may result in improved renal function Dipyridamole, warfarin and cyclophosphamide may also produce significant fall in urine protein, rise in serum albumin and improvement in creatinine clearance. 5. RECURRENT HEMATURIA - yndrome dominated by episodes of macroscopic hematuria, at times associated with loin pain and with tendency to exacerbations following viral upper respiratory infections or strenuous exercise. It most commonly affects boys and young males. Microscopic hematuria persists inbetween attacks and protenuria absent or moderate. Renal pathology in most cases is IgA nephropathy (Berger's disease) Course is often benign, some patients tend to develop progressive renal disease Treatment - None specific. 6. PERSISTENT ASYMPTOMATIC PROTEINURIA AND/OR HEMATURIA - in an apparently healthy person is detected on routine medical examination Causes - (a) Primary glomerulardisease - Mesangial proliferative GN, mesangiocapillary GN, membranous GN, focal segmental glomerulosclerosis (b) Multisystem disease - SLE, Henoch-Schonlein purpura (c) Miscellaneous - (i) Renal - Tumors, cystic disease of kidney, renal tuberculosis, tubointerstitial nephropathy. (ii) Non-renal - Urothelial tumors, prostatic disease Investigations -Assessment of renal structure and function including urine microscopy and culture, IVU and ultrasound. Renal biopsy if evidence of disease progression, particular/ if the process is amenable to therapy. 7. HYPERTENSION - Incidence of hypertension in patients with renal disease rises as renal function declines. Two major mechanisms are responsible. (a) Raised BP as a result of renal or renal vascular disease - (i) Increase in body sodium and water content. (ii) Inappropriately increased activity of the renin-angiotensin aldosterone system. (b) Renal damage as consequence of raised BP- The effect of hypertension depends on whether the raised pressure is in the benign phase or accelerated phase. In the latter, rapid progression to renal failure is the rule. 4. ACUTE RENAL FAILURE (ARF) Definition - ARF may be defined as an sudden fall in glomerular filtration rate sufficient to cause uremia. Oliguria (<>

- Either sex. Onset usually in third decade. (i) Pelvifemoral form - Weakness begins in pelvic girdle musculatur

dystrophy - Either sex. Onset usually in third decade. (i) Pelvifemoral form - Weakness begins in pelvic girdle musculature (psoas, glutei and quadriceps) and results in waddling lordotic gait with difficulty in climbing stairs. Winging of scapulae. (ii) Scapulohumeral form- Weakness confined initially to shoulder girdle and upper arm muscles. Deltoids are usually spared and may appear enlarged due to severe atrophy of upper arm muscles. Pelvic girdle musculature usually becomes affected at a later stage. The disease runs a variable course leading to severe disability in fourth or fifth decade. CPK is elevated and muscle biopsy shows non-specific dystrophic changes. (b) Scapuloperoneal muscular dystrophy - Presents in early adult life with foot drop due to weakness of anterior tibial and peroneal groups. Extensor digitorum muscle is characteristically spared and may be hypertrophied. The disease runs a benign course. Wasting and weakness in upper limbs is initially confined to scapular muscles but later spreacte to involve biceps, triceps, forearm extensors and sometimes small muscles of hand. (c) Congenital muscular dystrophy - One of the causes of the floppy infant. Myopathy manifests at birth or early life. Small, weak, hypotonic muscles, proximal usually more affected than distal. Both sexes. (3) Autosomal dominant muscular dystrophy - (a) Facioscapulohumeral dystrophy - Either sex. Onset usually in adolescence. Initial involvement, sometimes symmetrical, of facial and shoulder-girdle muscles, soon followed by weakness of anterior tibial and peroneal muscles, usually with spread within 20 or 30 years to pelvic muscles. Profound facial weakness produces pouting of the lips and a transverse smile. Slow insidious progression with periods of long arrest of the disease. (b) Distal muscular dystrophy of Welander - Very rare. Presents with slowly progressive, predominantly distal wasting and weakness. Muscle biopsy similar to myotonic dystrophy. (c) Ocular and oculopharyngeal muscular dystrophy - Presents in adult life with ptosis and extraocular weakness, usually without significant diplopia. Dysphagia is prominent in some families. Face and sternomastoicte are commonly affected and most patients develop weakness in the legs. Relatively benign course. Muscle biopsy shows vacuolar changes. Management - None specific. Principles are to treat complications such as respiratory and urinary infection if and when they occur, to avoid trauma which may easily result in fracture of limb bones and to keep the patient active as long as possible. II. Myotonic disorders -Failure of voluntary muscles to relax immediately innervation ceases. 1. MYOTONIC DYSTROPHY (Dystrophia myotonica) - (i) Onset - Most patients present in adult life with distal weakness and wasting in upper or lower limbs. (ii) Muscle weakness/wasting - (a) Myopathic facies - Ptosis, hanging jaw, haggard ap­pearance, temporal wasting. (b) Weakness of neck flexion, wasting of sternomastoicte. (c) Distal limb weakness with wasted brachioradialis. 3. Frontal baldness. Hyperostosis frontalis interna. 4. Cataracts (post. subcapsular) 5. Cardiac conduction defects (Heart block, at rial arrhythmias). Cardiomyopathy. 6. Hypoventilation, post-an aesthetic respiratory failure. 7. Hypersomnolence, mental retardation. 8. Hypogammaglobulinemia. 9. End-organ resistance to insulin (Impaired glucose tolerance). 10. Dysphagia, oesophageal dilatation. Investigations - (a) CPK - Normal or slightly elevated. (b) EMG - Characteristic myopathic picture with myotonic discharges. (c) Muscle biopsy - Chains of central nuclei, marked variation of

disintegrating agents. The contents of capsules other than Modified-release (Sustained-release) Capsules do not contain

fillers, wetting agents and disintegrating agents. The contents of capsules other than Modified-release (Sustained-release) Capsules do not contain any added colouring agent. Hard Capsules: Hard capsules contain the medicament(s) in the solid form. Where two mutually incompatible drugs are present in the mixture, one of the drugs can be put as a tablet or pellet or in small capsule and then enclosed with the other drug in a large capsule.Soft Capsules: Soft capsules shells are usually formed, filled with medicament and sealed in a combined operation on machines. In some cases, shells for extemporaneous use may be performed. The shells which are thicker than those of hard capsules are formed to produce capsules which are spherical, oval or cylindrical with hemispherical ends. The shells may sometimes contain a medicament. They may contain a preservative to prevent growth of fungi. The contents of soft capsules usually consist of liquids or solids dissolved or dispersed in suitable excipients to give a paste-like consistency but may also consist of powders or granules. As soft gelatin shells contain appreciable amounts of water, migration of capsule contents, particularly of% water-soluble ingredients, may occur. Modified-release Capsules: Modified-release (Sustained-release) Capsules are hard or soft capsules in which the contents or the shell, or both, contain auxiliary substances or are prepared by a special process designed to modify the rate at which the active ingredients are released Enteric Capsules: Enteric Capsules are hard or soft capsules prepared in such a manner that the shell resists the action of the gastric fluid but is attacked by the intestinal fluid to release the contents. STANDARDSContent of active ingredients: Determine the amount of active ingredient(s) by the method desctibed in the Assay and calculate the amount of active ingredient(s) in each capsule. The result lies within the range for the content of active ingredient(s) stated in the monograph. This range is based on the requirement that 20 capsules, or such other number as may be indicated in the monograph, are used in the Assay. Where 20 capsules cannot be obtained, a smaller number, which must not be less than 5, may be used, but to allow for sampling errors the tolerances are widened in accordance with Table 1. The requirements of Table 1 apply when the stated limits are between 90 and 110%. For limits other than 90 to 110%, proportionately smaller or larger allowances should be made. Uniformity of weight: This test is not applicable to capsules that are required to comply with the test for Uniformity of content for all active ingredients.Weigh an intact capsule. Open the capsule without losing any part of the shell and remove the contents as completely as possible. To remove the contents of a soft capsule the shell may be washed with ether or other suitable solvent and the shell allowed to stand until the odour of the solvent is no longer detectable. Weigh the shell. The weight of the contents is the difference between the weighings. Repeat the procedure with a further 19 capsules. Determine the average weight. Not more than two of the individual weights deviate from the average weight by more than the percentage deviation shown in Table 2 and none deviates by more than twice that percentage. TABLE 2Average weight of capsule Percentage deviation contents Less