MBBS UM (malaya) EXTENDERS

I'm BACK!!!

2011-05-16T00:49:00.003+08:00

there's been a while - i mean almost 1 year and half without post.. alot of things happen by and change me a lot..

For ur information, i've working at HSI for the past 1 year 5month+ as a Houseman

Currently in the 5th posting - orthopaedic posting where now left either Anaest or ED posting.

i've lot to share with u guys but i dont think i can post it within 1 night.

but anyway, i will definitely post what's will happen in my life after this.

nitenite~

PSP Custom Firmware 5.50 Gen-D3 Final Released

2009-12-19T01:35:00.004+08:00

As we all know, yesterday's release of Custom Firmware 5.50GEN-D3 didn't really went well as planned with some users reporting various problems using the firmware update. So what's the reasons behind the hiccups and what's new with the latest release?

As posted by voxuni over at PSPGEN (translated):

A little less than 24 hours after our previous release, here is the Custom Firmware 5.50 GEN-D3 fully functional, we will try to respond quickly to the question everyone asks:

But what happened anyway?
As you all noticed last night the server was "slightly" faltered under the weight of multiple connections, and F5 desperate that most of us were abused, awaiting the arrival of new custom firmware.
The editor allows us to create and publish our news has also been affected, and if we could publish, not without difficulty, the 5.03GEN-C, things are complicated when it came time to finalize the news on the 5.50GEN-D3. When we finally had the opportunity to access the editor, is a beta version already on our servers which has unfortunately been put online.

The version presented this morning in the emergency encountered numerous problems for some owners of PSP Slim. In fact, a bug prevented in the VSH to see the ISO files from the Memory Stick. This bug was not found on our PSP, Yoshihiro was soon given the job based on the feedback you've provided in the pages of our forums.

We apologize for the inconvenience, and we invite you to take advantage of this revised version. You can reinstall it safely over your version 5.50GEN-D3 current.

5.50GEN-D3 - 2

Improvements in the final version:

* Fix for bug eliminate the VSH menu, everyone can now enjoy the contents of its Memory Stick
* Update on backups that were seen as corrupt.
* Improved speed of access to Memory Stick during a game session
* Added support for IRSHELL D3 which will release shortly.

Only God Eater worries arise again, but we can hope that this update should address everyone. During this long day, we noticed that a lot of problems stem from improper installation, and we invite you to read the next page ...

Installation:
* Download the 5.50 GEN-D3 File below
* Connect your PSP via USB Mode
* Extract the 550.PBP and the PSP folder to the root of your Memory Stick (not MP_ROOT)
* Exit USB Mode
* Go to your Game Menu and run 5.50 GEN-D3 Quick Updater
* Follow the Instructions
* Done!

Changelog:
* Compatibility with all known PSN Game/Demo from on 15/12/2009
* Compatibility with all known UMD on 15/12/2009
* Add ISO SPeed MS loading (Beta version not really tested because we don't have any fake MS)
* Network update
* Fix for bug eliminate the VSH menu, everyone can now enjoy the contents of its Memory Stick
* Update on backups that were seen as corrupt
* Improved speed of access to Memory Stick during a game session
* Added support for IRSHELL D3 which will release shortly

Download: hotfile
Mirror1: mediaupload
Mirror2: mediafire

PSP Custom Firmware 5.50 Gen-D3 Is Now Out

2009-12-16T23:45:00.003+08:00

PSP Custom Firmware 5.50 GEN-D3 has been release by the famous PSP Custom Firmware Developer Team PSPGen just a few hours ago . PSP Custom Firmware 5.50 GEN-D3 – PSP CFW 5.50GEN-D3 , This new PSP Custom Firmware 5.50 GEN-D3 will give users more compatibility for the latest ISO and CSO game suppport that require highers firmware then 5.55 .

This release should also be able to connect to the PSN store now with this new PSP Custom Firmware 5.50 GEN-D3 release .

This is what the developer said will be new with new version of PSP Custom Firmware 5.50 GEN-D3

WARNING!

DO NOT ATTEMPT TO USE THIS PROGRAM ON TA088v3 PSP-2000 and PSP-3000 IN DANGER OF MAKING YOUR PSP TOTALLY UNUSABLE WITHOUT USING THE RECOVERING.

FOR OTHER READ THE FOLLOWING CAREFULLY TO AVOID MISTAKE IN HANDLING (installing official firmware for example).

Prerequisite:

This installer works on any PSP-1000 or PSP-2000 already custom firmware 4.01 M33 or higher (as 5.00M33 example) unless the 5.50GEN-B (1). You can install directly 5.50GEN-D3 since all these firmwares, without intermediate stages except the 5.50GEN-B (1) where it will, first, install the Custom Firmware 5.50GEN-B2 can then switch 5.50GEN -D3.

* Do not leave a custom theme on your PSP.
Settings> Themes Settings> Theme> Original

* Do not leave screen custom
Settings> Themes> Background> Original

Installation:

* Download XGen Updater for 5.50GEN-D3
* Connect your PSP to the computer via USB
* Take your PSP in “USB mode” with the option “USB Connection”
* Click the right mouse button on the file you downloaded,
* Choose “Extract Files …” (WinRAR is advised)
* Choose like destination the letter assigned to your PSP from your computer.
* Press OK and wait extraction files,
* Leave the “USB mode” on your PSP
* Go to the menu Thursday> Memory Stick to start XGen Updater for 5.50GEN-D3

Here is a list of some new games tested and compatible (UMD Backup and unpatched):

* Tekken 6
* Gundam vs. Gundam
* Phantasy Star Portable 2
* Naruto
* J-League Pro Soccer Club o Tsukurou 6 Pride of J
* Naruto Shippuden Narutimate Accel 3
* James Cameron Avatar The Game
* Phantasy Star Portable 2
* R-Type Tactics II Operation Bitter Chocolate
* Bleach Soul Carnival 2
* Battle Spirits Kiseki no Hasha
* Yamada
* Etc..

Both options are already installed and working perfectly.

* Compatibility with games / demos from the PSN sold until Listed
(Tekken 6, Gundam, etc..) – OK

* Compatible with UMD games sold until Listed
(Tekken 6, Gundam, etc..) – OK

Download:
5.50 GEN-D3

PSP F.A.Q. / Guide for PSP3000

2009-12-15T21:41:00.002+08:00

This document was taken from Dark-AleX.org Forum, from a thread created by n00b81.

Please, if you are going to copy anything of this, be kind of saying the original source.

"Released" on Sceners.org

----------------

Alright, so a ton of stuff has happened in the PSP scene during the past few weeks, so we decided that we should have a fresh new PSPfaq thread. My hopes are that this will answer some of the common questions about the chickHEN, and also combine some of the old data compiled by Jonatan10 (who did a great job by the way). Please read all of PSPfaq first to make sure your question hasn't been answered, before you make a new thread on the forums. If I have left anything out, or you would like to add something worth noting, please let me know so I can add it to the list.

Before I write anything, I first would like to make one thing clear: DO NOT flash ANYTHING on a TA-88v3 mobo or PSP 3000. Even though some files may work, it is strongly advised that you don't touch flash if you don't know what you are doing. This forum has unfortunately seen four members brick their PSPs, and I would hate to see a fifth. So please, don't try to flash custom firmware on a ta-88v3 slim or PSP 3000, you will end up with a brick.

So lets start out with the new stuff:

What is the ChickHEN, and how did it originate? The ChickHEN is a homebrew enabler written by Davee that allows most homebrews to run (with the exception of plugins for now). It takes advantage of a vulnerability in the way that the PSP handles alpha transperency in TIFF images. The vulnerability was found by Malloxis (the laughing man TIFF) and was exploited by MaTiAz. Davee later used this to take advantage of his kernel exploit, which he used to load the HEN.

So are the PSP 3000/ TA-88v3 mobos hackable? Well sort of. Firmwares up to 5.02 are hackable using the GripShift exploit, and firmwares up to 5.05 (NOT 5.50) are hackable using the laughing man TIFF exploit, although the HEN can only load on firmware 5.03. Still, many people would not consider the PSP 3000 hacked, as the pre-IPL has not been cracked yet. I guess it all depends on your perception of what "hacked" really is.

Wait a sec... I heard about a "libTIFF exploit for 5.50" can this be used to load the HEN? No. This was a mistake on QJ.net's part, and is not exploitable. Please refer to this for more details: viewtopic.php?f=83&t=14024

Ok.. so I have a TA-88v3 / PSP 3000 and I'm ready to start enjoyng homebrew! What will I need to successfully load the chickHEN? Well, if you have listened to most people's advice and have stayed on earlier firmwares waiting for a hack, you are probably on firmware 4.21 (shipped with PSP 3000) or maybe on 5.00+. In either case, unfortunately you will have to finally update your firmware, if you want to use the HEN. The HEN only works on 5.03 at the moment, so first you will want to download this: http://www.psp-hacks.com/file/1645. Use this to upgrade to 5.03. DO NOT upgrade to 5.50 or you will not be able to use the HEN. Remember to have fully charged your PSP first, and run it plugged into AC, so it doesn't loose power and brick during the upgrade process.

Once you have successfully updated to 5.03, you may proceed to download the chickHEN here: http://downloads.exophase.com/506/chick ... nabler-r2/

Follow the instructions in the readme to complete the installation.

So what exactly can I do with the chickHEN?

davee.x-fusion.co.uk escribió:
ChickHEN works as a homebrew enabler for all PSP models (1000, 2000 and 3000) and allows execution of homebrew games and apps on 5.03 Official firmware. It can allow you to play games such as Bugz!, Jellycar or run apps such as pspfiler and PSPTube. Homebrew enhances the experience of a normal PSP without any faulty side-effects.

What can't I do with the chickHEN?

davee.x-fusion.co.uk escribió:
- Run ISO, CSO or any other form of UMD backup.
- Run PSX Games
- Touch The Flash of your beloved PSP
- Magically allow the use of Custom Firmware (on TA-088v3 or PSP 3000)
- Load plugins

Can I unbrick a TA-088v3 ?
NO.
If you foolishly wrote on the flash of a TA-088v3 (for example, by trying to install a "full" custom firmware on it), it is bricked, and nothing can help you, even Pandora Batteries. Send the console to Sony's customer service. Or sell it for parts on eBay.

Can I unbrick a PSP 3000 ?
NO.
If you foolishly wrote on the flash of a PSP 3000 (for example, by trying to install a "full" custom firmware on it), it is bricked, and nothing can help you, even Pandora Batteries. Send the console to Sony's customer service. Or sell it for parts on eBay.

I ran Hellcat's recovery flasher on my TA-088v3/PSP3000 and now I only get a black screen, what can I do?
Congratulations, you decided not to read ALL the warnings about flashing these models of PSP, and got yourself a brick . See above.

Can I use LEDA(Legacy Software Loader) on the chickHEN? No. This will most likely brick your PSP (can't confirm for sure as no one's tried, nor would want to )

Is there anyway to make the HEN more "stable"? No. There isn't any technical way that could make this more stable. However, some people have put together some different packs of images that seem to help them boot it more often. Refer to these similar threads for tricks on how to get the HEN loaded more often:

viewtopic.php?f=83&t=13791&start=0

Some individuals have also reported that restoring system default settings, switching to "Original Theme", and changing the language settings, as well as formatting your media card helps to increase the chances of their PSP successfully loading into the HEN environment.

Can I run Game backups (ISO/CSO) on the chickHEN in R2 or later revisions? ISO/CSO game backups cannot run in the chickHEN envrinoment, nor will support ever be added in (at least on Davee's part).

I heard there is a working patch to get IRshell running on the chickHEN, where can I obtain these files? Thanks to Intense for kindly uploading the file. You can get it here: download/file.php?id=2706

When will chickHEN revision 3 be released, and what can we expect? Here are some of the features we can expect in the next revision:

* Hide TIFF in PHOTO
* Hide PIC1 Homebrew Icons
* Spoof system settings version
* Spoof mac address
* Redirect Network Updater
* Spoof firmware version
* Use Nandgaurd technology
* Store ChickHEN config
* Reboot PSP

Unfortunately, Davee is currently busy with other projects, so we may not see the release of chickHEN R3 for a while.

I used HellCat's recovery flasher from the chickHEN on a PSP 3000 to flash custom firmware, and now my PSP turns on with a green light, but all I get is a black screen, have I bricked it? What should I do? Yes, unfortunately you have a brick. You have two options: you could either send it in to Sony to repair, or wait for someone to hack the pre-IPL, and make a tool to get into service mode. And we all know that the chances of the pre-IPL ever being hacked is extremely slim, so you'll just have to send it in and get it back with 5.50 OFW

I heard that the TIFF file format is no longer supported anymore in 5.50, is this true? Partially. You can still view most TIFF images, just not ones that use extra alpha transpency layers (something along these lines ).

What region is my PSP?
For this you have to look for the number at the end of the serial code I guess its called at the sticker at the bottom.

It should be something like 100?, 200?, or 300?. Look at the last number. The last number refers to the region it belongs to.

So basically look at the last number and compare it to this.

PSP-X000-Japan

PSP-X001-US/North America

PSP-X002-Austrila/New Zealand

PSP-X003-UK

PSP-X004-Europe

PSP-X005-Korea

PSP-X006-Hong Kong/Singapore

PSP-X007-Taiwan

PSP-X008-Russia

PSP-X009-China

PSP-X010-Mexico
Thanks ilostchild and Blackbird256 for the info!

What PSP model do I have?

Ok with this as with the region you have you have to check the sticker at the bottom there at then end you will find one of the following:

PSP-100X This is the first PSP model the Phat

PSP-200X This is the second model the PSP Slim

PSP-300X This is the third and most recent model also known as the PSP Brite

Is DAX still working on the PSP 3000 and the PSP 2000 with the TA-88v3 motherboard?
Yes he is working on it diligently we just have to wait patiently for him to succeed and release it. He probably wont release news on it but Im certain he is working on it. If he wasnt he would have already announced it here and would have told us all but as he hasnt said that hes stopped working on them I believe he is. So please stop believing posts at other forums and comments. Just look on here at DAXs forums to check and then if he does say hes stopped working on it here then you should believe it.

7. What is a Magic Memory Stick also know as MMS?
Here's the definition from the PSP Dictionary

[quote]Magic Memory Stick: (MMS) An Memory Stick with the necessary files to boot with a JigKick Battery.]

More in depth its a memory stick with the necessary files and formatted in a way which with a jigkick battery it can be used to install CFW on most PSPs.

What PSP is the best?/Which PSP should I get?
To answer this question Ruyor has created a great powerpoint showing you each PSP and explaining the Pros and Cons of each. Also, the new version contains more detailed info and comparison of the different models (now with PSP Go! details).
----------------

250 Cases in Clinical Medicine

2009-12-08T03:01:00.006+08:00

Yup.. This is the best book for revision that i've ever had.. This book already runs for 7 years in med school and still among the best for revision either short or long case exam, neither final MBBS nor MRCP.

Bear in mind that my other blog posted the same thing before however the link was broken due to termination of the rapidshare account that i have earlier. Thus, this post is just another new update for the new link so that everyone who missed it can still have it. The file still maintain the pdf format, unlike the other circulating on the web which is a chm format. Password adalah nama saya. And if u dont know the password just use the YM next to u and ask.

Rating: 4 stars

Good Luck for ur finals and happy revision!

Rapidshare Premium Link Generator

2009-12-08T00:10:00.007+08:00

Rapidshare Megaupload Hotfile Premium Link Generator
Yup... no kidding.. ini bukan main2. and i've used it for quite sometime.. haha.. Sorry i cant share it to u earlier becoz of u know y rite? There are 2 websites which are currently working.

Basically the website will download the rapidshare file to their server(superfast server) and store it for a while and usually the download process from RS to their server will take about 1 minute.

Then later the web will generate a link to the server and then tada~ u can download it with your download manager. The link will dead if u did not start the download within the time limit. That's the overall process.

However, in order to open these websites, u need to answer a set of questionaire. The questionaire are merely a tool so that u will give your phone number and then u will be ask to sent an ON msg to certain number. Ala.. u know rite, type ON cinta and then send it to 22333. But wait.. I dont ask u to do that. This is one of thousand methods outside there a scam to trick your money just before u now it was a scam, your phone credit is already negative. Thus let us cheat them before they cheat us!

There are 2 ways:

1 All u need is a firefox and an addon that will bypass the CPAlead questionaire.
Download it here
Firefox
CPA blocker thanks to Joe Satriani for a nice script

I need to remind u that the CPA blocker will not actually 100% work. Thus u need to reload the page until it work. Mcm kaedah cuba jaya.

2. And the other one i really dont know wether its work or not, but u can give it a try
surveyblock.com

Hey wait.. I havent give the RS generator web's link rite? Here u go..

Rapidit.info
and
Rslinkgens.info

STREAMYX SUX

2009-12-04T02:02:00.005+08:00

see this pingtest run at pingtest.net

F- FAIL! - VERY POOR, REAL-TIME INTERNET APPLICATION PERFORMANCE WILL SUFFER GREATLY ON SUCH CONNECTION

WHY STREAMYX?? I've applied 1mbps, but i never get above 0.9. And last nite i got 0.3!!!!!! are u doing fair policy usage and limiting my bandwidth? COME ON LA STREAMYX! I never use any p2p and on agreement u never said about fair policy usage.. U sucks man.. Even my father fed up watching youtube becoz of u slower than chingciapore

iphone is the most expensive phone?

2009-12-03T20:24:00.005+08:00

I was searching for the cheapest 2nd hand iPhone 3Gs for my self, that i suddenly cross some wiki saying that the most expensive phone is the iPhone. Yup, seriously. But not the ordinary iPhone that we have in Malaysia. It the iPhone 3GS SUPREME..

The casing of the phone is being created with 271 grams of 22ct solid gold and the front bezel houses 136 flawless diamonds color F with total weighs of 68 cts.

Furthermore, the Apple logo of the phone is made of 53 flawless diamonds amounting 1ct and the front navigation button is home to a single cut very rare diamond at 7.1 cts. The luxury phone resides in an equally luxurious chest that has been made form a single block of Granite, in Kashmir gold with the inner lined with Nubuck top grain leather which weighs at 7kg.

According to Hughes who is the person who developed the iPhone Supreme, they have spent 10 months to create this luxury phone and more of the time was spent in trying to source the diamond for the navigation button.

The iPhone 3GS SUPREME is expected to be at the priced of $3.15 million. Now i wonder this iPhone can be jail break or not.. LOLZ

cufflinks geek!!

2009-11-28T02:34:00.001+08:00

I was trying to search for a nice cufflink and i saw some pretty cufflings to share with u guys..
Hoho.. this one surely for Dr haris..

James Bond USB Functional Cuff Links

Lego Cuffling

Rubic Cube
This is the best

apple.. another one for Dr haris.. lolz

WAA.. this cuffling can measure CVP!! lolz

Star Trek The Enterprise

This one Star Wars

Pac Man Mania!

Another free money using FB and paypal

2009-11-25T15:38:00.004+08:00

This is NOT a joke...No catches and definitely it's not April 1st.

PayPal is giving away $1 just to add an app (a wishlist) to your facebook account (absolutely no purchase required).
Visit this page: PayPal WishList
Within a minute create a small wishlist of 5 items and save it. Now submit your paypal email-id in the top-left side of the same page... congratulations you just earned 1 USD. But as the post-title says you can make up to $100 through this offer, here's what you have to do; ask your friends to make similar wihlists and for each additional wishlist, along with your friends you will earn a US Dollar too. Nobody has to pay a single penny, simply refer your friends and celebrate the festive season with them!

NOTE: It is important that your paypal account is a verified account to participate in this offer.

T&C (Don't worry nothing serious here, but read on...)
1. Offer ends at 23:59:59 SST on December 31st, 2009.

Eligibility:

1. successfully complete registration for a new PayPal account within the Promotion Period or already have an existing PayPal account prior to the Promotion Period;
2. submit to PayPal via the PayPal WishList and within the Promotion Period, the email address to which your PayPal account is linked;
3. be at least of 18 years of age, and have a PayPal account with a valid registration address in relation thereto located in India, Thailand, Malaysia, Korea, Vietnam, Philippines, Indonesia or Singapore (“Eligible Countries”);
4. have a PayPal account in Good Standing, with current contact information throughout the Promotion Period. In order for an account to be deemed in Good Standing as that term is used herein, the account must not have a hold status and/or be suspended or past due as of December 31st, 2009; and
5. complete the downloading of the PayPal WishList, and use the same to create a PayPal WishList, within the Promotion Period.

Prizes:
You may receive up to the maximum total sum of $100 USD, through this Promotion.

A tired weekend, GPMS and Shamsol Bahari

2009-11-23T21:22:00.007+08:00

1) Saya terpanggil ke KL oleh sahabat saya untuk menyertai persidangan kebangsaan GPMS pada kali pertama hujung minggu lepas. Saya diletakkan sebagai perwakilan daripada Johor Bahru. Bayangkan, saya tak pernah ada dalam GPMS tiba-tiba saya terus jadi perwakilan JB.

2) Ianya diadakan di kampus induk UITM, Shah Alam. Segalanya disediakan, dari segi pengangkutan, penginapan dan juga makanan.

3) Kerana ingin bantu sahabat saya, saya sanggup datang dari JB ke Shah Alam semata-mata untuk membantu dalam menaikkan undi kerana pengerusi GPMS Johor, saudara Rusdi ingin bertanding Presiden GPMS ekoran daripada senario DS Rezal Marican Naina Marican yang merupakan presiden GPMS 2006/09 menyatakan bahawa beliau tidak mahu mempertahankan jawatannya.

4) Saya bertolak dari JB pada hari khamis malam dan sampai ke UM menaiki bas. Saya bermalam di bilik sahabat saya, Mohd Najmi sebelum bertolak pada hari esok untuk ke UITM Shah Alam. Semasa di UM juga saya terpanggil untuk melawat kawan saya Samsol Bahari yang pada ketika itu koma akibat diabetes, namun kehadiran saya pada pukul 2 pagi tidak disedari staf jururawat lantas pintu ke ICU tidak dapat dibuka.

5) Mengikut pengamatan sahabat saya Najmi, 2 jam selepas itu, kawan saya yang koma selama 8 hari mula menyedarkan diri. Alhamdulillah, saya sempat berjumpa beliau pada hari Ahad sebelum saya pulang ke JB. Saya akan ceritakan pengalaman beliau semasa koma dibawah. Sebelum itu, berbalik kepada GPMS.

6) Mengapa saya kata tired? Sebab penat duduk di kerusi dengar orang bagi ceramah dan perbahasan. Majoritinya bosan walaupun ada yang best terutama babak2 ucapan daripada mantan Presiden GPMS Datuk Suhaimi Ibrahim.

7) Terlalu lama sehingga sakit belakang saya sampai saya nak tido pun tidak boleh. Teringat saya pada junior yang saya pernah oriented pada tahun 2 sampai budak itu sakit belakang sampai tak boleh bangun terus masuk wad PPUM. Barulah saya tahu bertapa teruknya bertahan 12 jam duduk.

Gabungan Pelajar Melayu Semenanjung (GPMS)

1) GPMS nama bak besar di mata rakyat, namun sayangnya ianya tidak seperti mana yang kita lihat di kaca TV.

2) Saya amat memandang tinggi pada persatuan ini sebelum ini namun segalanya berubah apabila datang ke persidangan ini.

3) Apa yang saya boleh simpulkan adalah kuasa lebih penting daripada persatuan. Majoriti saya lihat semuanya berpuak-puak, kenegerian, dan tamak kuasa merasakan diri lebih layak memegang jawatan di dalam GPMS.

Sebahagian daripada perwakilan negeri Selangor. Tua2 nampak.. tak macam perwakilan Johor yang rupa kebanyakan macam budak sekolah dan politeknik

Inilah pengerusi GPMS Johor, saudara Rusdi. Asalnya nak bertanding Presiden GPMS sebab merasakan beliau adalah paling senior, namun disebabkan mungkin 'perwakilan Johor' tidak seramai per'wakilan' daripada Pulau Pinang, lalu diserahkan Presiden kepada PP. Penat sahaja saya datang jauh2 ditambah sakit belakang.

4) Senarionya tidak berbeza sangat dengan suasana pemilihan seperti parti politik. Hari pertama perasmian oleh Dr Puad Zarkarshi, Timbalan Menteri Pelajaran, hari kedua ucapan dasar presiden dan juga perbahasan ucapan dasar presiden daripada wakil negeri disamping penamaan calon dan hari terakhir adalah hari pengundian dan juga penentuan siapa yang meneraju GPMS ataupun dengan kata lain siapakah yang akan dapat cable besar direct pergi kepada bapak2 menteri.

5) Ya, benar. Terus terang saya katakan GPMS saya lihat lebih kepada platform untuk menunjukkan atau menonjolkan diri kepada bapak2 menteri agar dapat nama, dapat jawatan, dan mungkin dapat tender kot daripada dilihat dalam membantu pelajar-pelajar melayu dalam pelajaran.

6) Saya kurang faham apa sebenarnya telah terjadi kepada GPMS sejak kebelakangan 3 tahun ini semenjak krisis GPMS yang terbahagi kepada 2 pada tahun 2006. Namun 3 hari saya bersama GPMS telah cukup untuk memberitahu saya tentang begitu nazaknya GPMS ketika ini lagi teruk daripada krisis MCA yang dihadapi sekarang.

7) GPMS merupakan sebuah NGO yang non partisan, namun persepsi yang ada menunjukkan ianya tidak begitu. Kononnya pada persidangan ini, ada kata-kata ingin menjadikan GPMS non partisan seolah-olah hanya menaruh air di daun keladi dan tidak berpijak di bumi yang nyata. Lihat sahaja mantan presiden merupakan Ketua Penerangan Pemuda UMNO

8) Saya merasakan persidangan GPMS kali ini lebih kepada kenduri kawen. Perjalanan majlis banyak kali terlewat. Waktu mengundi pun terpaksa dilewatkan selama 2 jam setelah mesen photostat rosak dan tidak boleh mengprint kertas undi.. Lawak2.. Ada pula AJK persidangan mengadu, Presiden DS Reezal Marican mara kat depa sebab majlis tak lancar, dan mulalah adegan tuduh menuduh, tak berterima kasih, ungkit wang berbanding usaha, memang layak Reezal kalah Pemuda UMNO lah dan bermacam2 lagi. Namun saya tak nafikan, pasti akan ada masalah dalam apa sahaja pun majlis yang dianjurkan secara besar-besaran.

9) Tak cukup dengan itu perwakilan yang saya rasakan tahap budak-budak sekolah, memakai jeans dan juga selipar mencacatkan perjalanan majlis. Mungkin sebab main tangkap muat 3 kuota sahaja nak masukkan dalam perwakilan cawangan masing, perwakilan pun tak sempat saring, pilih saja mat rempit dan mat punk utk naik ke atas pentas masukkan undi mereka..

10) Di sini secara ringkas apa yang saya boleh simpulkan tentang GPMS

a) Kuasa - apa saja yang boleh dilakukan utk mendapatkan jawatan adalah halal.
b) Puak-puak - wujudnya sikap bermuka-muka dan tikam menikam dibelakang kawan
c) Sekadar NGO yang hanya syok sendiri, tak ada pun jentera untuk menguatkan GPMS negeri.
d) Time persidangan berlangsung, time itula wujudnya cawangan-cawangan dan ahli-ahli baru dengan harapan untuk meningkatkan lagi undi masing-masing agar jawatan tak terlepas.
e) Sistem ahli yang tidak telus dan bersistematik memudahkan lagi penyelewengan.
f) Senioriti penting gila sampai ada budak umur 23 tahun masuk bertanding jawatan sehingga neliau sendiri pun terasa tercabar utk sama2 bertanding
g) GPMS memang NGO UMNO sebab nak tanding jawatan tertinggi pun kene mintak kebenaran Timbalan PM dulu oi...
h) Dah tak da harapan lagi lah di dalam GPMS sebab ianya majoriti diketuai oleh orang yang hanya pentingkan orang2 dia dalam 'kabinet dia'. Orang lain dipijak dan tak dijaga lalu rugilah GPMS kehilangan orang yang benar2 memperjuangkan pelajar melayu.

11) Dahla.. saya tak mahu sebut lagi pasal GPMS.. cukup la 3 hari tu.. lu pikirlah sendiri. Harapan, objektif GPMS untuk membantu membela dan memperkasa pelajar-pelajar melayu benar-benar dilakukan.

Pengalaman Koma Samsol Bahari

1) Saya bernasib baik sebab saya masih sempat jengok Samsol pada hari Ahad selepas tidak berjaya melawat beliau pada hari Jumaat lepas. Nasib baik tidak ada aktiviti yang saya pada asalnya menjangkakan hari tersebut akan pack dengan aktiviti riadah bersama seorang kawan.

2) Dengar Samsol sedar sahaja saya terus lawat beliau. Beliau menyatakan sayalah kawan pertama yang menjenguk beliau sewaktu beliau sedar 100%. Najmi ada menjenguk sewaktu mula2 regain conscious namun Samsol tak teringat.

3) Staf nurse ICU tanya saya lalu saya dengan gaya medical student(MS) memakai labcoat memperkenalkan diri sebagai MS. HAHA..

4) Tiba di hujung pintu, Samsol terus angkat tangan isyarat salam, lantas saya bertanyakan condition dan progress beliau. Alhamdulillah, beliau telah 100% sedar dan mampu berbual dengan saya tanpa ada masalah ingatan kira GCS 15 la... Beliau akan dipindahkan ke wad endocrine pada keesokan harinya.

5) Untuk pengetahuan Samsol bahari terlantar di ICU koma selama 8 hari setelah beliau terkena Diabetic ketoasidosis dikomplikasikan lagi dengan sepsis atau jangkitan kuman dalam darah.

6) Beliau merupakan batch 2001/2006 dan tahun ini merupakan peluang terakhir beliau untuk menduduki peperiksaan. Berkat usaha beliau akhirnya beliau lulus MBBS bersama2 saya dan rakan2. Namun tidak sampai 4 hari selepas lulus, beliau mengalami sesak nafas dan keliru. Lalu beliau tidak sedarkan diri dan diintubasi. Pemakanan beliau juga dilakukan secara parentral iaitu salur darah. Agak gembira beliau sedar lebih awal dari jangkaan para doktor iaitu 1 bulan.

7) Dengan tidak sabarnya hati di dada ini lantas saya bertanyakan apa pengalaman mimpi yang beliau lalui sewaktu koma? Pengalaman koma tidak semua dapat rasa ini saya rasakan sesuatu pengalaman yang tidak ternilai dan saya harap tak ada lagi kawan2 saya yang mengalami situasi sebegini.

8) Sewaktu di dalam koma, beliau bermimpi mengalami perkara yang sama. Bayangkan beliau dalam keadaan itu tahu beliau didiagnose DKA. Beliau telah mimpi terlantar di ICU, diberi oksigen, tangan dan kaki beliau tidak boleh bergerak. Namun beliau tidak mendengar kata2 yang cuba disampaikan oleh ibunya. Pada detik beliau mula sedar, beliau dapat mengingat sedikit sahaja peristiwa yang berlaku kerana beliau mengatakan beliau masih lagi confuse.

9) Mengikut kata-kata beliau, beliau telah mengalami confusion dan sedikit pening sewaktu viva border lagi. Ditambah beliau, pada waktu itu mungkin ada examiner sudah perasan simptom penyakit itu. Apa pun, beliau bernasib baik pada ketika itu, beliau bersama keluarga yang baru sahaja sampai daripada sabah.

10) Saya menasihatkan beliau agar terus berehat dan tidak perlu sangat memikirkan induksi yang bakal tiba tidak lama lagi. Sama-samalah kita mendoakan kesihatan Samsol.

Sekian itu sahaja.. Terima kasih kerana membaca.

another spam

2009-11-23T19:58:00.003+08:00

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Biet tin gi chua, vao day coi di http://nhattruongquang.0catch.com

Solution? It's simply the same solution like I've post before..

Men Are Like...

2009-11-16T23:14:00.000+08:00

Men Are Like...

... Blenders.
You need one, but you're not quite sure why.

... Chocolate Bars.
Sweet, smooth, and they usually head right for your hips.

... Coffee.
The best ones are rich, warm, and can keep you up all night long.

... Commercials.
You can't believe a word they say.

... Computers.
Hard to figure out and never have enough memory.

... Coolers.
Load them with beer and you can take them anywhere.

... Copiers.
You need them for reproduction, but that's about it.

... Curling Irons.
They're always hot, and they're always in your hair.

... Government Bonds.
They take way too long to mature.

... Horoscopes.
They always tell you what to do and are usually wrong.

... Lava Lamps.
Fun to look at, but not all that bright.

... Mascara.
They usually run at the first sign of emotion.

... Parking Spots.
The good ones are already taken and the ones that are left are either handicapped or extremely small.

... Popcorn.
They satisfy you, but only for a little while.

... Weather.
Nothing can be done to change either one of them.

Pokjatt dan Fatishah

2009-11-15T23:28:00.011+08:00

To MBBS UM batch 2004/2009,

On behalf of my best friend pokjatt, im requesting the honour of your presence at the marriage of

Tg Nuramiriah Fatishah
to
PokJatt (Izzad Johari)

Date: Saturday, 26th December 2009
Time: 11.30am to 5.30pm (bersanding at 2.30pm)
Venue: Dewan Azalea, Lot 17882, Jalan Gertak Merah, 80000, Johor Bahru, Johor Darul Ta'zim.
YM: izzad_jatt@yahoo.com

--------

BM version
Kepada batch MBBS UM 2004/2009,
aku bagi pihak pokjatt ingin memberikan jemputan kepada seluruh batch tak kira melayu, cina atau india atau bumiputra atau lain2

Jemputan ke Majlis Perkahwinan Pokjatt dan Fatishah

Majlis persandingan

Tarikh: 26 Disember 2009
Jam: 11.30 pagi - 5.30 petang(bersanding at 2.30pm)
Tempat: Dewan Azalea, Lot 17882, Jalan Gertak Merah, 80000, Johor Bahru, Johor Darul Ta'zim

Majlis nikah

Tarikh: 25 Disember 2009
Jam: Confirm nanti
Tempat: Masjid Abu Bakar sebelah maahad dan Pusat Islam Johor.

Moonwater

2009-11-14T14:41:00.005+08:00

(click to enlarge)
This image provided Friday, Nov. 13, 2009 by NASA shows the ejecta plume created by the LCROSS Centaur upper stage rocket about 20 seconds after after impact Oct. 9, 2009. It turns out there's plenty of water on the moon- at least near the lunar south pole, scientists said Friday. (AP Photo/NASA)

HOHOOHO.. the moon got water!!we can now live on the moon if 2012 is really the end of the world..lolz

Splash! NASA moon crash struck lots of water

By ALICIA CHANG (AP)

LOS ANGELES — Suddenly, the moon looks exciting again. It has lots of water, scientists said Friday — a thrilling discovery that sent a ripple of hope for a future astronaut outpost in a place that has always seemed barren and inhospitable.
Experts have long suspected there was water on the moon. Confirmation came from data churned up by two NASA spacecraft that intentionally slammed into a lunar crater last month.
"Indeed, yes, we found water. And we didn't find just a little bit. We found a significant amount," said Anthony Colaprete, lead scientist for the mission, holding up a white water bucket for emphasis.
The lunar crash kicked up at least 25 gallons and that's only what scientists could see from the plumes of the impact, Colaprete said.
Some space policy experts say that makes the moon attractive for exploration again. Having an abundance of water would make it easier to set up a base camp for astronauts, supplying drinking water and a key ingredient for rocket fuel.
"Having definitive evidence that there is substantial water is a significant step forward in making the moon an interesting place to go," said George Washington University space policy scholar John Logsdon.
Even so, members of the blue-ribbon panel reviewing NASA's future plans said it doesn't change their conclusion that the program needs more money to get beyond near-Earth orbit. The panel wants NASA to look at other potential destinations like asteroids and Mars.
"This new and terrific result reassures us about lunar resources, but ... the challenges currently facing the human spaceflight program remain," Chris Chyba, a Princeton astrophysicist who is on the panel, said in an e-mail.
President George W. Bush had proposed a more than $100 billion plan to return astronauts to the moon, then go on to Mars; a test flight of an early version of a new rocket was a success last month. President Barack Obama appointed the special panel to look at the entire moon exploration program. The decision is now up to the White House, and NASA's lunar plans are somewhat on hold until then.
As for unmanned exploration, previous missions had detected the presence of hydrogen in lunar craters near the moon's poles, possible evidence of ice. In September, scientists reported finding tiny amounts of water in the lunar soil all over the moon's surface.
But it was NASA's Oct. 9 mission involving the Lunar Crater Observation and Sensing Satellite, LCROSS, that provided the stunning confirmation announced Friday — water, in the forms of ice and vapor.
"Rather than a dead and unchanging world, it could in fact be a very dynamic and interesting one," said Greg Delory of the University of California, Berkeley, who was not involved in the mission, led by NASA's Ames Research Center in Mountain View, Calif.
The LCROSS spacecraft only hit one spot on the moon and it's unclear how much water there is across the entire moon.
The October mission involved two strikes into a permanently shadowed crater near the south pole. First, an empty rocket hull slammed into the Cabeus crater. Then, a trailing spacecraft recorded the drama live before it also crashed into the same spot four minutes later.
Though scientists were overjoyed with the plethora of data beamed back to Earth, the mission was a public relations dud. Space enthusiasts who stayed up all night to watch the spectacle did not see the promised giant plume of debris.
NASA scientists had predicted the twin impacts would spew six miles of dust into the sunlight. Instead, images revealed only a mile-high plume, and it was not visible to many amateur astronomers peering through telescopes.
Scientists spent a month analyzing data from the spacecraft's spectrometers, instruments that can detect strong signals of water molecules in the plume.
"We've had hints that there is water. This was almost like tasting it," said Peter Schultz, professor of geological sciences at Brown University and a co-investigator on the LCROSS mission.
Astronaut Buzz Aldrin, who in 1969 made his historic Apollo 11 moonwalk with Neil Armstrong, was pleased to hear the latest discovery, but still believes the U.S. should focus on colonizing Mars.
"People will overreact to this news and say, `Let's have a water rush to the moon,'" Aldrin said. "It doesn't justify that."
Mission scientists said it would take more time to tease out what else was kicked up in the moon dust.

AP Science Writer Seth Borenstein contributed to this report.

Copyright © 2009 The Associated Press. All rights reserved.

Congratulations Guys

2009-11-12T00:55:00.007+08:00

no more extenders(i hope so, no pls.. no more even in HO time).. i need to change the blog's title.. (click to enlarge those pictcha)

no more extenders(i hope so, no pls.. no more even in HO time).. i need to change the blog's title..

Aku Bukan Superman

2009-09-02T08:38:00.001+08:00

The Lucky Laki - Bukan Superman Lyrics Mp3

[Top Lirik Lagu]
Aku bukanlah superman
Aku juga bisa nangis
Jika kekasih hatiku
Pergi meninggalkan aku

Ayahku selalu berkata padaku
Laki-laki tak boleh nangis
Harus selalu kuat harus selalu tangguh
Harus bisa jadi tahan banting

Tapi ternyata sakitnya cinta
Buat aku menangis

Back to [Top Lirik Lagu]:

Ayahku selalu memarahi aku
Jika jatuh air mataku
Kata ayah selalu air mata itu
Adalah tanda kelemahan
Tapi ternyata air mataku
Ternyata jatuh juga

Black Testicles

2009-09-01T20:32:00.002+08:00

Copy from Tim's Note,

Black Testicles

A male patient is lying in bed in the hospital, wearing an oxygen mask over his mouth and nose.. A young student nurse appears to give him a partial sponge bath.

"Nurse,"' he mumbles from behind the mask, "are my testicles black?"

Embarrassed, the young nurse replies, "I don't know, Sir. I'm only here to wash your upper body and feet."

He struggles to ask again, "Nurse, please check for me. Are my testicles black?"

Concerned that he might elevate his blood pressure and heart rate from worrying about his testicles, she overcomes her embarrassment and pulls back the covers..

She raises his gown, holds his manhood in one hand and his testicles in the other.

She looks very closely and says, "There's nothing wrong with them, Sir. They look fine."

The man slowly pulls off his oxygen mask, smiles at her, and says very slowly, "Thank you very much. That was wonderful. Now listen very, very closely: Are - my - test - results - back?"

HAHAHAHAHAHAHAHAHAHAHAHAHAAHAHAHAHAHA.. lawak giler

Testing Pop Up Image

2009-08-30T08:03:00.009+08:00

Which style do u like?

Click to enlarge

Doctor who migrate to other country

2009-08-21T17:53:00.004+08:00

From Chedet.co.cc

1. I gave a talk after I was conferred an honorary degree by the International Medical University. I directed a major part of my talk to the new graduates.

2. I explained that medicine is not just a profession, a qualification for earning a good income. It is a vocation, a calling which involves dedication to the job of healing the sick and caring for them.

3. What their qualification confers upon them is not just a degree but as doctors they have been elevated to a special status and endowed with special powers. They would have in them the capacity to inspire confidence and trust in their patient. The confidence and trust are such that people would literally entrust their lives to them, allowing them to cut open their bodies and do things which could kill if done by others.

4. The skill and the power they acquire owe much to the society in which they were brought up and their access to education up to the highest level. Not all human society can do this. A poor society, an unstable society, an uncaring society would not be able to give them even primary education, much less training to become a doctor. The cost borne by the society is high.Whether they get a scholarship or their parents pay for their education, they all owe a debt to society. It behoves them to repay to society through the service in which they are trained.

5. They should therefore be ready to offer their services to the society in which they lived. It may be by serving the Government or if this is not attractive enough, at least their country. They can earn a good income in Malaysia's private sector.

6. But some easily forget their debt and are easily enticed by higher pay in other countries. These countries paid nothing for their education and training and yet for a little bit more money they get the services of the people we paid a lot to train whether in Government school and universities or in private ones. Quite often the countries which get the service of our doctors are developed and rich.

7. The nation loses a lot when the people we train opts to work in other countries.

8. But the association of doctors make matters worse by refusing entry to foreign doctors to practice. It wants to keep the opportunities for making money in this country to its members only. It does not mind Malaysian doctors going out but foreign doctors may not come in. Only if they work with the Government can they come in.

9. The flow is one-way. Our doctors can leave the country but foreign doctors cannot replace them. We are losing the brains that we develop without the foreign brain coming in.

10. Despite all the Government's efforts we are losing especially the much-needed specialists.

11. There is something wrong here. If the Malaysian Medical Association (MMA) wishes to close the country to outsiders then it should also object to Malaysian doctors from leaving the country. As it is the MMA seem to be wanting to have their cake and to eating it as well.

12. I am not suggesting that as we have embraced globalisation and the free flow of capital etc that we should now allow foreign doctors to come and open their hospitals here. But I do think that if local hospitals need to employ foreign doctors then they should be allowed to.

Some of my batch gone to Singapore, and most of them are the best students in the faculty.

Of coz we can blame them just because gov has support their education eventhough they only apply loan (ptptn), but still of fee about RM1800/year (RM9000)is the cheapest fee to produce a doctor compare to the private medical school which nearly cost RM200,000. But do they care eventhough they were using 'rakyat' money ?

We are currently shortage of doctor, overall a doctor to patient ratio is about 1:1,145. Tan Sri Ismail Merican, director of health said in 2012 the ratio would be 1:600.

Calculation numbers of HOs:

Currently my batch 170. Those who go to singapore are about 10+, those who fail including me are 21 students. That doesn't include pass but then quit medicine which i think less than 5 students. So how much/percentage of doctors currently practice in GOV hospital? - about 75% only! I don't know other university, but i assume it's the same. Can we get our target of 1:600?

I do agree that some of them are too arrogant but can we blame them just because they are not practicing in Malaysia? We cant totally blame them. Working in gov hospital is like working in HELL although we've not been there, yet. Some said doctors should do charity, helping people, bla bla bla etc. Of coz we are helping ppl, but in the end what we get?

Scolded by the patients?
Almost all not appreciate what doctors do?
Low salary?
On Call 3 times/week?
No time for luxury/entertainment/family?
Working like in a factory with polluted air?
Sweating even at night because there is no air-cond?
Lost 5Kgs every months because too busy and forgot to eat?
Getting HIV because of needle prick?

I also do agree on the other hand, most of the doctors are certainly very loyal to the Gov hosp. But try asking them, do they willing to work at gov for the rest of their life if nothing change? Some of them even lost hope to Malaysian Gov, which are just waiting their bond to finish.

Practice in singapore, with only 4 night shifts/months, Salary of $3000++ --> convert RM7000 (eventhough they said they live in singapore the cost of living is high, bullshit i said to them. Do they have savings? They might have about $1000 then later come back to Malaysia once a month and blanje sakan! waaa ternganga mulut aku...) comparing to Gov hosp here basic RM2500. So basically can get about RM 3500++. RM7000-3500 = 3500.. So u actually need to work 4 times harder here to earn that singapore money.. This is HO u know.. Not a MO, Specialist, or Consultant.

So think again, by going to singapore, eventhough we feels like rakyat have been betrayed, whatever u tried to label them such as mata duitan, tak kenang budi, tak semangat patriotik, lupe daratan, selfish doctor, etc, do they care after a lot of benefits and privilege they got. Adding summore, there is no law to prevent them working outside of the country

Of coz malaysia cant support their salary to be as good as our neighbour to prevent loss, but we certainly can put an act. This law should be strict and if ever broken, immediate action such as terminate their license to practice or the worst the university should take back their degree.

What can i said is, Malaysia need a new hope. That's all. If the BN can't do it, who else can do it? PR? such a loser..

H1N1 - 5 JUTA RAKYAT AKAN DIJANGKITI

2009-08-15T20:02:00.002+08:00

5 juta rakyat Malaysia akan dijangkiti H1N1

15/08/2009 7:37pm

BUKIT MERTAJAM 15 Ogos — Pertubuhan Kesihatan Sedunia (WHO) menganggarkan lima juta atau 20 peratus rakyat negara ini berisiko dijangkiti virus selesema babi atau influenza A (H1N1) jika langkah pencegahan tidak diambil secara serius oleh orang ramai.

Menteri Kesihatan, Datuk Seri Liow Tiong Lai berkata, kajian WHO juga menjangkakan penularan wabak itu mungkin berlarutan antara enam bulan hingga setahun lagi.

“Kajian itu menyebut bahawa jika penularan virus H1N1 di sesebuah negara tidak berjaya ditangani dengan berkesan, 20 peratus penduduknya akan terdedah dengan jangkitan virus itu,” katanya kepada pemberita selepas melawat Hospital Bukit Mertajam di sini hari ini.

- BERNAMA

SCIENCE AND MATHEMATICS IN MALAY

2009-08-14T18:32:00.003+08:00

1. The Government has decided that the teaching of science and mathematics would revert to Malay in the Government school, with Chinese in Chinese schools and Tamil in Tamil schools. How this is going to help integrate Malaysians I do not know.

2. Since then I had conducted a poll on my blog. The result is 84 per cent want to retain English as the language medium for these subjects.

3. Admittedly the poll was conducted in the English language and English language speakers might be biased in favour of English.

4. But some parents and teachers had also conducted a survey and the majority are again in favour of English. A petition to the Prime Minister by parents and teachers was copied to me and they were in favour of retaining English. At least one senior non-Malay politician had left a Barisan Nasional component party and joined the opposition because of the switch back to Malay, Tamil and Chinese. He claimed that he could not afford to send his grandchildren abroad as some who advocate Malay as the medium had been doing.

5. I meet a lot of people at the various forums I am invited to speak. During the usual post-meeting tea most of the participants who got to talk with me, mostly Malays regretted the Government's decision to use Malay for Science and Mathematics.

6. The reason that has been given is that Malays, particularly kampung Malays just could not do well when the two subjects were taught in English. If we follow this kind of argument we should also stop trying to get Malays to do business because they really cannot do well in that field. They are best at working as wage-earners, particularly in Government service. We should encourage them not to try to go into business.

7. If we do this then the current anger over the New Economic Policy on the part of the non-Malays would be reduced.

8. Similarly with learning English. Malays just cannot learn and speak English. We should stop teaching it so that the language would not drag down the Malays in their exams. We should see better results.

9. Malays do best at paddy planting and fishing with rods and net. They should be taught to do this, probably with new technology.

10. By switching back to Malay, we can expect them to vote for the Government party at the next election. Similarly we can expect at least some who believe their children's future has been blighted by this decision to think again about voting for the BN.

11. I cannot read Chinese but Utusan Malaysia kindly translated the editorial in the Sin Chew Jit Poh. The editorial basically said that giving "Ang Pow" would not win over the voters.

Sokong sangat2 kata Dr M. Kalau Melayu tak boleh nak buat sume bende ni, lebih baik jangan tolong melayu dalam apa2 pun. Melayu takkan berubah. Sampai akhir zaman pun macam ni. Selagi melayu berkuasa, macam ni la jawabnya. Kene dengan penangan bila kaum lain memerintah Malaysia, melayu hilang kuasa, baru la sibuk nak perjuang bangsa, ketika itu nasi pun da jadi bubur. Tgk saja singapore, pulau tergadai dek tertipu igtkan melayu masih berkuasa sebab presiden yusof ishak, bahasa melayu dijadikan bahasa kebangsaan, pastu tak nampak pula belang pemimpin nak bela nasib melayu bahasa pembelajaran pula kesemuanya BI, baru melayu kat situ nak blajar bersaing, terkial2 baru nak naik kejar kaum lain.

Kaum lain berada 1000 langkah dihadapan, kita masih lagi terkial2 dengan langkah pertama. Tapi masih lagi ada guru yang menentang PPSMI (yang aku assume semuanya cikgu agama dan BM yang memang tak da kene mengena dengan PPSMI). mungkin cikgu ni memang tak nak anak murid dia berjaya kot. Die lebih suka anak murid terkial2 masa akan datang. Almaklumlah, kerja beliau senang, tak perlu translate2, anak murid dan anak sendiri pun senang paham bile BM, duit pun senang dapat. Tak perlu terkial2 cakap BI. Makan gaji je la cikgu2 oi. Aku rasa cikgu2 yang ajar aku sejak sekolah dari darjah satu mesti sokong PPSMI kalau dia tgk aku skg ni..

Jgn kerana kononnya nak mempertahankan dan memperjuangkan 'perlembagaan' tetapi masa depan nanti anak2 kita yang sendiri belot pada perlembagaan kerana terlalu bodoh dan hilang kuasa.

CPC - August 14 - Epilepsy

2009-08-14T13:23:00.011+08:00

Clinico-pathological Conference, 14th August 2009

A 23-year-old man was admitted to the hospital because of complex partial seizures that had become generalized.

The patient, who was from El Salvador, had been well until the age of 15 years, when he had three seizures during a two-month period. He was told that the seizures were caused by a "parasite." A medication, which has not been identified, was prescribed, and there was no recurrence. At the age of 16 years, he had a series of episodes of "panic," each lasting as long as three days. Soon after these episodes, he emigrated to the United States after a four-week stay in Mexico. Ten months later, a tonic–clonic seizure occurred.

The patient was evaluated at this hospital at the age of 17 years. The results of neurologic and hematologic examinations, blood chemical analyses, and screening of the serum for toxic substances were negative; radiographs of the chest were normal. Computed tomographic (CT) scanning of the brain, performed without the administration of contrast material, revealed a focal area of dense calcification, less than 1 cm in diameter, in the region of the left hippocampus, adjacent to the choroid fissure. A lumbar puncture was performed (Table 1). An electroencephalogram was normal while the patient was awake and while he was asleep. Treatment with phenytoin was begun, but the patient discontinued it because of anorexia. A seizure occurred, and carbamazepine was administered.

Table 1

One year later, another cranial CT study, performed before and after the intravenous administration of contrast material, showed no change in the calcific lesion in the left temporal lobe. A tuberculin skin test (purified protein derivative, 5 TU) was positive, producing a 13-mm induration. A serologic test for cryptococcal antigen was negative. Microscopical examination of a stool specimen revealed giardia. A test for antinuclear antibodies and serologic tests for histoplasmosis, blastomycosis, and coccidioidomycosis were negative. Metronidazole was prescribed. A serologic test for paragonimiasis was negative. Another electroencephalogram was normal, both while the patient was awake and while he was asleep. Radiographs of the chest remained normal. Isoniazid, rifampin, and pyridoxine were administered. The patient was subsequently lost to follow-up for five years.

At the age of 23 years, the patient returned to this hospital. He reported that his seizures had begun when he was 15 years old, after he had been struck on the right side of the head by his father and had lost consciousness. The seizures were preceded by an aura of warmth on the right side of the head; occasionally, he had brief myoclonic jerks before losing awareness. His brother added that the patient would look to the right and then fall, stiffen, and shake for several minutes. Tongue biting and incontinence accompanied the seizures, which were followed by confusion and sometimes combativeness for as long as 30 minutes. The seizures occurred as often as six times weekly but usually occurred two or three times a week. The patient had had only minor injuries as a result of the falls. He had been taking 200 mg of carbamazepine three times daily, presumably on a regular basis, during the two weeks before this presentation. He also reported having generalized fatigue, malaise, and severe headaches. He was admitted to the Epilepsy Service.

The patient's birth and development had been normal. He did not have a history of encephalitis or febrile convulsions and did not use tobacco, alcohol, or illicit drugs. He was unmarried and, because of his symptoms, was unemployed. He resided with his brother. There was no family history of seizures or other neurologic disease.

The temperature was 36.6°C, the pulse 76, and the respirations 18. The blood pressure was 130/75 mm Hg.

A general physical examination revealed no important abnormalities. On neurologic examination, the patient was fully alert and oriented; his speech was fluent. The retinas were normal. The cranial-nerve functions were intact. Motor strength was 5/5 throughout, with normal bulk and tone. Sensation, tendon reflexes, coordination, stance, and gait were normal.

The urine was normal. Hematologic and blood chemical tests (Table 2) and a lumbar puncture (Table 1) were performed. Magnetic resonance imaging (MRI) of the head, performed without the use of contrast material, showed a focus of abnormal magnetic susceptibility in the medial portion of the left temporal lobe, as well as mucosal thickening in the right sphenoid and ethmoid sinuses. Radiographs of the chest were normal. A CT scan of the brain, obtained without the administration of contrast material, revealed a calcific lesion within the tip of the left temporal lobe (Figure 1). A positron-emission tomographic (PET) study of the brain, performed after the intravenous injection of 18F-fluorodeoxyglucose, showed reduced accumulation in the left temporal lobe. No evidence of abnormal 18F-fluorodeoxyglucose uptake was observed elsewhere in the brain.

Table 2

Figure 1: CT Scan Obtained without the Administration of Contrast Material, Showing a Round, High-Density Lesion in the Medial Portion of the Left Temporal Lobe (Arrow).

The dose of carbamazepine was reduced, and then the drug was withdrawn. Continuous video electroencephalographic monitoring for a period of five days showed six typical seizures, each of which was characterized by an initial spike, followed by rhythmic activity in the left temporal region; interictal epileptiform discharges were recorded in a similar pattern. There was no obvious background abnormality in the left temporal region.

Carbamazepine therapy was resumed at the usual dose, and the patient was discharged on the sixth hospital day. He subsequently had one or two seizures per week.

A diagnostic procedure was performed.

------------------------------------------------

Discussion

Ok then.. Did u get the case given? Time to put on a diagnosis and some differentials.

This patient had had partial, or focal,seizures since adolescence. The tendency of these seizures tobegin with the same type of aura suggests that they arose froma single cortical area. Partial seizures, which are classifiedas partial even if they become generalized, are more commonthan seizures generalized at onset. In patients with partialepilepsy, the temporal lobe, particularly its medial portion,is often the site at which seizures are generated. The mostcommon underlying pathological lesion is mesial temporal sclerosis,which is characterized by a specific pattern of neuronal loss,gliosis, and axonal reorganization in the hippocampal formation,but other lesions in this region can have similar clinical manifestation.

Neuroimaging studies were performed over a period of several years. On the CT scan of the head that was obtained on admission to the Epilepsy Service, the only abnormality is a high-density, apparently calcified focus in the medial portion of the left temporal lobe (Figure 1). The lesion appears to be unchanged from that seen on the previous CT scan. On the T2-weighted images from the MRI studies, there is a focus of hypointensity in the same region, which is consistent with the presence of calcification.

Team also performed a pulse-sequence study with sensitivity to magnetic susceptibility in order to help differentiate between the presence of blood products and calcification. The focus of hypointensity did not appear to be enlarged on the pulse-sequence study, a finding that confirmed its calcific nature. On the coronal T1-weighted image, the calcification appeared to be near or within the left choroid fissure.

Before we discuss the differential diagnosis of this lesion, we must decide whether it caused the patient's epilepsy. The first step in localizing the focus of a seizure is to take a detailed history. We have also learned, however, that clinical findings do not always pinpoint the site of a seizure, since many common manifestations of seizures reflect spread of the electrical discharge from a clinically silent cortical area. In the present case, the usual warning was a sensation of warmth on the right side of the head. Unilateral sensory phenomena (with the exception of head pain) reliably indicate a site in the contralateral hemisphere. One cannot assume, however, that within that hemisphere the seizure arose in the primary sensory cortex of the postcentral gyrus; it may instead have spread to that region from the temporal lobe or elsewhere. Even areas outside the parietal lobe, such as the second sensory area of the frontal operculum, can generate such somatosensory phenomena.

When a partial seizure begins to generalize, deviation of the head and eyes toward the right — as reported in this case — suggests that the seizure originated in the left hemisphere (although when temporal-lobe seizures do not become generalized, the head usually turns toward the side of onset of the seizure). Seizures arising from the medial temporal lobe are commonly associated with a visceral, cognitive, or psychic aura and with oral movements after loss of consciousness. Such features did not accompany this patient's seizures. Furthermore, there was no reliable history of isolated simple partial or complex partial seizures, which are almost always more frequent than secondarily generalized seizures in cases of epilepsy involving the medial temporal lobe. It is possible, however, that the patient and those around him did not remember the more subtle events.

In the hospital, the withdrawal of medication would have made secondary generalization more rapid and frequent, possibly masking the early features of the seizures. The prolonged episodes of panic that occurred several years before the current admission could have been a manifestation of simple partial seizures, but a duration of two to three days would suggest simple partial status epilepticus, a very rare condition. Furthermore, the panic did not immediately precede loss of awareness, which would be expected in the case of a true epileptic aura.

In the absence of definitive phenomenologic data, we must rely on ancillary testing, primarily electroencephalographic studies. Localization of both ictal and interictal abnormalities to the left temporal region is very helpful, and if clinical findings suggest involvement of the left hemisphere, the likelihood of a focus in the left temporal lobe is high. The presence of glucose hypometabolism in the left temporal lobe on PET, which is seen in 70 to 80 percent of patients with temporal-lobe epilepsy who have undergone surgery, also supports the possibility of a focus in the left temporal lobe. For these reasons, the calcification seen in the left medial temporal region on the MRI and CT scans is probably of causative importance. Finally, one should not be dissuaded by the small size of the lesion; even very small lesions can cause intractable epilepsy.

Causes of cerebral calcification

Cerebral calcification can have a metabolic, neoplastic, vascular, congenital or developmental, traumatic, or infectious or noninfectious inflammatory cause.

Metabolic processes, such as hypoparathyroidism and other disorders of calcium and phosphorus metabolism, can result in bilateral calcification, which typically involves the basal ganglia and can therefore be dismissed from further consideration. The same is true of other systemic diseases that are occasionally associated with cerebral calcification, such as systemic lupus erythematosus.13

A neoplasm of low-grade malignancy must be carefully considered in this case. Tumors that are found during surgery for chronic epilepsy often lack radiologic characteristics that are typical of other tumors, including edema, mass effect, and contrast enhancement. Furthermore, their radiologic appearance does not change over the course of many years. The types of tumor identified on pathological examination include low-grade astrocytomas, oligodendrogliomas, gangliogliomas, and the more recently recognized dysembryoplastic neuroepithelial tumors. Calcification can be a manifestation of any of these tumors, especially on CT scans, but on MRI scans they typically appear as heterogeneous masses rather than as a uniform focus of calcification, such as that seen in the case under discussion.

Vascular lesions that may give rise to epilepsy include infarcts, primary intracerebral hemorrhages, and congenital vascular anomalies. This patient's history rules out all but the last category, which comprises arteriovenous malformations, venous angiomas, capillary telangiectasias, and cavernous angiomas. Arteriovenous malformations consist of anomalous vessels that have the characteristics of both arteries and veins, with intervening parenchymal tissue, and that are visible on MRI or conventional angiography; MRI scans characteristically show multiple flow voids. Since these features are not present in the case under discussion, an arteriovenous malformation is unlikely, although a small, thrombosed malformation cannot be ruled out. Magnetic-susceptibility studies are helpful in cases in which vascular lesions are suspected.

Venous angiomas have a linear or radial appearance and typically do not cause seizures or calcify. Capillary telangiectasias usually appear in the brain stem and do not cause seizures. Cavernous angiomas are present in about 0.5 percent of the general population and are frequently associated with epilepsy when they are symptomatic. The lesions are characteristically heterogeneous and do not appear as a solid, calcified focus; typically, there is a hyperintense center with a hypointense rim, corresponding to the presence of hemoglobin-breakdown products from previous small, usually asymptomatic hemorrhages. Other surgically important lesions are thrombosed aneurysms of the internal carotid artery or of the circle of Willis, but these are rarely associated with epilepsy and would not be intraparenchymal at a distance from the relevant signal voids on MRI scans. In this case, therefore, the lesion is probably not of vascular origin.

Hamartomas, among other congenital lesions, can appear on CT scans as isolated, nonenhancing foci of calcification. On MRI scans, however, they usually are associated with anomalies now recognized as areas of dysplastic cortex.

Traumatic lesions rarely calcify, and when they do, the calcification is generally seen in an area of bleeding associated with a cerebral contusion. The history of head trauma in this case does not strongly suggest such an injury, and the density of the calcification and the absence of associated encephalomalacia make this an unlikely explanation for the lesion. Cranial irradiation is another form of trauma that can lead to cerebral calcification, but there was no history of it in this case.

With respect to possible infectious or noninfectious inflammatory causes of the calcified lesion, the patient's fatigue, malaise, and headache at the time of the third presentation at this hospital raise the possibility of an active infection, although infection of the central nervous system is improbable, since the cerebrospinal fluid was normal and the lesion had been stable for many years. Among specific causes, viral, bacterial, mycobacterial, or parasitic infections merit consideration.

Multiple areas of calcification may develop after neonatal herpes or cytomegalovirus encephalitis, and a single case of an isolated, calcified temporal-lobe focus in an adult who had had herpes encephalitis has been reported. The history in the present case, however, does not suggest either of these viral diagnoses. There is also no clinical evidence of syphilis, which would be associated with abnormal findings in the cerebrospinal fluid and a positive serologic test, or any other bacterial process.

The possibility of a mycobacterial lesion, however, merits serious consideration. The patient's positive tuberculin skin test indicates that he was exposed to tuberculosis, but positive tests are common among immigrants from developing countries and do not necessarily indicate the presence of symptomatic disease either at the time of the evaluation or in the past. The long course of the patient's illness and the absence of abnormal findings in the cerebrospinal fluid eliminate tuberculous meningitis from consideration. Although isolated tuberculomas can occur, usually they are more than 2 cm in diameter and are enhanced with the use of contrast material, and they rarely calcify. Other granulomatous diseases, such as sarcoidosis, are also unlikely, given the normal cerebrospinal fluid and the absence of contrast enhancement.

Toxoplasmosis is a common parasitic disease that often results in cerebral calcification when it occurs in newborns, but there are almost always multiple calcified foci. In older children and adults, cerebral infection is usually associated with immunosuppressive disorders, particularly the acquired immunodeficiency syndrome. The lesions in those cases, however, are frequently multiple and usually enhance, and the clinical course is much shorter than that in the present case. Trematodes such as schistosoma and paragonimus, both of which are found in Asia and Africa rather than Central America, may infect the cerebrum but typically also invade other organs, such as the liver or lungs, and usually cause seizures only in the acute stage of the disease. Giardia, a common intestinal parasite in developing countries, was found in this patient, but this organism does not cause cerebral infection.

Cysticercosis may be the most common cause of symptomatic epilepsy in the world. The disease is caused by the larval form of the pork tapeworm, Taenia solium, and is endemic in much of Central America and South America, as well as Asia. It is associated with poor sanitation and is acquired through consumption of infected food or by fecal-to-oral transmission. The infected food may be pork, but more commonly transmission occurs through consumption of fruits and vegetables grown in soil fertilized with contaminated pig or human waste.

T. solium is the only tapeworm for which humans can be both the intermediate host, harboring the larval form of the worm, and the definitive host, harboring the adult form. The embryos, or oncospheres, are ingested and absorbed through the intestinal blood vessels into the venous circulation. They pass through the lungs and then embolize systemically, ultimately lodging in skeletal muscle, the eyes, and the central nervous system. In the central nervous system, the oncospheres may lodge in the gray matter, at the junction of the gray and white matter, or in the subarachnoid space. In tissue, the embryos develop into encapsulated larval forms called cysticerci, which are filled with clear fluid and contain a viable scolex. When contaminated meat is ingested by humans, the cysticerci may attach to the intestinal mucosa and develop into mature tapeworms 2 to 8 m in length. The worms are composed of hundreds of proglottids, each of which contains oncospheres that repeat the cycle when the proglottid is shed in feces.

Cerebral lesions typically evolve from an active to a transitional form and then to an inactive form. On CT or MRI scans, the active form appears as a thin-walled, fluid-filled cyst with a mural nodule (the live scolex); it causes no inflammatory reaction. The transitional form is a more proteinaceous, encapsulated cyst with ring enhancement; this cyst becomes a granulomatous, irregularly enhancing lesion as the organism dies. The inactive lesion contains the dead organism and is densely calcified, with no enhancement. At any of these stages there may be multiple lesions, but often the lesions are solitary. Seizures are the most common clinical manifestation at all stages of intraparenchymal infestation, although headaches and focal symptoms are common during the active and transitional stages. Meningeal and intraventricular cysts can result in hydrocephalus.

Solitary areas of calcification are usually supratentorial and less than 1 cm in diameter, without a mass effect, as in the case under discussion; lesions located in the hippocampus have been reported. The negative results on serologic testing in this case do not rule out cysticercosis. Indeed, when inflammation is absent, even the most accurate test, the enzyme-linked immunotransfer blot, is negative in 60 to 80 percent of cases and probably in more than 80 percent of cases involving only a single lesion. Treatment with the antihelminthic drug praziquantel or albendazole may be beneficial during the active and transitional stages of neurocysticercosis and may even help control seizures, but this type of treatment is unlikely to be effective when the disease is inactive.

I believe that the diagnostic procedure in this case was resection of the calcified lesion in the left medial temporal lobe, along with tissue from the adjacent anterior hippocampus and amygdala. When epilepsy results from a solitary lesion, seizure control depends mainly on complete resection of the lesion; whether electrically active tissue should also be removed is controversial. The pathological examination probably showed a degenerated cysticercus organism surrounded by gliosis, without appreciable inflammation. A less likely finding would be a small, thrombosed arteriovenous malformation, a cavernous angioma, or a low-grade astrocytoma. Control of the patient's seizures should be markedly improved as a result of the surgical procedure.

Clinical Diagnosis

Neurocysticercosis, with epilepsy.

Neurocysticercosis, inactive, with temporal-lobe epilepsy.

Pathological Discussion

The patient underwent a left temporal craniotomy. Three fragments of brain tissue were obtained from the junction of the hippocampus and the amygdala. The largest fragment was 3.5 by 2.3 by 1.7 cm. Two of these fragments were grossly normal, but the third contained a round, firm nodule, 3.0 mm in diameter, filled with granular, tan–yellow material and surrounded by a capsule and attached parenchyma.

Histopathological examination revealed a cyst (Figure 2) that was circumscribed by a collagenous capsule, 0.2 mm thick, and attached to a portion of the hippocampus. The lumen of the cyst contained acellular, eosinophilic debris (Figure 3), with scattered, round, basophilic concretions, as well as a dense, homogeneous, refractile cuticle that was serpentine in shape and that rested on a less dense but thicker layer studded with calcified particles. Beneath the second layer were spaces containing debris. The serpentine fragment was probably the remnant of a desiccated scolex, although it was not possible to confirm the identification of the parasite.

Cyst Circumscribed by a Capsule Composed of Dense Collagenous Tissue with Chronic Inflammatory Cells (Arrows) (Hematoxylin and Eosin, x30).

Figure 3. Acellular, Eosinophilic Debris within the Lumen of the Cyst (Hematoxylin and Eosin, x250).
The portion with a serpentine shape (S) probably represents a desiccated scolex.

A dense, lymphoplasmacytic infiltrate that included rare eosinophils, macrophages containing hemosiderin, and Russell bodies involved the capsule (Figure 4) and the parenchymal vessels (Figure 5).

Figure 4. Dense, Lymphoplasmacytic Infiltrate in the Capsule (Hematoxylin and Eosin, x250).
The eosinophilic, hyaline corpuscles are Russell bodies

Figure 5. Dense Infiltrate of Lymphoplasmacytic Cells in the Wall of an Intraparenchymal Vessel (Hematoxylin and Eosin, x250).

The portion of the hippocampus near the capsule was gliotic, with focal neuronal loss (Figure 6). Some of the remaining neurons were encrusted with granular, ferruginous material. There were also foci of perivascular or vascular chronic inflammation.

Figure 6. Neuronal Loss in the Pyramidal Layer of the Hippocampal Formation near the Cyst (Hematoxylin and Eosin, x500). Some of the neurons that remain are ferruginous (arrow).

These findings are consistent with a diagnosis of cysticercosis involving the cerebrum, with features that are characteristically observed 2 to 10 years or even longer after infestation.33 The central nervous system is involved in 90 percent of cases of human cysticercosis.34 The presence of a single cerebral cysticercus in this case is unusual, however, since in 80 percent of the cases multiple cysts are found.35

Four types of central nervous system cysts are encountered in cysticercosis. Parenchymal cysts are usually found in the cerebral cortex, including the cortical–subcortical junction; the white matter is rarely involved. Meningeal cysts form in the meninges overlying the base of the brain more often than in the meninges overlying the convex surface, sometimes causing hydrocephalus and strokes. Ventricular cysts are usually located in the fourth ventricle and cause intermittent hydrocephalus and, occasionally, sudden death. Spinal cord cysts are rare.

The host can tolerate the worm as long as the embryo is alive. It usually dies two to six years after infection, and the ensuing disintegration of the parasite triggers a vigorous tissue reaction. The dead parasite eventually decays into grumose or eosinophilic, desiccated material. The final stage of this process is characterized by the presence of a calcified nodule, presumably the result of dystrophic calcification of the necrotic larva.

Small Talk

The patient has been free of seizures since his left temporal lobectomy.

If the development of seizures is related to an inflammatory process, how does it increase excitability?

The mechanism is not known, but one hypothesis is that the lesion disturbs the microenvironment of the surrounding neurons, either by affecting neurotransmitters or by stimulating axonal reorganization in ways that favor excitation over inhibition. Inflammation does not always accompany the lesions that cause seizures, however.

Does the sensitivity of serologic testing change over time?

Several studies suggest that the sensitivity of serologic testing decreases considerably late in the course of the disease, especially when only a single lesion is present.

Anatomical Diagnoses

Neurocysticercosis, left temporal lobe, end-stage, with calcification.

Epilepsy.

Death Certificate

Will continue adding later

References
CPC Faculty of Medicine, University of Malaya
http://content.nejm.org/cgi/content/full/343/6/420
http://www.neurology.org/cgi/content/full/57/2/177

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2009-08-14T00:58:00.005+08:00

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2009-08-13T17:32:00.004+08:00

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Related articles
1 YAY.. DUIT NUFFNANG DA DAPAT!!!!
2 Claiming Nuffnang Money

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2009-08-12T22:52:00.003+08:00

Update: PUO case

2009-08-12T21:25:00.005+08:00

This post is a follow up on a case which i discuss earlier. In case if you wanna know a bit about the patient history or you are lost, care to click here.

Patient currently on week 2 and currently on day 4 of oral augmentin course change from previous IV augmentin due to development of rashes based on Prof MT Koh saying that the cause of the rashes which raised on the patient trunk and the limbs could be from the antibiotic given. I'm start to think, patient was already on IV augmentin for 12 days and if the rashes really due to the antibiotics given, shouldn't it comes early? And if the patient really have the rash problem due to antibiotic, is the route of administration of the drug makes the rash goes away eventhough it using the same antibiotics? but anyway, the rashes was still there for the past 3 days.

Currently, oncology team lead by Prof MT Koh, makes the working diagnosis as Haemophagocytic Lymphohistiocytosis, which is a rare disorder of the immune system. The disease clinically manifests as fever, hepatosplenomegaly, pancytopenia(which the patient's platelet is normal), lymphadenopathy, and rash(and no rashes initially) often comprise the initial presentation.

Hemophagocytic Lymphohistiocytosis

The diagnostic criteria set forth by the Histiocyte Society for inclusion in the International Registry for Hemophagocytic Lymphohistiocytosis (HLH) is as follows. All 5 criteria must be met to establish a diagnosis of hemophagocytic lymphohistiocytosis:

* Fever - Seven or more days of a temperature as high as 38.5°C (101.3°F)
* Splenomegaly - A palpable spleen greater than 3 cm below the costal margin
* Cytopenia - Counts below the specified range in at least 2 of the following cell lineages:
o Absolute neutrophils less than 1000/µL
o Platelets less than 100,000/µL
o Hemoglobin less than 9.0 g/dL
* Hypofibrinogenemia or hypertriglyceridemia - (1) Fibrinogen less than 1.5 g/L or levels greater than 3 standard deviations below the age adjusted reference range value or (2) fasting triglycerides greater than 2 mmol/L or levels greater than 3 standard deviations above the age-adjusted reference range value
* Hemophagocytosis - Must have tissue demonstration from lymph node, spleen, or bone marrow without evidence of malignancy
* Rash - Skin findings in more than half of patients;1 scaly and waxy lesions; rashes on the scalp and behind the ear
* Other - Swollen or hemorrhagic gums that can result in tooth loss; feeding problems (especially prominent in infants); abdominal pain, vomiting, diarrhea, and weight loss

Light microscopic image of bone marrow showing stromal macrophages containing numerous red blood cells in their cytoplasm

Discussion

I don't know why they were searching for all those rare things. If i answer this HLH in my long case final exam, sure GG. They are currently planning to have some blood investigations to confirm the HLH by doing fasting TG, fibrinogen, and waiting for trephine report.

When i ask one of the doctor there, why would they haven't done their lymphnode biopsy, the answer somewhat like this

"This is a generalised lymphadenopathy. How could we biopsy all the lymphnodes?????"

I don't know wether its true or not, but currently there is no plan for lymphnode biopsy yet.

A big suprise where today was the first time the patient is 24 hour free from fever. Maybe an oral antibiotic is working after all..

Pyrexia of Unknown Origin

2009-08-07T03:18:00.003+08:00

Today i've managed to present one case of a 4 year old child with fever for 4 weeks with no other clinical symptom except loss of appetite, lost of wt of 1 kg and a bit lethargic and less active. There was no RTI, GIT, CNS symptom. Fever was reduce by antibiotics. No night sweat. Then later was referred from a GP due to fever and palpable cervical lymphnodes. Got a history contact to TB patient(grandmother). Vaccination was complete.

Physical examination reveals fever, palor, with hepatomegally (1cm) and generalised lymphadenopathy. No bcg scar noted

So differentials would be
1) Tuberculosis
Points favour - History contact with TB, loss of wt and appetite. PE reveals fever, palor, hepatospleenomegally and also generalised lymphadenopathy and no BCG scar.
points agains - No cough, haemoptysis, and night sweat.

2) Leukaemia
Points favour - Lethargy, fever, palor, hepatomegally, lymphadenopathy
Points against - No bleeding tendency, no family history of blood malignancy, no spleenomegaly

3) Lymphoma
Points favour - B symptom? (must really need to clarify is there any night sweat because patient was in an aircond when sleeping) and also lymphadenopathy
Points agains - i couldn't think of... maybe u can give me a comment

4) HIV - fever
points against - No hx of blood transfusion,

5) Thyphoid/thyphus
Points favour - PUO, lymphadenopathy, hepatomegally
Points against - no spleenomegally, no

6) autoimmune? connective tissue disease?

Investigation that was done and some I think should be done base on the differentials given are:

1)FBC
Investigation fbc reveals hb low, white cell low, but platelet and wcc differentials are normal.

2)PBF shows normocytic and normochromic anaemia. No blast cell seen

3)Mantoux test
negative

4)Chest xray
No mediastinal lmphadenopathy noted.

5)Bone marrow film
No abnormal/malignant cell noted. Comment said that we should look for viral causes.

6)Lymphnode biopsy
Not done yet

7) HIV screening (permission should be taken 1st when doing HIV screen), Hepatitis screening
-ve

8) Toxoplasmosis?
No plan yet for this toxoplasma screen

9) Infectious Mononucleosis??

10) Blood culture
-ve for all bacteria, virus,

11) Thyphoid/Thyphus
-ve

12)

Diagnosis

PUO and currently on investigation.

Comment

Currently, patient on IV antibiotics, fever are up and down, and relief with PCM. Antibiotics given shown to have positive result, but they are trying to off it to let see if the fever spike up again.

Platelet count was normal despite HB and WBC low. wbc was low until 2 and this is what we call febrile neutropaenia. Prof Amir has said that if a patient come with febrile neutropaenia, we should do a septic screen (blood culture, urine culture, oral swab etc..). However all the test was negative.

Mantoux test was negative however it doesn't mean that the diagnosis should be exclude. there was no BCG scar showing that

Bone marrow was also negative of malignant cell, however, if the bone marrow is negative we can do a lymph node biopsy. Correct me if I'm wrong.

I will follow-up the patient progress and post it on here later. Anything in mind can contact me. Thanks in advance.

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2009-08-07T02:32:00.007+08:00

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Ibu baru bersalin korban H1N1

2009-08-04T05:26:00.000+08:00

Ibu baru bersalin korban pertama di Sarawak

KUALA LUMPUR 3 Ogos - Seorang wanita berusia 23 tahun yang baru dua minggu bersalin menjadi korban ketujuh virus selesema babi atau influenza A (H1N1) di negara ini.

Mangsa merupakan kes kematian pertama H1N1 di Sarawak.

Ketua Pengarah Kesihatan, Tan Sri Dr. Mohd. Ismail Merican berkata, mangsa meninggal dunia pada pukul 4 pagi ini setelah dimasukkan ke Unit Rawatan Rapi (ICU), Hospital Miri, Sarawak sejak 22 Julai lalu.

''Dia dimasukkan ke ICU kerana mengalami komplikasi pada paru-paru dan disahkan dijangkiti H1N1 pada 23 Julai lalu. Dia telah bersalin di hospital sama dua hari sebelum itu,'' katanya dalam kenyataan di sini hari ini.

Beliau berkata, wanita itu didapati menghidap pneumonia yang teruk selepas bersalin selain mengalami simptom demam dan batuk empat hari sebelum bersalin.

''Bayi wanita itu didapati selamat dan disahkan bebas daripada H1N1. Penyebab kematian direkodkan sebagai pneumonia akibat jangkitan H1N1,'' jelas beliau.

Mohd. Ismail menambah, sebanyak 17 kes baru H1N1 termasuk satu kes kematian dilaporkan di negara ini menjadikan jumlah kes terkumpul H1N1 meningkat kepada 1,446 kes.

''Kesemua kes baru itu adalah jangkitan tempatan yang melibatkan rakyat Malaysia. Jumlah kematian akibat H1N1 di negara ini setakat ini adalah sebanyak tujuh orang,'' katanya.

Menurutnya, daripada 1,446 kes terkumpul H1N1, sebanyak 574 merupakan kes import dan 872 adalah kes jangkitan tempatan.

''Daripada jumlah ini, 1,408 kes telah sembuh, hanya 29 kes sahaja yang sedang menerima rawatan antiviral di hospital yang mana lapan daripadanya berada di ICU. Sembilan orang sedang menerima rawatan antiviral di rumah,'' katanya.

Beliau berkata, daripada lapan kes di ICU, empat daripada mereka mempunyai faktor risiko iaitu obesiti (1), wanita hamil (1) dan imuniti rendah (2).

Mohd. Ismail berkata, bagi 17 kes terpencil, tujuh kes dirawat di wad pengasingan hospital, satu kes di ICU dan sembilan orang menerima rawatan pesakit luar.

Merujuk kepada situasi global sehingga hari ini, beliau memberitahu, sejumlah 183,854 kes H1N1 dengan 1,307 kematian telah dilaporkan daripada 167 negara.

''Ia melibatkan peningkatan sebanyak 28 kes termasuk enam kes kematian berbanding dengan hari sebelumnya,'' katanya.

Beliau berkata, orang ramai yang mempunyai gejala jangkitan H1N1 berterusan dan bertambah teruk disaran mendapatkan rawatan di klinik serta hospital yang berdekatan.

''Kes-kes yang mempunyai simptom jangkitan influenza serta faktor risiko seperti mengandung, obesiti, asma, penyakit paru-paru kronik, diabetes dan golongan imuniti rendah akan diberi rawatan antiviral influenza serta-merta tanpa perlu membuat ujian pengesahan H1N1.

''Ini adalah untuk kes-kes yang dikesan dalam masa 48 jam selepas mereka mula mengalami simptom jangkitan influenza. Ujian pengesahan jangkitan influenza hanya perlu untuk kes-kes yang dirawat di hospital,'' katanya.

Beginning of my paediatric posting

2009-08-03T12:27:00.002+08:00

1) Today started my new posting - paediatric. Prof Asma was very critical to our history taking and i managed to get something from her class today this morning.

2) Although the first case was very simple, a respiratory infection, it seems that there are a lot we still don't know.

3) The way we should took a history is to let the patient tell the event from the beginning until the end without us interrupting in the middle.

4) After the patient finish talking, then we clarify the gaps and take further history which are relevant.

5) English, again are very important, enough say.

6) We don't create a history. Read back what we took. Is the history was really a logic event? If it not, clarify again with the patient.

7) Prior to admission, is the 'key' date. In the mean while, we can also use the 'day of illness' for associated symptom. How many days did the patient has admitted is also an important history.

8) 4C's should be in the history - chief complain, causes, complication, and course of the disease. Thus we really need to know how was the patient progress.

9) Current situation such we're having now - H1N1 should bear in our mind now.

10) The 2nd case is a dengue haemorrhagic fever.

11) I should admit it, this was the first time i saw the rashes like the patient had. If Prof Asma don't tell me it's rashes, i wont know.

12) The last time i saw a dengue rashes was a bit different from this. I should see and identify a lot of different presentations of dengue rashes.

13) There was 3 other differentials based on history - acute glomerulonephritis, hepatitis, and urinary tract infection.

14) Investigation that has been done are FBC - to see the platelet level, haematocrit, UFEME. Prof said we need to exclude the differential also by doing ASOT or ESR.

15) Treat dengue by giving IV maintenance half saline and check for heart rate, resp rate, urine output, and also sign of ascites and pleural effusion.

16) Lastly, thanks Prof Asma. I was hoping my URTI heals faster.

H1N1 have reached 1000+ cases

2009-07-26T23:51:00.000+08:00

Kes H1N1 cecah 1,000
Jul 26, 09 8:22pm
Jangkitan influenza A (H1N1) di Malaysia kini mencecah 1,000 kes apabila 54 lagi kes baru dilaporkan di seluruh negara hari ini, kata Ketua Pengarah Kementerian Kesihatan Tan Sri Dr Ismail Merican.

Katanya, daripada jumlah kes baru itu, 43 kes merupakan kejadian dari tujuh kluster baru, lima daripada kluster sedia ada manakala enam lagi adalah kes terpencil termasuk satu kes import.

"Sehingga kini, 1,075 kes dicatatkan dengan satu kematian, dengan 574 kes atau 53 peratus adalah kes import manakala 501 kes atau 47 peratus kes jangkitan tempatan.

"Hanya empat kes atau satu peratus sahaja yang sedang menerima rawatan anti-viral di hospital," katanya dalam satu kenyataan, lapor Bernama.

Sehubungan itu, beliau berkata pihak Kementerian akan terus memantau kejadian kes H1N1 mahupun "Influenza-like illness"(ILI) yang dimasukkan ke hospital.

Beliau menasihatkan orang ramai termasuk pihak pengurusan institusi pendidikan dan tempat kerja supaya lebih peka dan berinformasi mengenai penyakit berjangkit ini.

Ismail juga meminta orang ramai melaporkan segera kepada Jabatan Kesihatan terdekat sekiranya terdapat tanda-tanda orang di sekeliling mereka menampakkan simptom yang menjurus kepada jangkitan H1N1 dan ILI.

"Mereka yang mendapat gejala yang teruk atau berisiko tinggi perlu segera mendapatkan rawatan di hospital berdekatan," katanya

Penularan wabak

Mengenai langkah untuk memperlahankan penularan wabak itu, Ismail berkata orang ramai perlu patuhi beberapa peraturan yang digariskan termasuk mengamalkan kebersihan diri terutama membasuh tangan secara rutin serta mengamalkan duduk berjarak sekurang-kurangnya satu meter dengan individu lain di samping mengurangkan majlis perjumpaan.

"Kes yang bergejala ringan boleh berehat di rumah tetapi perlu sentiasa mengamalkan kebersihan diri dan persekitaran di tahap yang optimum dan memakai topeng mulut dan hidung dan jika gejala bertambah teruk, segeralah mendapatkan rawatan," katanya.

Mengenai kes kedatangan yang berkurangan disebabkan demam, batuk dan selesema sama ada di sekolah mahupun di tempat kerja, Dr Ismail berkata perkara itu perlu dilaporkan segera ke Pejabat Kesihatan Daerah yang terdekat.

"Bagi pelajar yang sekolah dan institusi mereka terlibat dengan arahan penutupan sementara, adalah dimaklumkan hanya mereka yang bebas dari tanda-tanda H1N1 atau ILI sahaja yang dibenarkan pulang.

"Bagaimanapun, bagi mereka yang masih ada tanda penyakit itu, kita nasihatkan mereka untuk terus berehat kerana mereka masih mempunyai risiko untuk menularkan virus di kalangan rakan masing-masing," katanya.

Di LABUAN, lapan pelajar dari dua sekolah menengah yang baru pulang dari Melaka mengikuti program kadet pertahanan awam anjuran Jabatan Pendidikan Labuan dimasukkan ke hospital pada Ahad selepas didapati positif H1N1.

Mereka adalah antara 17 pelajar dari Sekolah Menengah Pantai dan 17 dari Sekolah Menengah Sungai Bedaun yang menaiki penerbangan Air Asia AK5177 dari Kuala Lumpur yang tiba di lapangan terbang Labuan 10.40 pagi ini.

Baki 26 pelajar bersama dua orang guru yang mengiringi mereka diarahkan menjalani kuarantin di rumah selama tujuh hari mulai hari ini.

Pengarah Kesihatan Labuan, Dr Zaini Hussin memberitahu Bernama bahawa lapan pelajar itu dimasukkan ke hospital selama tujuh hari.

Ahli Parlimen Labuan Datuk Haji Yussof Mahal menasihatkan pelajar dan ibu bapa mereka jangan panik tetapi sentiasa mematuhi prosedur perubatan.

Wow.. penis stuck in metal park bench

2009-07-25T20:36:00.002+08:00

A MAN is lucky to still have a penis after he inserted it in a metal park bench and became stuck, doctors say.
At least a dozen police and emergency services workers were called to the park in Hong Kong after 41-year-old Le Xing’s penis became trapped in a hole, apparently after he became aroused.

According to reports from Hong Kong, the “lonely and disturbed” Mr Xing told police he thought it would be fun to have sex with the bench, UK’s The Telegraph reported.

Unfortunately for Mr Xing, news crews descended on the park to film the rescue effort:

Doctors had tried to drain some of Mr Xing’s blood in an attempt to loosen his penis, but to no avail.

Rescuers eventually cut away part of the bench and Mr Xing was taken to hospital where doctors took another four hours to free him.

They said if Mr Xing had been stuck for another hour they would have had to amputate his penis.

Xing, 41, is in LanTian park. It's night time.

Reports diecrine Mr Xing as “lonely and disturbed”. But had only he been disturbed he may have been to wary to lodge his member in a steel sit-up bench.

The bench, features “numerous small holes”. In Xing went. But out he did not emerge.

He calls the police. If anyone can cool his ardour and enable him to come lose, it is they.

When doctors arrived on the scene they tried to release some of the pressure by removing some of his blood, but the penis was so swollen that they ended up having to cut the entire bench free and take it, with Xian attached, to the hospital.

Four hours later, Xing is free.

H1N1 - First Death in Malaysia

2009-07-24T14:32:00.002+08:00

First H1N1-related death in Malaysia

2009/07/24

PUTRAJAYA: Malaysia recorded its first influenza A (H1N1)-related death in a 30-year-old Indonesian student who died of heart complications.

Tengku Abdullah Syahputra from Medan was a first-year student of the International Centre for Education in Islamic Finance in Kuala Lumpur.

His body has been claimed by his family and taken back to Medan.

He was on holiday in Indonesia and returned to Malaysia on July 5. He had fever and cough but the symptoms were mild.

On July 20, he started to have high fever and cough and was lethargic.

The next day, the student sought medical treatment at a private medical centre in Kampung Baru, Kuala Lumpur.

While waiting for his medication, the student fainted and was given emergency medical treatment but he failed to respond.

He was declared dead at 11.50am.

The medical centre declared the cause of death as cardiac arrest due to ventricular fibrillation (irregular heartbeat).

In extending his condolences to the victim’s family, Health Minister Datuk Seri Liow Tiong Lai stressed that the student did not die of H1N1 virus.

“Based on the preliminary post-mortem results, although he was a H1N1 patient, his death was not directly due to H1N1 as he suffered from other complications,” he said at a press conference in the ministry yesterday.

Post-mortem conducted by Hospital Kuala Lumpur found that besides being obese, there were signs of pneumonia in the lungs, enlarged heart and liver, high level of white blood cells and “pus-like material” at the trachea.

Additionally, influenza A (H1N1), dengue, TB, HIV and leptospira tests were conducted on the body and the results were negative.

Liow said the ministry was still waiting for the results of toxicology, biochemical and histology tests.

“There are lots of factors that could be the cause of death. We will only get the full report tomorrow,” Liow said at a press conference at the ministry yesterday.

In illustrating an example, Liow said any H1N1 death would not cause the white blood cells to increase.

“Normally, H1N1 will attack the lungs. The high presence of white blood cells in the victim is due to bacteria,” he said.

Elaborating further, Health director-general Tan Sri Ismail Merican said because of all the complications, it was highly likely that the cause was “something else”.

Nevertheless, Liow said the ministry had taken precautions by directing 25 employees of the private medical centre who had come into contact with the victim to quarantine themselves for seven days.

They were also given anti-viral treatment.

The ministry had also identified seven people who were roommates and part of the victim’s study group. Only one was given treatment. The others were told to take care of their health

Next KL International Motorshow set for 2010

2009-07-23T03:36:00.003+08:00

KLIMS 2010

The MAA have announced that the Kuala Lumpur International Motor Show will be held in December next year - between the 3rd and 12th December 2010 to be exact.

KLIMS10’s motto will be “We CARE”, and CARE is supposed to stand for Commitment, Advancement, Reliability and Environment. The KLIMS organising committee says the show will take up 30,000 square meters of space at the PWTC and expects to attract over 200 exhibitors and over 330,000 visitors.

That’s a long time to wait. See you at KLIMS next year then!

It reminds me the old time. I have nice pictures with all the chicks there at the last KLMIS.. Hopefully this 10th KLIMS would be more and more models! oopppss.. I mean more sophisticated supercars!! =P

setting the internet

2009-07-20T22:40:00.001+08:00

Crimping the network wire was my specialty. It some sort like a micro surgery.. hahaha..

Curik Ptm wireless.. LoLz.. Dun get me wrong. This internet wireless was there 5 years ago, and the wireless was replaced by the latest PTM wireless network with a different environment. This internet source was not use and we managed to use it as our internet source.

Make sure the wire colour at the correct sequence.

After crimping, let this naked guy do the rest.. hahaha...

Matric card

2009-07-19T20:16:00.004+08:00

Last week, I've found a matric card at Dewan Makan. Later i found out that the matric card was a bit unusual. I've managed to take a picture of her matric card.. Lolz.. Sorry guys. Due to privacy, i need to hidden the identity of this matric card owner.

It's because the matric card owner is not a medical student. It's science. How on earth would a science student matric card in a DM of medical student hostel?

Ok, it's searching time. At first I've tried searching using the facebook search. No result (because the owner use different name). Then i tried googling and i found 3 sites of her name with contact number next to it! ok. I try the first one, and it was unsuccessful, when she didn't reply my sms. Then the second one which not include her phone number but contain admin's website number, however when i contact him, he won't allowed me to have her phone number. And last the third. At first, I thought that was not her number again, then after 3 hours around 1 a.m she replied my sms! Good things that I haven't sleep. Thanked god. Luckily i found the owner.

So I set a date on Sunday 3pm.. She met me with a friends. malu2. kecil2 je orangnya. Tak sangka she can play softball.U might wonder (if u click the 3rd site), the owner plays softball. haha...

We met for only 1 minute face to face. She tried to give me RM10.. lol.. Nevermind i said. Seems to me that the owner feels very happy that she've found back her matric card.

p/s: I was wondering if someone could return Hasem's camera that i lost at Pusat Sukan last year, the same way like i did.. A lot of info in the camera including my face. Unless the founder want take it. sigh..

Malaysia vs Manchester United

2009-07-19T01:39:00.000+08:00

Muahahahah.. Malaysia managed to get 2 goals from Amri Yahya. It would be great if Malaysia manage to get it draw. Below are the pictures that I've taken at the event in Bukit Jalil Stadium.

Parking jauh giler..

Not many ppl arived yet but the parking was 2 KM away from the stadium..

The sea of red with a small dot2 of yellow islands.. Lolz

Starting

Practice session 15 minutes before kick off

I sat on the cheapest section, the violet section. Fergie managed to put his best 1st team at 1st half. Seriously, I was a bit shock. I thought he'll put his 3rd team. Rooney, Berbatov, Nani, Anderson, Evra, Van Der Sar etc, all playing!! Even Michael Owen played the 2nd half. Unlike the Livepool Asia Tour, Gerrard, Fernando Torres will not be playing. gg lor Thai and Singapore.

2nd half break, the pancaragam comes in

Rooney was set to have a kick

Even indons came

Fedrico Manchida (kiko) warming up before enter

In the end, a good fight from Malaysian side and i hope we can continue on the next rematch..

Update: we lost 0-2 but Man U could only found the 2 goals at the first half. A goal again from former liverpool player, Michael Owen. Ferguson must be cheerful

New FUTSAL shoes!!

2009-07-19T00:59:00.000+08:00

hihihi
Cheap saja.. for 3 months play2 is sufficient for me.. nway, i'm not a pro to use expensive extragiantza shoes. I bought it at Pertama Complex at Jalan Tar. Bought it at RM40++.. Topper Brand. Not a reject shoes, i hope so. I hope it'll last until I finished my 6 months (3++ months left).. Cuak giler..

In a yellow plastic

nice topper.. hehehe...

Alert! Do not give your account info

2009-07-18T03:04:00.006+08:00

I sense something fishy going on from above mail. The sender is from center.alert@yahoo.com. makes me wonder is this really from yahoo or is just a scam? why would yahoo want something like this? All make sense when i started to replying with the fake id and password then i saw this

Account Alert

Dear Valued Member,

Due to the congestion in all Yahoo, There will be removal of all unused Yahoo Accounts,Yahoo would be shutting down all unused Accounts,You will have to confirm your E-mail by filling out your Login Info below after clicking the reply bottom, or your account will be suspended within 24 hours for security reasons.

UserName:...........................

Password:............................

Date of Birth:.....................

Country Or Territory:....................

After following the instructions in the sheet, your account will not be interrupted and will continue as normal.

Thanks for your attention to this request. We apologize for any inconvenience.

Warning code:.................VX2G99AAJ
Account owner that refuses to update his or her account before two weeks of receiving this warning will lose his or her account permanently.

.

WTF!!!!!!!!! pls readers, do not give any information about ur login or password to anyone who ask for it. It's VERY DANGEROUS!!!!

Kenapa aku menyokong PPSMI?

2009-07-13T01:00:00.003+08:00

Bersemangatnya org2 ini berdemo.. Aku tak paham org2 pas ni. Nik aziz cakap tak perlu berjuang kerana bangsa sebab dalam isle tak da perjuangan bangsa. Tapi bab bahasa melayu, diorang duk perjuangkan walaupun diorang tak tau apa objektif sebenar PPSMI.

Kenapa nak anak2 mereka menjadi seperti aku? Agak2 kenapa aku fail exam? Aku dibesarkan dengan sains dan math dalam BM. Dari sekolah sampai ke matrikulasi, even universiti tahun 1, fisiologi aku dalam BM. Aku jawab juga dalam BM. Tak pernah dibuat org, jawab anatomy dalam BM. Aku malu.

Naik tahun 2, BI sepenuhnya. Aku mula beradaptasi. Aku mula merasakan kepayahan yang teramat sgt. Akibat dari itu, aku fail exam. Masuk supplementary exam selama 2 bulan! Naik fasa 3a, kemahiran berkomunikasi diperlukan dalam klinikal exam. Agak2 aku lulus ke? Aku fail klinikal sampai terpaksa repeat klinikal nasib baik tak perlu repeat semuanya. Da 4 tahun dibesarkan dengan BI, adakah aku masih mahir dalam BI?

Skg ni aku tunjuk video aku sebelum persediaan MBBS final yang aku fail masa tu.. Tu baru aku kat study week. Korang tak tgk lagi aku bercakap BI kat depan external examiner yang bukan dari Malaysia. Agak2 koranglah, kalau aku xda masalah blaja sains dalam BI, adakah aku akan macam ni?

Padang Besar Man U jersey baru

2009-07-12T01:39:00.007+08:00

Bahasa Melayu

Sapa ada contact2 org padang besar. Nak tanya yang jersey baru Manchester United yang tak ori da kuar ke? Padang besar sememangnya syurga untuk membeli jersey2 yang ciplak.. Sila bagitau di comment yer.. Aku tak nak bli yang mahal2 nyer.. Membazir..

Untuk yang datang ke blog ni cari jersey ni, nah esok hari last untuk sapa2 yang nak PRE ORDER dan berpeluang utk bertemu bintang2 man u
-----------------

Bahasa Inggeris

As I told you before, Malaysian will be the very first to see the Manchester United play in the brand new kit. The new home kit was made by Nike and will be launch this July 16, just 2 days before Malaysia vs Manchester United match at Bukit Jalil Stadium.

The new 2009/10 Manchester United Kit will hit the stores nationwide on 16 July 2009 but Nike Malaysia is organizing an exclusive PRE-ORDER PROMOTION for the new kits to ensure these die-hard supporters will have the opportunity to be clad in the new team colours when the Red Devils touchdown in Kuala Lumpur. So…no need for you to pre order online at Manutd.com store or Kitbags store to get this new kit.

Place the order now at selected NIKE & AL-IKHSAN outlets and you will get the jersey on 16 July 2009 PLUS you will stand a chance to win tickets to the Manchester United vs Malaysia Game, training passes and the chance to meet the Manchester United stars at an exclusive Nike5 event at KLCC Outdoor Car Park.

Pre orders for the jersey will start from 1st to 13th July 2009 at below selected outlets..

NIKE OUTLETS at;
Sunway Pyramid,
Pavilion KL,
Mid Valley Megamall,
Suria KLCC,
One Utama

AL-IKHSAN STORES at;
Bukit Bintang Plaza,
Sunway Pyramid,
Alamanda
Shah Alam.

Be the first to wear it on launch day – 16.07.2009!!

http://manutd.diyanazman.com/2009/07/08/pre-order-nike-200910-manchester-united-new-home-kit-in-malaysia-and-get-a-chance-to-meet-manutd-players/

-----------------

Upin Ipin Sebenar!!!

2009-07-10T22:37:00.006+08:00

Upin Ipin Sebenar!!! Betol tak diorang ni comel? Betol, Betol, Betol...

My Old website closing

2009-07-10T14:25:00.010+08:00

AAAAAaaaaa... Pretty sad. My old free web hosting, Yahoo! Geocities is closing.. They will terminate the service on 26th October 2009. This was the first website that i ever build using HTML code. I've started using the service since 1999, however it does managed to serve until 2006. After that the web was dead.. haha.. But there is nothing really important on that website anyway. In case u wanna know and eager to go to my old website, care to click here. Bear in mind that there was nothing left.. Haha. I've managed to download all the files back to my hard disk because they are deleting all the files in geocities and no one can recover back the files that have been deleted.

Good bye my old Geocities.....

Snapshot from my old website

This is my first music flash swf in the web! lolz...

HAPPY BIRTHDAY, Tun Dr. Mahathir

2009-07-10T02:54:00.004+08:00

Today is former Prime Minister Tun Dr. Mahathir Mohamad’s 84th birthday. He was born in Jalan Kilang Ais, Seberang Perak, Alor Setar.

Upon graduation in 1953, with Tun Dr. Siti Hasmah

May Allah s.w.t. bless you, for many more productive years.

PPSMI mansuh

2009-07-09T00:48:00.005+08:00

I feel sad that my future generation will become like me one day when they enter the university. I've difficulty and culture shock when i first started my medicine course. Without learning basic science in english, I've difficulty in many aspect. Thus i don't see why some people outside there are not thinking about their children later. Enough arguing about Science in English when we already knew the benefits for the students in the future! By learning science in BM just showed that you are just becoming a jaguh kampung. Think about it. The one who suffers not the one who arguing PPSMI, those who suffers are their children. I don't want my juniors at the back just because they are trying to translate it to BM and those who mastered the English have gone 100 steps beyond us.

The stupidest reasons of not having PPSMI that i ever heard and they even said that we 'dewa' the English.

Here are the sound bite from Tun Mahathir about PPSMI

PENGAJARAN DAN PEMBELAJARAN SAINS DAN MATEMATIK DALAM BAHASA INGGERIS (PPSMI)

1. Saya berasa amat sedih apabila membaca laporan berkenaan demonstrasi yang dipimpin oleh tokoh sastera Melayu menentang pengajaran sains dan matematik dalam bahasa Inggeris.

2. Kononnya ini akan menidakkan kebolehan bahasa Melayu sebagai bahasa pengantar dalam ilmu ini. Konon ia akan mengurangkan perkembangan bahasa Melayu sebagai bahasa kebangsaan.

3. Kita harus ingat bahawa pelajaran bukan semata-mata untuk memaju atau mengembangkan bahasa. Pelajaran adalah untuk penguasaan ilmu, pelbagai jenis ilmu.

4. Yang boleh meningkatkan taraf dan kemajuan bahasa ialah matapelajaran bahasa itu sendiri dan diperingkat yang lebih tinggi mata pelajaran sastera.

5. Sains dan matematik tidak mungkin menolong kemajuan bahasa, khususnya bahasa Melayu.

6. Ini disebabkan bahasa sains dan matematik bukan daripada bahasa Melayu. Sebahagian besar daripada perkataan-perkataan dalam mata pelajaran ini adalah dalam bahasa Latin yang di-Inggeriskan.

7. Memang benar kita boleh Melayu-kan perkataan-perkataan ini, seperti juga kita Melayu-kan perkataan daripada lain-lain bahasa.

8. Memang boleh tetapi perkataan-perkataan sains bukan satu dua tapi beratus-ratus. Dan perkataan ini menjadi asas kepada perkataan yang mempunyai makna yang amat berlainan.

9. Umpamanya perkataan Oxygen (Oksigen) - satu jenis gas. Derivative (cabang) daripada perkataan ini adalah seperti berikut;

• Oxygenation

• Oxidation

• Oxide

• Oxidants

• Deoxydation

• Oxidise

• Oxidification

• Dioxide

• Monoxide

• Peroxide

10. Ini hanya bagi satu elemen daripada sebanyak 120 (118) elemen.

11. Tiap satu mempunyai banyak derivative. Tetapi ada perkataan-perkataan lain yang hanya untuk ilmu sains. Jika semuanya nak di-Melayukan, bahasa Melayu akan bertukar menjadi bahasa Inggeris, ejaan lain bunyi semacam. Sebenarnya ia bukan bahasa Melayu lagi.

12. Ilmu sains dan matematik bukan ilmu yang statik. Ilmu-ilmu ini berkembang sepanjang masa. Tiap hari ada hasil kaji selidik, penerokaan, ciptaan dan perluasan yang diperkenal melalui ratusan kertas-kertas yang ditulis.

13. Hampir semua ditulis dalam bahasa Inggeris. Untuk menterjemah tulisan ini kita perlu orang yang fasih dalam bahasa Melayu dan bahasa Inggeris dan faham ilmu yang hendak diterjemah.

14. Kita ada beberapa kerat sahaja orang yang berkebolehan seperti ini. Itupun dalam dua tiga bidang sahaja. Orang yang layak seperti ini tidak berminat menjadi penterjemah seumur hidup. Apabila sains dan matematik diajar dalam bahasa Melayu, orang seperti ini tidak akan ada lagi. Bagaimanakah kita hendak ikuti perkembangan ilmu sains?

15. Sebaliknya kertas ilmiah akan terus dikeluarkan beratus-ratus lagi, semuanya dalam bahasa Inggeris atau bahasa-bahasa lain. Maka tanpa kebolehan menterjemah semua ilmu baru ini akan tertinggallah orang Melayu dalam bidang ilmu yang amat penting di zaman ini.

16. Kalau kita masih tidak dapat menerima kenyataan di atas, kaji sahaja jumlah Phd dalam bidang sains yang hanya belajar sains dalam bahasa Melayu dan tidak faham bahasa Inggeris. Berapa ramaikah daripada pakar dalam bidang perubatan yang hanya belajar dalam bahasa Melayu, tanpa buku dalam bahasa Inggeris sebagai buku teks.

17. Apakah penuntut luar bandar tidak dapat menguasai bahasa Inggeris?

18. Sekali lagi perhitungan perlu dibuat berkenaan jumlah mereka yang dari kampung yang memegang jawatan tinggi dalam Kerajaan dan swasta kerana lulus dalam bahasa Inggeris dan mampu berhujah dalam bahasa berkenaan. Yang menentang PPSMI pun dari kampung juga tetapi dapat kelulusan bahasa Inggeris. Bahkan mereka sering berbahasa Inggeris.

19. Duta dan diplomat kita, berapa ramaikah yang hanya boleh bertutur kata dalam bahasa Melayu yang memegang jawatan penting dalam Kementerian Luar?

20. Pakar sains dan perubatan dan juga pegawai tinggi Kerajaan sering dikehendaki mengambil bahagian dalam persidangan antarabangsa. Apakah mereka dapat berhujah dan mengambil bahagian secara berkesan dengan mengguna hanya bahasa Melayu?

21. Saya bukan hendak memandang rendah bahasa bangsa saya sendiri. Tetapi saya perlu terima hakikat yang sebenar.

22. Bahasa sesuatu bangsa akan dipelajari oleh orang asing jika bangsa itu amat maju dan terkenal dengan ilmu yang dimiliki dan diterokai olehnya. Demikian sebelum abad ke-15 Masihi orang Eropah terpaksa belajar bahasa Arab kerana tamadun Islam pada masa itu gah dan amat dihormati. Tetapi selepas orang Islam ketepikan sains, ilmu perubatan dan hisab, orang Eropah tidak lagi mempelajari bahasa Arab. Sebaliknya orang Arab dan Islam terpaksa belajar bahasa Eropah.

23. Jika kita ingin bahasa Melayu digunakan dengan meluas kita perlu majukan diri kita dalam semua bidang terutama bidang ilmu dahulu. Sebelum daripada itu minat untuk belajar bahasa Melayu akan terhad kepada sekumpulan kecil sahaja.

24. Kita belajar sains dan matematik untuk memajukan bangsa kita supaya satu hari mungkin kita akan terkenal berkenaan dengan penerokaan dan kajiselidik oleh kita dan orang lain akan belajar bahasa kita untuk mendapat ilmu yang diteroka oleh kita.

25. Penguasaan ilmu amat penting bagi masa depan seseorang. Janganlah kita perjudikan masa depan anak orang kerana kononnya kita seorang nasionalis yang begitu sayang kepada bahasa kita. Sayang bahasa tidak boleh melebihi sayang bangsa. Mereka yang sayang bangsa mereka ingin lihat bangsa mereka maju, berilmu dan dihormati dunia. Hanya kerana boleh bertuturkata dalam bahasa sendiri tidak akan menjadikan bangsa kita dihormati dan disegani orang.

26. Akan rosaklah bangsa dan negara jika dasar negara ditentukan oleh orang yang berdemonstrasi. Lebih rosak lagi jika yang berdemonstrasi didalangi oleh politik pembangkang.

Dr M calls for doctors to help build the nation

2009-07-08T00:44:00.002+08:00

TUN Dr Mahathir Mohamad has called on doctors and future doctors in the country to contribute towards nation-building by serving the people.

The former prime minister who spoke on 'brain drain', said that loyalty to the country was very important "if you want to build this country".
According to Dr Mahathir, everyone who was born in this country was "helped" by the country, to be where they were today, be it a doctor or any other profession.
"So, if you think that you owe the people who helped you, then I don't think you will leave the country so easy," he said in a dialogue with International Medical University Malaysia students and staff at the university here today.
Dr Mahathir said that it was alright for a medical student to go overseas to study but upon completion, they should return and serve the country and the people.
"I don't think it (not returning to serve the nation) is compatible with a character a doctor should have," he added.
While it could not be denied that a doctor could earn more if he chose to go to a country which offered better pay, Dr Mahathir pointed out that the cost of living there, could be higher.
To a question from a student, the doctor-turned politician who helmed the country for almost 22 years, said that it was not wrong for a medical student to pay attention to political developments, but it should not be at the expense of his studies.
"(In fact)...medical education helps you to become a good politician. Doctors ask patients the history and symptoms. They have developed a very good methodology to solve problems," he noted.
He said the standard of the medical profession and the character of doctors must always be maintained.

PSP CRACKING BERJAYA

2009-07-06T10:06:00.008+08:00

Few weeks ago, i dengan gatalnya updating Najmi's PSP with a new firmware which is not an M33 firmware. Aiseyman.. Brick la pulak.. I panic.. no idea how to unbrick. Then i borrow my buddy kecik's psp 2000, i igtkan can settle, but his PSP's motherboard is TA-85a! aaaaaaa! This motherboard cant create Pandora battery by soft-moded. Then skg, no one else got PSP, and if they do got, they don't want to lend us their psp, and then the only way to unbrick is by creating pandora using my PSP and my PSP at johor that time. ARGHHh.. good thing that adik went home last week. She went back to KL and managed to get the PSP last night! Akhirnya berjaya crack the PSP using despertar del cementerio v6.. Please don't ask me why not using v8. Because i'm using windows 7 and the latest Pandora Deluxe is not working with it!

PSP untuk dilelong.. Panas2.. Satu RM10.

Stupid act by UMers

2009-07-03T01:21:00.004+08:00

1. The title was a bit harsh.

2. I'm actually talking about one of University Malaya (UM) student from Academy of Islamic Studies (API) which is also the President of PMIUM currently doing stupid act.

3. I'm not talking about politics. I'm not a politician, and i hate politics thus, there is no way that I'm gonna talk politics here.

4. Because I'm the most seniors undergrad stud in UM currently, it's important for me to address this messages to him. I care my junior, is that a problem? My junior have a duty and responsible to their parents.

5. Firstly, for me his act is certainly not an intellectual move which is supposedly to be expected from every student from UM.

6. We are not a politician, not an extremist, not a another 'RPK'. We're only a 'Mahasiswa Biasa'.

7. You might seem big to us because you're President of PMI, but do you think you are big enough out here?

8. Do you think that you big enough you can do anything against the law and because of that you run from getting caught from the cops?

9. You're the 'role model' of all the student in UM. Do you think this act should be done on every students here?

10. Or you just want to have a 'publisiti murahan' so that all Malaysians know you.

11. Don't make assumption, where u based only on youtube video without any fact.

12. Don't make a statement threaten to the university admins of having a riot. If you do, i do agree if AUKU is implemented on you.

13. I suggest you shouldn't be doing it. Better for you to do good deeds and welfare to the students.

14. Where is your 'kurangkan yuran universiti' and also 'Riba PTPTN' fight anyway? My yuran is so expensive, and yet i don't have any $$ left in my pocket!

15. University can throw you away anytime they want, because you have done the DUMBESS act which is against the law.

16. And yet they have not done it because they think that you're the Leaders of Islamic Student? Of course not, because the investigation have not been concluded and you've not been prove to be the culprit who behind this DS Rosmah C4 wall painting.

17. If DS Rosmah was really doing all those nasty things, dont you think by putting an oil/petrol on the carpet and try to harm her by putting up a fire are the best way to punish her?

18. Do you think you wont be having a fair trials? Do you think that Anwar Ibrahim and RPK doesn't have a fair trial? Do you think that you'll be beaten at the eye and having a 'panda eye' like Anwar Ibrahim in the lockups?

19. If you have all this you might having a delusion of persecutory which might indicate you a schizophrenic. If it does, you should meet me, here, in Psychiatric ward in UMMC.

20. Maybe, i mean it, maybe, you might or will be given an exemption from the trial.

21. So please don't ask your friends to become one like you.

22. Don't you think that by AUKU is important now?

MBBS vs MD

2009-06-30T13:30:00.003+08:00

Haha.. I was a bit surprise when i saw one of the keyword from the readers.

perbezaan M.D dan MBBS

I wonder why would someone really cares about the difference between Medicine Bachelor and Bachelor of Surgery (MBBS) and Doctor of Medicine(MD)? Both of them doctors, and both of them study the same things. The only differences are the name and one is British system, one is American. That's all. I wonder if i put this article, more and more will come to this site. LOL

H1N1/Influenza A/Swine Flu/Selsema babi..

2009-06-29T02:40:00.010+08:00

Prof. Datuk Dr. Adiba Kamarulzaman, my professor of Infectious Disease in Dept Medicine, recently came out in hello Malaysia one of the segment/talk/tv shows in Bernama TV, Astro.. To those who still doesn't know what is Influenza A, can watch this video.. Meanwhile, when i'm writing this article, our cases have reached to 124!

(Click the image to view the video)
p.s.: You need to have real player plugin to view this video..

Sorry guys, We're back!

2009-06-27T11:05:00.009+08:00

First of all we're sorry for the missing days guys.. We're too busy for this current posting. Actually, we've been in Obstetric and Gynaecology posting for 1 weeks already. Our posting require us to make 2 case summaries, 3 case presentation, and 5 DELIVERIES!!! sux man, because, we shouldn't be doing deliveries anymore because we've done it before. The department was really strict on us. I can still remember i fail my posting with only 0.1 mark to pass (i got my marks 49.9) because I didn't get the chance to pass out my last case summary only because of I'm late for a day. Anyways guys, I'll try to put up some post and maybe some picture of us later what we've done for the next 2 weeks in O&G.

Next, how was your life then? Many of my batch mates have already been posted to their respective hospital! Good luck guys in the coming days. Do not extend your posting.. LOLZ..

Meanwhile, it's the end of the months now and this would be the most suitable day to cash out my NUFFNANG blogging money! maybe tomorrow would be nice! I would like to thank to you all guys for clicking the ads here by nuffnang. Until then, I'll post about it the moment i got that check..

Intestinal Obstruction - Xray

2009-06-18T21:35:00.016+08:00

Topic today would be identifying Intestinal Obstruction in an abdominal X-ray. It's more or less like a quiz. Let's get started

Case 1
A 36 year old male with vomiting- for 1/7

Ok. How to interpret this?
It looks normal isn't it? Of coz it's normal. We need to know which one is normal. But if this normal, u still need to comment. What to look for in a 'normal' x-ray anyway?

Things to look for are

Technical – Is the X-ray adequate?
Is the gas in the correct place?
Is there abnormal calcification or mass?
Is the visualised bone and soft tissue normal?
Any foreign bodies?

Case 2
8year old boy with abdominal pain

Hoho.. what do u think? Looks a bit shiny isn't it?

It's a metallic foreign body projected over the left iliac fossa
No dilated bowel loops
Very unlikely to cause intestinal obstruction

Case 3
50 year old male with vomiting and NBO for 5/7

Look a bit bizarre rite? Take a proper look at the right side of the inguinal region. Is that a bowel?
This is actually an inguinal hernia basically a clinical diagnosis. Why do we do an Xray then? To rull out intestinal obstruction.

Radiograph shows dilated small bowel in abdomen
Bowel in the left inguinal region extending into the scrotum

Case 4
52 year old female with abdominal distension and vomiting for 2 days with a previous history of appendicectomy

Based from the history, adhesion would be more likely to cause intestinal obstruction due to adhesions from the previous appendicectomy.

Note the multiple air fluid levels on the erect AXR
On the supine radiograph – dilated loops of air filled small bowel

There is one question so common to ask in viva - How do you differentiate dilated small and large bowel?

Easy - Look a the bowel fold
Small bowel folds extend from one end of the bowel wall to the other
Large bowel folds- Haustra extend about one third of the way
Small bowel is also more central in position in the abdomen

Case 5
45 year old female with abdominal distension for 5 months

This one abit difficult. Where is the bowel actually? This is a large abdominal mass!
Bowel loops are displaced laterally and superiorly by a large soft tissue mass which appears to arise from the pelvis. Note a dilated small bowel loop in the right lumbar region.

Case 6
48 year old male – post gastrectomy 1 day

This could be paralytic ileus. I forgot to tell u that apart from adhesion, paralytic ileus could also be the cause of Intestinal Obstruction. However, an ileus can be diagnose based on abdominal examination by absence of bowel sound.
Note dilated small and large bowel. Apart from paralytic ileus, sub acute distal large bowel obstruction can give a identical appearance

Case 7
76 year old female with loss of weight for 3 months and now presents with NBO for 3 days.

Note the dilated air filled large bowel, from the caecum to the splenic flexure. This is a large bowel obstruction at the level of the splenic flexure.
This was due to carcinoma of the colon. A colonscopy would confirm this diagnosis
Ba Enema (Limited)- would also confirm the diagnosis. A CT would show the mass and is useful for staging

Case 8
30 year old female with non specific abdominal pain – 1 year

Non specific abdominal pain.. If you see this in Primary Care, sure you handle this as an irritable bowel syndrome.. HAHA.. yup this one is a normal small bowel enema. Note the “small bowel enema tube”. Normal small bowel folds which become less prominent in the ileum

Case 9
33 year old male with loss of weight – 4 months and vomiting for 5/7

There is thickened small bowel folds and strictures

Diagnosis?
.
.
.
.
It's a Lymphoma

Case 10
43 year old male with vomiting and lower abdominal pain- 1/7

This is a dilated loop of Large bowel. Inverted ‘U’ shaped loop of large bowel arising from the pelvis. Inverted ‘U’ shaped loop of large bowel arising from the pelvis. Suspect a volvulus (twist) of the sigmoid colon. How to confirm?

By doing a barium enema
Note the site of twist. This has been called the ‘Bird’s Beak’ sign

Case 11
20 year old male with history of chronic constipation since childhood

Diagnosis: Hirschprung Disease
Grossly dilated large bowel
Filled with faeces

We've got our 1st Influenza A transmission Man to Man

2009-06-17T17:30:00.008+08:00

Hey, first of all i don't know it's real or not because it's from Malaysiakini.com. But if this is real, this would be the very bad. Why? Because this patient was send to UMMC!!!!!!!!
Damn I don't want to go to the ward after this!! An irresponsible act by a 17 year old girl who don't contact to the ministry after getting exposure to patient of the 12th case of Influenza A in Malaysia. This would be the 19th case and just now, the 20th case has just been reported! Because of this, no wonder WHO has declaring pandemic, the Influenza A gene has evolve from swine to human transmission, to human to human transmission! Good thing that there is no death case reported here. And when there is death case, it would be very very bad to our country.

Updated: Meanwhile our cases have reached 23rd cases with 5 new cases today according to the MOH here.
Nevermind. The patient has been transferred to HKL already.. My bad.. No excuse not to go to the ward..

kemaskini 4.59pm Jangkitan selesema A (H1N1) semakin serius di negara ini, susulan berlakunya penularan wabak tersebut di peringkat tempatan yang pertama pada pesakit ke-19 daripada 23 kes, sejak sebulan lalu.

Pesakit berkenaan, seorang pelajar perempuan 17 tahun, dijangkiti daripada pesakit ke-12 akibat kegagalan kuarantin apabila tidak memaklumkan pernah berhubung dengan pelajar perubatan kes terdahulu.

Akibatnya, menurut satu kenyataan Kementerian Kesihatan hari ini, kegagalan itu menyebabkan 20 orang lagi berkemungkinan terdedah kepada jangkitan H1N1.

Kementerian juga memaklumkan bahawa lima lagi kes influenza itu dikesan dalam tempoh 24 jam yang lalu.

"Salah satu dari kes yang disahkan positif Influenza A (H1N1) adalah kes penularan tempatan yang pertama berlaku di negara ini," kata Ketua Pengarah kesihatan, Tan Sri Dr Mohd Ismail Merican.

"Kes pertama penularan tempatan (kes ke-19) adalah seorang pelajar perempuan berumur 17 tahun, warganegara Malaysia yang tidak mempunyai sejarah melawat negara (asing) yang telah diisytiharkan berlaku wabak Influenza A(H1N1).

"Beliau telah mula menunjukkan simptom batuk dan selesema pada 14 Jun 2009 jam 9 malam, dan mula demam pada keesokan harinya. Pada pagi 15 Jun 2009, kes telah pergi ke Pusat Perubatan Universiti Malaya seterusnya dirujuk ke Hospital Sungai Buloh jam 10.00 pagi.

"Semasa penyiasatan, kes ke-19 melaporkan bahawa beliau adalah kontak kepada kes ke-12 iaitu pelajar perubatan yang telah disahkan positif Influenza A(H1N1) pada 13 Jun 2009.

"Namun sebelum ini beliau tidak pernah diisytiharkan sebagai salah seorang kontak kepada kes ke-12.

"Ini menyebabkan pengawasan dan kuarantin awal ke atas kes ke-19 ini gagal dilakukan dan menyebabkan 20 orang lagi (kontak) terdedah kepada jangkitan influenza A(H1N1)."

Dr Mohd Ismail menambah, sangat penting semua kes yang disahkan
positif H1N1 memberikan maklumat lengkap supaya pengawasan dan kuarantin awal dapat dilakukan kepada semua orang yang pernah berhubung dengan mangsa, seterusnya mengelakkan risiko penularan kepada orang lain.

"Tindakan undang-undang bawah Akta Pencegahan dan Pengawalan Penyakit Berjangkit 1988 boleh diambil sekiranya mereka gagal memberikan maklumat yang lengkap," katanya.

Tambahnya lagi, sesuai dengan keputusan Mesyuarat Jawatankuasa Teknikal Kejadian Influenza A(H1N1) bil. 5/2009, kementerian juga mengeluarkan arahan seperti berikut:

Orang awam tidak digalakkan untuk melawat hospital. Kanak-kanak berumur bawah 12 tahun dilarang pergi atau dibawa melawat ke hospital kecuali untuk mendapatkan rawatan.

Setiap pesakit hanya dibenarkan menerima dua orang pelawat berumur lebih 12 tahun pada satu-satu masa. Masa lawatan di hospital kerajaan dan swasta akan dipendekkan.

Saringan demam akan dilakukan kepada semua pelawat yang
datang melawat pesakit di semua hospital kerajaan dan swasta.

Kementerian Kesihatan juga memohon kerjasama kepada penumpang, anak kapal dan kontak kepada kes agar menghubungi melalui talian 03-88 81 02 00 atau 03-88 81 03 00 untuk mendapatkan nasihat kesihatan termasuk keperluan kuarantin di rumah.

Which one better SLR or Compact?

2009-06-17T01:18:00.004+08:00

Nowdays, camera seems to be the second gadget that we must have and I'm wondering to get one but I don't know which one suits me. It it SLR or compact camera.
Of course in terms of budget, I should buy a compact camera, but for long term, SLR might be worth for. So i've look up for some 2nd opinions from the net. Then i found something interesting. 'TheBigCameraDebate' by the two Fly FM DJs, Ben and Phat Fabes sponsored by Olympus PEN E-P1
They are fighting about this two type of camera, Ben - SLR and Compact - Phat Fabes. But the one actually fighting are not them, the users which are debating for their side. The criteria was, those who want to wins needs to have the most messages/debates from the users and in the end of the day, the winner will be granted one wish which make the loser to do his command.. LOLZ.. Wait till u see the videos.. Too bad, Phat Fabes is the one who lost mostly. So, did the SLR wins? haha.. U have to see it for yourself.

In the mean time, the debate was closed but u can still watch the recent video they've put up on their site. Click here to watch the videos.

HAPPY BIRTHDAY

2009-06-17T00:48:00.006+08:00

HAPPY BIRTHDAY TO 'ONE OF US'! SYUHADA!

(Versi Melayu-Classic)

ALLAH SELAMATKAN KAMU,
ALLAH SELAMATKAN KAMU,
ALLAH SELAMATKAN NOR SYUHADA,
ALLAH SELAMATKAN KAMU.......

(Versi English)

Happy Birthday to you,
happy birthday to you,
Happy Birthday, Nor Syu...
Happy Birthday to you!



(Versi Arab)

سنة حلوة يا جميل

سنة حلوة يا جميل

سنة حلوة يا حبيبي

سنة حلوة يا جميل

(dalam ruminya,)

Sana 7elwa ya gamiil,

Sana 7elwa ya gamiil,

Sana 7elwa ya Nor Syuhada,

Sana 7elwa ya gamiil,

New Template!!

2009-06-16T03:35:00.013+08:00

Yes! We've managed to put up a new, hey but wait. I need to address something much2 more important

First of all, We're sorry for those who went to our page using Internet Explorer before. I've noticed that there was a problem when viewing using IE either using old or latest (8). The problem was crash and terminate the connection to the net. However there is no problem using Firefox 3.0. I don't know about the other browser such as Chrome or Safari which i've stopped using it for a while because no RSS function. We're really regret it and sorry for any inconvenience when surfing our page.

We're so excited about this new template. I've managed to got it from here. I feel that we've just being born again! It's like a new beginning. LOLZ.. Feel free to come back to read for our articles. More to come!

Orthopaedic examination

2009-06-15T17:27:00.004+08:00

Nice class today with Dr Shamsul Ortho. Syud dengan tak malunya, made a video of kah kian yang malu.. LOLZ.. hope she can put it up here

Type and Indication of Blood Transfusion

2009-06-13T21:15:00.007+08:00

The second short note question would be about blood transfusion. Safe blood products, used correctly, can be life-saving. However, even where quality standards are very high, transfusion carries some risks. If standards are poor or inconsistent, transfusion may be extremely risky. No blood or blood product should be administered unless all nationally required tests have been carried out.

Blood component:
1 A constituent of blood, separated from whole blood, such as:

Red cell concentrate
Red cell suspension
Plasma
Platelet concentrates

2 Plasma or platelets
3 Cryoprecipitate, prepared from fresh frozen plasma: rich in Factor VIII and fibrinogen

Plasma derivative
Human plasma proteins prepared under pharmaceutical manufacturing conditions, such as:

Albumin
Coagulation factor concentrates
Immunoglobulins

WHOLE BLOOD

450 ml donor blood
63 ml anticoagulant-preservative solution
Haemoglobin approximately 12 g/ml
Haematocrit 35%–45%
No functional platelets
No labile coagulation factors (V and VIII)

Indication

Red cell replacement in acute blood loss with hypovolaemia
Exchange transfusion
Patients needing red cell transfusions where red cell concentrates or suspensions are not available

RED CELL CONCENTRATE

150–200 ml red cells from which most of the plasma has been removed
Haemoglobin approximately 20 g/100 ml (not less than 45 g per unit)
Haematocrit 55%–75%

Indication

Replacement of red cells in anaemic patients
Use with crystalloid replacement fluids or colloid solution in acute blood loss

LEUCOCYTE-DEPLETED RED CELLS

A red cell suspension or concentrate containing <5>
Haemoglobin concentration and haematocrit depend on whether the product is whole blood, red cell concentrate or red cell suspension
Leucocyte depletion significantly reduces the risk of transmission of cytomegalovirus (CMV)

Indication

Minimizes white cell immunization in patients receiving repeated transfusions but, to achieve this, all blood components given to the patient must be leucocyte-depleted
Reduces risk of CMV transmission in special situations
Patients who have experienced two or more previous febrile reactions to red cell transfusion

PLATELET CONCENTRATES
Single donor unit in a volume of 50–60 ml of plasma should contain:

At least 55 x 109 platelets
<1.2>
<0.12>

Indications

Treatment of bleeding due to:
— Thrombocytopenia
— Platelet function defects
Prevention of bleeding due to thrombocytopenia, suchas in bone marrow failure

FRESH FROZEN PLASMA

Pack containing the plasma separated from one whole blood donation within 6 hours of collection and then rapidly frozen to –25°C or colder
Contains normal plasma levels of stable clotting factors, albumin and immunoglobulin
Factor VIII level at least 70% of normal fresh plasma level

Indications

Replacement of multiple coagulation factor deficiencies: e.g.
— Liver disease
— Warfarin (anticoagulant) overdose
— Depletion of coagulation factors in patients receiving large volume transfusions
Disseminated intravascular coagulation (DIC)
Thrombotic thrombocytopenic purpura (TTP)

CRYOPRECIPITATE

Prepared from fresh frozen plasma by collecting the precipitate formed during controlled thawing at +4°C and resuspending it in 10–20 ml plasma
Contains about half of the Factor VIII and fibrinogen in the donated whole blood: e.g. Factor VIII: 80–100 iu/ pack; fibrinogen: 150–300 mg/pack

Indication
* As an alternative to Factor VIII concentrate in the treatment of inherited deficiencies of:
— von Willebrand Factor (von Willebrand’s disease)
— Factor VIII (haemophilia A)
— Factor XIII
* As a source of fibrinogen in acquired coagulopathies:
e.g. disseminated intravascular coagulation (DIC)

HUMAN ALBUMIN SOLUTIONS
Prepared by fractionation of large pools of donated plasma

Indication

Replacement fluid in therapeutic plasma exchange: use albumin 5%
Treatment of diuretic-resistant oedema in hypoproteinaemic patients: e.g. nephrotic syndrome
or ascites. Use albumin 20% with a diuretic
Although 5% human albumin is currently licensed for a wide range of indications (e.g. volume replacement, burns and hypoalbuminaemia), there is no evidence that it is superior to saline solution or other crystalloid replacement fluids for acute plasma volume replacement

COAGULATION FACTORS

Factor VIII concentrate

Treatment of haemophilia A
Treatment of von Willebrand’s disease: use only preparations that contain von Willebrand Factor

PLASMA DERIVATIVES CONTAINING FACTOR IX
Prothrombin complex concentrate (PCC)
Factor IX concentrate

Treatment of haemophilia B (Christmas disease)
Immediate correction of prolonged prothrombin time

POSTOPERATIVE MANAGEMENT

2009-06-12T16:49:00.003+08:00

End of Posting Written Test
Lolz.. This morning short note test come out to be complication of operation.. Damn i don't like this kinda question. I hate short notes.. really.. But nway, i've made an article for us to look what we've answer and filling all the blanks that we have.. But hey, this is not an answer scheme or what so ever. It just for our understanding and merely a revision before we get ourself into a House Officer..

The role of the junior doctor postoperatively is to check that the patient has recovered from the anaesthetic, look at their observation charts and check their fluid balance. The operation note should have a section on specific postoperative management written by the surgeon, and is a guide that should be followed. For example, following a vascular graft operation — say, to the leg — you should always check the pulses, capillary refill and toe movement in the involved leg to ensure that the graft has not blocked off. A common question for exams concerns complications of surgery.

Complications
All operations carry a risk of complications. These can be divided into general and specific.

* General complications include those pertaining to the anaesthesia itself and those that can occur after any operation, such as a chest infection or DVT.
* Specific complications are those that occur because of the individual operation itself, such as cutting a nerve.

You can subdivide this classification by time, into complications that occur immediately, within the first 24 h; early, within the first week or so; late postoperative, occurring within the first month or so; and long term.

General immediate complications include those due to the anaesthetic, such as direct trauma to the mouth when intubating and reactions to the anaesthetic (inherited disorders or idiosyncratic reactions).

Other early complications including
* Chest infections
* Urinary retention or infections
* Deep vein thrombosis
* Bed sores.

Specific complications depend on the nature of the operation. In this category haemorrhage and wound infection are important.

Haemorrhage
This can be divided into primary, reactionary and secondary haemorrhage.

* Primary haemorrhage occurs during the operation, when a vessel is cut.
* Reactionary haemorrhage is when at the end of the operation the wound looks dry, but when the patient’s blood pressure and cardiac output rise to normal levels, bleeding begins, presumably from vessels that were not properly ligated during the operation.
* Secondary haemorrhage, occurring several days after the operation, is usually attributed to infection that erodes through a vessel.

Wound Infections
These are most commonly caused by S. aureus (increasingly MRSA), although coliforms such as E. coli are also important. Wound infection is more likely if

• The operation is dirty (e.g. abdominal surgery)
• The duration of the operation is long (greater than 2 h)
• The patient is more susceptible (e.g. old age, immunosuppression, diabetes)

Minor wound infections, with a little redness and slight discharge, are relatively common and usually need just simple measures, such as regular wound dressing and perhaps antibiotics. More severe infections, common after abdominal operations, usually occur in the first week or so. The wound looks inflamed, and there may be cellulitis, discharge or localised abscess formation. The wound should be swabbed and maybe antibiotics started, but the only correct treatment for an abscess is drainage. This may mean simply removing a few of the surgical clips, and probing the wound, allowing the pus to discharge, or a further surgical procedure to open up the wound. The wound is then left to heal by secondary intention (i.e. to heal itself from within, with no further suturing).

Wound Dehiscence
This is an uncommon problem. It is usually due to an inadequate repair of the tissues (but infection, poor blood supply, malnutrition and steroids may all play a part in poor wound healing). Dehiscence usually occurs about a week after the operation. A warning sign is a serosanguinous discharge from the wound a few days before. The wound suddenly bursts open and in the case of a laparotomy the bowel protrudes outwards and is extremely alarming for the patient and the nursing staff. Sterile soaked swabs should be placed over the wound and the patient taken back to the theatre for repair.

serasenguinous discharge

An example of general and specific complications pertaining to a - gastrectomy is outlined below.

Click to enlarge

The commonest reason that a junior doctor gets called to the ward is to write up fluids or to see a patient with postoperative pyrexia or poor urine output.

POSTOPERATIVE PYREXIA
A small rise in temperature is common postoperatively. If the temperature spikes above 38'C or persists, then you should consider and look for the seven C's as potential causes. This is a common viva question.

1. Chest. Chest infection
2. Catheter. UTI
3. CVP line. Infected
4. Cannula. Superficial thrombophlebitis (solved by removing the cannula)
5. Cut. Wound infection
6. Collection. Subphrenic or pelvic abscess (may indicate a failure of anastomosis)
7. Calves. DVT (rumbling pyrexia in second postoperative week)

A chest infection is very common postoperatively, especially in patients who smoke or have pre-existing poor respiratory function. The mucus secretions are not cleared; these then clog up the smaller bronchi, which leads to collapse of the air spaces distal to the blockage (atelectasis). Inhaled organisms then infect the collapsed segments. In addition, thoracic and upper abdominal incisions cause pain and stop the patients from coughing up the secretions, and so they are much more likely to have basal atelectasis and develop chest infections. These patients should therefore be given adequate analgesia, have vigorous physiotherapy, and be encouraged
to cough up the phlegm (ideally whilst holding their wounds — applicable for chest and abdominal wounds).

Abscesses
A deep collection, such as a subphrenic or pelvic abscess, can occur after the patient has had generalised peritonitis. The patient usually presents with general malaise, nausea, pain (a subphrenic abscess may also cause pain felt in the shoulder tip), a swinging pyrexia and localised peritonitis.

A pelvic abscess often occurs 4–10 days postop., whereas a subphrenic abscess usually occurs a bit later, 7–21 days postop. Clinically, the patient appears to be recovering well, but then develops a fever and starts to feel unwell. The white cell count may be raised and a collection is identified on ultrasound or CT. Treatment is by drainage, either percutaneously under ultrasound or CT guidance, or by an open procedure. A drain is usually left in situ.

Anastamotic leak
A small anastomotic leak usually causes a localised abscess which becomes sealed off by the omentum and the bowel. Clinically, the patient is slow to recover, but usually improves with intravenous antibiotics and fluids and delayed return to food. A larger anastomotic breakdown causes the patient to be very unwell, with anything from local peritonitis through to a rigid abdomen and septicaemia. The abscess needs to be drained, the peritoneal cavity washed out, and the two ends of the failed anastomosis can be brought out as temporary stomas.

Thrombosis
A diagnosis of DVT and pulmonary embolus (PE) in the first instance is essentially a clinical one, as treatment is usually instituted before definitive diagnosis is made. A PE usually presents with pleuritic chest pain (stabbing and worse on inspiration). The textbooks tend to describe the findings you would see in a massive PE, although more commonly in the smaller PEs the findings are less impressive. Usually, the patient is tachycardic, maybe with a low-grade fever and maybe tachypnoeic, but not much else and they may even be asymptomatic. The ECG usually shows sinus tachycardia (the classic S1Q3T3, which most students know about, occurs when there is a large amount of right heart strain, in a large PE, and is rarely seen). The CXR is usually unhelpful but may show a small area of linear atelectasis.

S1Q3T3

Blood gas analysis is essential and you would expect to find a low PO2 (due to ventilation/perfusion mismatches) and a low PCO2 due to hyperventilation. Examination of the calves may or may not reveal evidence of a DVT. If a DVT or PE is suspected, a heparin infusion can be started before investigation but always check with a senior colleague before doing that, especially if the patient has had recent surgery.

To diagnose a DVT you can use duplex ultrasound (or a venogram). To diagnose a PE you can request a ventilation–perfusion scan, although the gold-standard is pulmonary angiography (note nowadays a spiral CT is used in some centres).

Other less common causes for a fever include infective diarrhoeas, drug reactions and blood transfusion reactions. If faced with a patient with a pyrexia you would obviously find out a little history and examine the patient properly. In a long case exam situation you could answer along the lines of, ‘I would listen to the chest, examine the abdomen, check the cannula sites, inspect the wound, etc. … My investigations would depend on my clinical findings but may involve sending a urine specimen, a full blood count and blood cultures, sending wound swabs or the tip of the central line for culture, etc.’

DRAINS
Collections within a wound (especially if they contain blood) are the perfect medium for colonisation of bacteria and hence infection.

A drain can be used to remove anticipated collections within a wound, but should never be used as a substitute for adequate haemostasis at the time of surgery.

Drains can be closed or open:

Closed drainage includes suction drainage (e.g. Redivac) where the collection is attracted into a container either by gravity or suction. This can then potentially reduce the risk of infection when used for large spaces or cavities, such as after a mastectomy or joint replacement. Drains are usually removed as soon as possible (usually 24–48 h) or as soon as the losses begin to tail off. Drains can also introduce infections and so they should not be left in for any longer than needed.

Open drainage (e.g. a piece of corrugated tubing with one end in the wound and the other in the dressing), allows small losses to escape from the wound. This is often employed in established abscesses after incision and drainage to allow any remaining collection a passage out of the wound. Some surgeons like to withdraw this type of drain in stages to allow the track to collapse behind it.

Other drains commonly asked about in exams include chest drains, T-tubes and percutaneous nephrostomies.

POSTOPERATIVE POOR URINE OUTPUT
This is a common exam question and can be classified as prerenal, renal or postrenal. The commonest causes of failure to pass urine postoperatively are postrenal.

Postrenal problems (commoner in males) include obstruction caused by a large prostate or a blocked catheter. Also, the patient may find initiation of micturition difficult for the following reasons:

1. Anticholinergic drugs or those with alpha adrenergic effects (e.g. the anaesthetic)
2. Pain (e.g. after a hernia repair)
3. Inhibition (e.g. because of strange surroundings or a nurse continually asking them if they have passed urine)
4. Opiates or epidural anaesthetics

Once the bladder reaches a certain volume of distension it fails to function properly and the patient goes into retention. Benign prostatic hypertrophy is an important predisposition and these patients are more likely to go into retention.

Prerenal causes are due to renal hypoperfusion because of either hypovolaemia or heart failure.

Renal causes — Acute renal failure is usually due to acute tubular necrosis.

How to handle?
Junior doctors are commonly called to see patients who have failed to pass urine postoperatively. Often this will be a patient you are covering but have not met before. It is, therefore, worth spending a little time getting a history and reading the patient’s notes. You should find out the type and date of operation and also search for clues pointing to whether the problem is prerenal or postrenal. Ask if there is any pain; an enlarged bladder causes suprapubic pain, although this is difficult to differentiate from pain in an abdominal wound (one exception is when there is an epidural in situ and there is no pain).

On examination you should look for signs of hypovolaemia (dry mucous membranes, decreased skin turgor, tachycardia, etc.), signs of heart failure (shortness of breath, tachycardia, raised CVP or JVP and bibasilar crepitations, peripheral oedema, etc.). A distended bladder palpable just above the pubis is dull to percussion and usually tender, making the patient want to pass urine, when compressed.

You can initially try conservative measures such as analgesia, privacy, sitting in a warm bath, etc., but if that fails then catheterisation is indicated. If you suspect that the cause is postrenal (i.e., distended bladder and discomfort), then the diagnosis is proven by catheterisation. A large residual volume of urine should drain (usually about 500 ml or more).

If the patient already has a catheter in situ, then the catheter should be flushed to ensure it is not blocked. If the urine coming out of the catheter is small amounts of concentrated dark urine, then the cause is likely to be prerenal anyway. You could dipstick the urine, testing for a high specific gravity (more than 1020) to prove this.

You should check the fluid balance charts (IO chart). Observe how much fluid has gone in before, during and since the operation and the measured urine output. Remember that a long laparotomy can lead to large losses of fluid by evaporation and this will not be measured on the charts. A urine output of less than about 30 ml/h is poor (oliguria). The patient should be catheterised anyway at this point to measure the hourly urine output.

U & Es should be sent; if there is a prerenal cause, the urea will be raised. If from your clinical examination and your assessment of the fluid balance charts you think the patient has a prerenal cause, then you should try a fluid challenge.

Fluid Challenge — 250–500 ml of normal saline given as a stat dose (unless you suspect blood loss as the cause, in which case the patient may be shocked and should be given colloids and blood). Then, observe the urine output over the next hour. If the urine output picks up, you have shown the patient to be in need of more fluid and the next bag should be speeded up.

If the patient has heart failure, the urine output will not pick up and the patient may become a little more breathless and the CVP might rise. If this occurs, a bolus dose of a loop diuretic, such as 40 mg of frusemide, will lead to a diuresis and a fall in the CVP. If the patient does not have a central line in at this point, you should ask a senior colleague for advice, as a central line is really necessary for knowing exactly what the state of vascular filling is and will help in the management.

Only after you have excluded a postrenal and a prerenal cause can you assume that there may be a renal problem and acute tubular necrosis has occurred. The creatinine will be raised and you should measure the urine and plasma osmolalities. The ratio of urine to plasma osmolality will be less than 1 (as opposed to prerenal oliguria, where the ratio will be more than 1). Advice from a renal physician should be sought early.

That's all folks.. Hope can help you a bit. I need a great night sleep tonight after tired using my brain for 12 hours straight. Good night.

£80 million for Ronaldo.. Damn Real..

2009-06-11T17:39:00.003+08:00

Manchester United have accepted an £80m offer from Real Madrid for Cristiano Ronaldo.

A statement on the United website confirmed that a deal for the 24-year-old should be completed by the end of the month.

''Manchester United have received a world-record, unconditional offer of £80million for Cristiano Ronaldo from Real Madrid.

''At Cristiano's request - who has again expressed his desire to leave - and after discussion with the player's representatives, United have agreed to give Real Madrid permission to talk to the player.

''Matters are expected to be concluded by 30 June. The club will not comment until further notice.''

Ronaldo has long been a target for the Spanish giants, whose president Florentino Perez vowed earlier this week to do ''everything possible'' to take the 24-year-old to the Bernabeu.

Cristiano Ronaldo's last game for United was the Champions League final defeat to Barca

It is now certain that a second era of "Galacticos" has begun at Madird, with news of Ronaldo's £80m deal coming in the same week Perez agreed a £59, deal to sign Kaka.

The news is bound to be greeted with some scepticism by United fans who have repeatedly been told no deal had been agreed for the sale of FIFA's world player of the year in the face of regular statements from Spain the former Sporting Lisbon star was bound for the Bernabeu.

It was even suggested Ronaldo would be due a £20m compensation fee from Real if the deal did not go through by June 30, the date United now state themselves is when they expect matters to be concluded.

As it now seems a matter of when, rather than if a world record transfer will be completed, Sir Alex Ferguson might wish to explain why he has gone back on his famous comment in December last year that he would not ''sell that mob a virus''.

It is the first time for many years United would have allowed a player to leave they were not happy about losing.

Yet some supporters may be pleased that at least another drawn-out transfer saga, such as the one 12 months ago, is not played out in public.

And, at least the money could be reinvested in a squad that almost, but not quite proved good enough to win back-to-back Champions League trophies, in addition to a hat-trick of Premier League titles.

Wow a New Upin and Ipin Movie

2009-06-10T19:45:00.011+08:00

After the success of Geng:Pengembaraan Bermula last February, the popular 3D animation characters from the movie - Upin and Ipin will be back for yet another adventure in an all-new feature film called Upin & Ipin: Angkasa. The announcement was made yesterday by Les' Copaque Production, the company behind the film, on their official production blog.

Together with the announcement, the production company has also revealed the film's official website. In the teaser available at the site, Upin and Ipin are shown on the moon and clad in space suits. Right after they plant Malaysian flag on the surface, a shadowy alien figure suddenly dashes by them, setting the twin brothers off on yet another investigative adventure.

There is no mention of an exact release date for the film, but according to the official website, Upin & Ipin: Angkasa will be out in 2011.

Busy week

2009-06-10T08:49:00.011+08:00

I'm a bit busy this week. A lot of things to share with u guys.. a bit sad i couldn't share with u guys in this blog.. nway, i'll be in facebook... Sorry guys..

at Dr Vivek trauma seminar

UPNM terima kumpulan pertama pelajar perubatan tahun hadapan

2009-06-08T20:04:00.005+08:00

UTUSAN

KUALA LUMPUR 8 Jun — Universiti Pertahanan Nasional Malaysia (UPNM) akan menerima kumpulan pertama 40 penuntut Fakulti Perubatan Ketenteraan pada tahun depan, kata Menteri Pertahanan Datuk Seri Dr Ahmad Zahid Hamidi hari ini.

Beliau berkata pengenalan fakulti baru itu sejajar dengan hasrat UPNM menjadi sebuah universiti yang berteraskan kecemerlangan bukan sahaja dalam aspek akademik tetapi mencakupi sahsiah, kepimpinan dan pembangunan kendiri.

“Kita memiliki aset seperti hospital tentera serta pusat pemeriksaan kesihatan sendiri dan kita telah kenalpasti beberapa hospital tentera yang akan dijadikan pusat latihan amali bagi pelajar tersebut,” katanya kepada pemberita selepas melakukan lawatan rasmi ke UPNM di Kem Sungai Besi di sini hari ini. - Bernama

Agak2nya what do you think their title is? MBBS? MD? MBBchb?MB BChir? BM BCh? MB BCh? MB ChB? BM BS? or AD(army doctor) or SD (soldier doctor) lolz

Teringat kat Amru...

kepada classmate ku

2009-06-08T19:44:00.001+08:00

Datang la ward, clinic dan juga kelas.. Ya? ok? ble la.. 2 minggu je lagi.. Aku malas nak wat hal dengan department ataupun pejabat dekan..

Hehehehe

2009-06-07T23:49:00.004+08:00

I've bought 2 tickets to the Malaysia XI vs Manchester United match! Bought it a the rockgarden, Gardens Mid Valley! hehe jgn jealous yer

apa itu cinta?

2009-06-07T01:18:00.010+08:00

Hehe.. mesti pelik blog ni asalnyer citer pasal medical tibe2 citer pasal bende bukan2? Knape tak le ke dak medic bercinta2 nih?

I'm just jealous that a lot of blogs outside there posting about love, cinta2 la, etc2.. So that now I'm in blues, blues giler2 babeng, apa kata I talk about Cinta plak.. hehe.. so layan kan saja yek.. Kalau tak nak layan don't click proceed.. LOLZ.. I'm just having delusion for now..

Apa itu Cinta?

Setiap orang mempunyai makna cinta yang tersendiri. Ada yang kata, cinta itu menyakitkan dan jangan kau hampirinya. Tetapi, ada juga yang kata, cinta itu mengasyikkan sehingga kau akan terbawa-bawa dengan ombak asmaranya. Dan ada juga yang kata, cinta itu indah dan tiada ungkapan yang dapat menyatakan maksud cinta yang sebenar.

Berdosakah bercinta ?

Cinta adalah kecenderungan hati kepada sesuatu, Oleh itu, ia adalah kerja hati, bukan kerja anggota badan yang zahir. Cinta seorang lelaki kepada seorang wanita atau cinta seorang wanita kepada lelaki adalah harus kerana ia adalah fitrah manusia.

Oh cinta,

Banyaknya versi, ada yang normal, bercinta kepada Tuhan, agama, sesama manusia(what i mean normal paham2 ea). Ada yang pelik skit, cinta pada dunia, wang, emas, coklat. Dan ada yang extreme tu sampai nak bunuh diri.. Sad2..

Tapi rasa sedih juga kalau cinta yang kita harapkan itu tak kesampaian. Ada pula cinta yang kita berikan tetapi tidak pula dikembalikan. Itu yang memang bercinta tak pe lagi. Ini ada yang cinta, tapi tak pernah memulakan langsung percintaannya itu kerana tak berani menanggung risiko cintanya ditolak sebelum dimulakan. Oh sedihnya kalau cinta tu ditolak.

Sesungguhnya berterus terang itu lebih baik daripada kecewa seumur hidup terlepas. Perlukah kita takut sampai kita kehilangan cinta yang dicari itu Apa salahnya kan. Mengaku saja la. Mungkin ada rezeki jodoh bersama? Barula brani.. Kerana kegagalan membawa kita kepada kejayaan yang lebih manis..

So, Setiap insan yang sedang bercinta patutnya bersyukur dan menghargai cinta itu. Tetapi, kalau setakat kita hargai saja tapi tak cinta pada sidia tak gune jugak.. Bagaimana pula cinta yang sudah pudar atau tiada setelah bertahun2 menabur bakti akibat terluka hati? Adakah perlu kita berpura2 utk bercinta? Conflictnya dunia ini.. Adakah perlu cinta itu dipaksa? Tapi bukan kah teruk kalau bertepuk sebelah tangan?

Perlukah kita terseksa dengan cinta sebegitu? Perlukah cinta yang mati itu disambung talian hayatnya? Perlukah cinta memberi satu lagi peluang? Adanya itu, baru sahaja putus cinta, lantas ketemu cinta baru. Mesti sahaja cinta itu kecundang disebabkan orang ketiga. (oppss..). ya mungkin juga. Tapi mana mungkin hati ini terobat sekelip mata.

Ok ok.. da tak nak da ngarut2 nih.. So this is my summary of cinta:

Yang ku tau, Cinta itu tidak bisa di ungkapkan, Cinta itu tidak bisa di rasa, Cinta itu tidak bisa dimiliki. Cinta itu berbentuk2 berubah2..... Cinta itu hanya milik dirinya sendiri....

argh.. bosannyer cite ngarut2.. nway, kalau korang sudi menerangkan what is CHINTA, do not hesitate to put in as a comment down there.. Hehe... mungkin korang ada versi2 masing2.. Sorry mate, sj nak berjiwang2..rasanya da 5 tahun tak berjiwang2 ni...

p/s: cerita ini tiada kaitan kepada sesiapapun walaupun anda terasa dan gambar2 diatas hanyalah sebagai satu hiasan yang tiada kene mengena dengan article tersebut..
p/s/s: Aku da tak nak post entry mcm ni lagi.. soo gurlish.. aduhai..

PRE-OPERATIVE MANAGEMENT

2009-06-05T20:11:00.009+08:00

I'm wondering to have an article about what a House Officer should do when they in the surgery posting. I hope this helpful for my 'old classmates' who are going to have and induksi this week. Congrates to them they are going to start their work! When you are a surgical house officer (or Formula One), part of your role preoperatively will be to clerk the patients and prepare them for the theatre or their investigations.

A clerking consists of the history of the presenting complaint, past medical history, drug history, family history and social history. You should then examine the patient fully, looking first at their general health and whether they are fit enough for the operation, and if not you should be thinking of ways to optimise their health, such as using preoperative nebulisers for an asthmatic. The clerking also allows other problems to be picked up.

If, when the patient arrives on the ward, you feel that the diagnosis made in the out-patient clinic has changed, you should inform a senior colleague before the operation is booked. For example, if a patient was admitted for an excisional biopsy of a lymph node that has completely disappeared when you examine them, you should inform your consultant, as the operation might need to be cancelled.

In the main, appropriate investigations should be performed before surgery and this is often a good question for a viva examination. For example, before a laparascopic cholecystectomy is performed the patient should have had an ultrasound to confirm the presence of gallstones, and a set of liver function tests. The house officer should discuss the order of patients on the operating list with the operating surgeon. Usually, children are placed first on the list, as this is nicer for the child and the parents; also they find it hard to go without food for long periods. If special equipment is needed in the theatre, such as the image intensifier for X-rays or laparascopic equipment, then these should be discussed with the theatre staff (and radiographers) the day before.

Specialist nurses who have expertise in certain areas such as breast disease, wound management and stomas should be involved preoperatively in all appropriate cases. For example, a patient who is likely to need a colostomy or ileostomy should be seen by the stoma nurse specialist several days before the operation. This allows for patient education (i.e. answering of any questions and worries), and also the site where the stoma will be cited is marked (note that the patient should be standing, so
as to position it in the most appropriate place).

Comorbidity

Many patients have problems other than the one that is being operated upon. These may be social and as such need a social work or occupational therapy referral. For example, if the patient has difficulty climbing stairs and there is no lift, then there may be a need to arrange for a stair lift or rehouse into ground floor accommodation.

The patients may have intercurrent medical problems such as diabetes, hypertension or chronic obstructive pulmonary disease (COPD). They may also be on drugs such as steroids or anticoagulants. When clerking the patient you should be looking out for these, and if you think they may affect the operation, then you should inform the anaesthetist or the consultant in charge of the patient.

As a house officer the tests you need to consider preoperatively include blood tests, such as a full blood count, a sickle screen if at risk (this includes anyone of Afro-Caribbean origin), and either a group and save or a cross-match. You should X-match any patient at risk of blood loss extensive enough to need replacing — for example, the anticipated blood loss from an anterior resection is about two units, but to be safe we usually X-match four units. The blood is kept in the refrigerator ready for use. If it is not used it goes back to the blood bank for storage.

A young healthy person, in general, requires no preoperative investigations, but if at all unsure then you should ask the anaesthetist what they would like performed (for example, some anaesthetists like to have a recent full blood count on all females of childbearing age). The National Institute for Clinical Excellence (NICE) have issued guidelines on preoperative
investigation available here. If the patient is hypertensive or on diuretics then a U & E (urea, creatinine and electrolytes) to assess renal function must be performed. An ECG is necessary on anyone who is hypertensive or has a history of heart disease, and a chest X-ray on anyone
with respiratory disease, including a personal or family history of TB.

In most hospitals the requirement is to order an ECG and CXR as a baseline on the elderly (aged over 60), but check the policy in your hospital. The management of medical problems in surgical patients is essentially the same as that you read about in medical textbooks. We will, however,
cover just a few topics.

DIABETES

Diabetics have an increased incidence of perioperative complications. The stress of surgery can lead to an increased production of catabolic hormones, such as glucagon and catecholamines, which antagonize the action of insulin, making control more difficult, especially as the patient will also be nil by mouth. These patients are at an increased risk of infection (wound, chest, IV access sites and urine), peripheral vascular disease, pressure sores and ischaemic heart disease. The aim is to maintain the patient’s blood sugar level between 5 and 9 mmol/l. Preoperatively you should dipstick the urine to check for protein, send off a laboratory blood
glucose, check the electrolytes and creatinine and order an ECG.
Management depends on the types of diabetes.

Insulin-dependent Diabetics
For anything other than minor surgery it is probably best to put these patients on an insulin sliding scale to establish good control. This means they are on a drip of dextrose or dextrose saline (as they are not eating), together with a continuous infusion of fast-acting insulin (‘Actrpid’). The rate of infusion of insulin will depend on their blood sugar level, which can be monitored by hourly BM stix (a finger prick testing stick specific for glucose). If the BM is low the infusion is decreased or stopped, and if the BM is high the insulin rate can be increased to bring the sugar level down. It is important that you add potassium to each bag of fluids you give, since the insulin causes cellular uptake of potassium and can lead to hypokalaemia. The sliding scales regimen differs in different hospitals and
you should try and get hold of a sliding scale protocol at your hospital.

This is one example:

Diabetics Controlled with Oral Hypoglycaemics

Long-acting oral hypoglycaemics such as metformin should be changed to a short-acting sulphonylurea (e.g. Gliclazide) a few days before the operation. Ask the diabetic team for advice. On the morning of the operation omit the dose of oral hypoglycaemic. This can be resumed once the patient starts eating postoperatively. The BMs should be measured, and if very high the blood sugar can be brought down by small doses of subcutaneous soluble insulin (e.g. 6 units of actrapid). If this fails to control the sugar level or in the case of major surgery, you cannot go wrong by simply converting the treatment to a sliding scale as above. Diabetics should really go first on the list, as the starting time is predictable and this allows better management of sugar levels.

Diabetics Controlled by Diet Alone

These patients rarely need any special measures. Remember that provided they have not been given any insulin or oral hypoglycaemics the patients cannot become hypoglycaemic (unless they have an insulinoma); if anything, their sugar level will be high. A BM stix will tell you where you stand if you are worried. If you find their control is poor, then you should refer the patients back to their diabetologist.

STEROIDS

Patients on steroids are liable to impaired healing and postoperative infections. Also, long-term corticosteroids can lead to adrenal insufficiency, where the adrenals are unable secrete the increased glucocorticoids necessary in response to the stresses of surgery. This can lead to an Addisonian crisis, where the patient becomes shocked. Patients who have been on long-term oral steroids should therefore be treated with perioperative steroids. This usually means intravenous hydrocortisone before and after the operation until the patient can resume their oral intake.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Surgery and anaesthesia predispose patients to basal lung collapse (atelectasis),
aspiration pneumonitis and chest infection. This is especially true of operations on the abdomen, since the patient may be in pain and therefore does not cough up the secretions. Any pre-existing respiratory disease, such as chronic obstructive pulmonary disease (COPD), increases the risk of chest complications, as do smoking, obesity and old age. Preoperatively, therefore, you should arrange for a chest X-ray and lung function tests in any patient with pre-existing chronic airways disease.
You should also do a baseline blood gas analysis if hypoxia or carbon dioxide retention is anticipated. You can assess the degree of reversibility of the airway disease by measuring peak flows before and after bronchodilators are given by nebuliser.

If there is a degree of reversibility, then prescription of nebulisers may help optimise lung function. Physiotherapy is an important modality in these patients and preoperative breathing exercises can help prevent a chest infection. Postoperatively physiotherapy should be initiated early to help remove airway secretions, especially in abdominal operations. Smokers should be encouraged to stop smoking at least 4 weeks prior to elective surgery.

DEEP VEIN THROMBOSIS

All surgical patients are at risk of deep vein thrombosis (DVT). In some hospitals prophylaxis with subcutaneous low molecular weight heparin injections and thromboembolic deterrent (TED) stockings is given to all surgical patients, whereas other hospitals only give this to patients at medium-to-high risk of DVT. Risk factors for DVT include previous thrombosis or pulmonary embolus, long periods of immobility, pelvic or hip operations, obesity, cancer and use of the oral contraceptive pill. Find out what the DVT prophylaxis protocol is in your hospital.
Intermittent limb compression is where an inflatable device is wrapped around the legs and periodically blown up, from the distal to the proximal end, encouraging venous return. Also available is low molecular weight (LMW) heparin, which is thought to work on the antiplatelet factor antithrombin III and therefore has little effect on the intrinsic clotting cascade.

In normal prophylactic doses LMW heparin does not require monitoring; it is longer acting and thus only needs to be given once daily. LMW heparin is as effective as unfractionated heparins. Newer drugs such as direct thrombin inhibitors are also now available.

In most cases, early mobilisation in combination with one or more of the above options is acceptable.

ANTIBIOTICS

Antibiotic cover is necessary for surgery if there is an increased risk of infection. This could be due to patient-related factors or those related to
the type of operation. Contaminated operations, such as those where the bowel contents can leak out, carry a high risk of infection, as do operations where a prosthetic implant is used (e.g. joint replacement), and antibiotics should always be given in these cases.

An example of a patient-related factor is mitral valve disease and the subsequent risk of developing endocarditis. We usually give prophylactic antibiotics intravenously at induction of anaesthesia, so that blood levels are high during the operation, followed by two subsequent doses postoperatively (usually after about 8 and 16 h).

If a tourniquet is being used, then the antibiotics must be given before the
tourniquet is inflated. You should have a rough idea of which organisms are likely to be responsible for the infection and which antibiotics should therefore be
used. A common question concerns methicillin-resistant Staphylococcus aureus (MRSA), which is an increasing problem in many hospitals. It is especially worrying when it infects patients with prosthetic implants such as hip replacements or vascular bypasses.

Operations Involving the Bowel
Organisms
Mainly Gram-negative bacilli, i.e. coliforms, but also faecal anaerobes (bacteroides) and S. aureus from the skin. In the gut there is also Enterococcus faecalis (also known as strep faecalis), but this causes infection less commonly. In bile, the majority of infections are with gut bacteria, such as Escherichia coli, and, rarely, pseudomonas, which is more difficult to treat.
Prophylaxis
We tend to use a cephalosporin to cover the Gram-negative organisms together with metronidazole to cover anaerobes. If you are concerned about strep faecalis you should add amoxycillin, as the cephalosporins do not cover this well. For operations on the biliary tree, such as a laparascopic cholecystectomy, you could either use the same regimen as above or just use a cephalosporin alone, as most infections are with Gram-negative bacilli (mainly E. coli). One dose at induction is sufficient. For improved biliary penetration such as before and after an ERCP or for ascending cholangitis, a broad-spectrum B-lactam such as pipericillin is often used. This also covers for pseudomonas.

Operations Involving Prosthetic Implants
Organisms
Skin organisms are usually responsible. S. aureus is the commonest pathogen, but also S. epidermidis tends to colonise the newer plastic prostheses. Rarely, coliforms are responsible.
Prophylaxis
Either a broad-spectrum cephalosporin or flucloxacillin. Orthopaedic operations involving metalwork require a dose of intravenous antibiotics (usually a cephalosporin) at induction and for about 24 h postoperatively. Similarly, valve replacements are usually given amoxycillin (or a cephalosporin) and gentamycin. If MRSA is a particular worry, then vancomycin may be used.The British National Formulary contains up-to-date advice on this topic. Remember that if ischaemic or necrotic tissue is involved, then spores of clostridium tetani may cause gas gangrene. Benzylpenicillin, to which the organism is highly susceptible, is the prophylaxis (and treatment) of choice against this (this includes penetrating wounds and compound fractures).

The mnemonic “ABCD LMNOPs” is helpful in remembering preoperative management:
A — Antibiotics/anaesthetist
B — Bloods (including X-match)/bowel preparation
C — Consent/CXR
D — Drug chart/DVT prophylaxis
E — ECG
F — Fluids (especially if NBM or if the patient is vomiting)
L — List (put in the theatre list)/lung function tests
M — Mark the area or limb (should be done by the operating surgeon)
N — Notes should be filed correctly
O — Operating theatre staff (e.g. book special equipment/radiology)
P — Physiotherapy
S — Specialist nurses (e.g. breast care or stoma care nurses)

Royal Pains: A new TV series!!

2009-06-05T15:44:00.009+08:00

I'm Bored coz my everytime favourite TV series - House - season 5 will only come out next year.. Pathetic of waiting, suddenly i found a new medical series!! Royal Pains!

Here is the premiere of USA medical drama “Royal Pains”, which is about A down and out surgeon who has a chance to redeem himself as a small town physician in the wealthy beach community of East Hampton, NY. 720p is from CTU!

Here's the synopsisEP 1.1 Pilot

When a Hospital trustee dies on Dr. Hank Lawson’s watch, he is shunned by the medical community. Months later, at a party in the Hamptons, he saves the life of a guest and stumbles upon a new career as an on call doctor for high society.

If you want to download this series, i've found links for you

http://rapidshare.com/files/240987071/royal.pains.s01e01.hdtv.xvid-fqm.part1.rar
http://rapidshare.com/files/240988059/royal.pains.s01e01.hdtv.xvid-fqm.part2.rar
http://rapidshare.com/files/240987406/royal.pains.s01e01.hdtv.xvid-fqm.part3.rar
http://rapidshare.com/files/240987899/royal.pains.s01e01.hdtv.xvid-fqm.part4.rar
http://rapidshare.com/files/240987743/royal.pains.s01e01.hdtv.xvid-fqm.part5.rar
http://rapidshare.com/files/240988082/royal.pains.s01e01.hdtv.xvid-fqm.part6.rar
http://rapidshare.com/files/240988312/royal.pains.s01e01.hdtv.xvid-fqm.part7.rar

waaaa.. Nak PSP - GO baru ni!!

2009-06-04T08:08:00.004+08:00

New PSP Go (N1000) Goes On Sale For $249 Beginning October 1st in US!
Sony Computer Entertainment Inc. (SCEI) has officially announced the launch of its new evolution of PSP handheld entertainment system - PSP Go (PSP-N1000), which the company said to be 50% smaller (128 x 16.5 x 69 mm) and 40% lighter (5.6 ounces) than the original PSP, aiming to enhance the unmatched portable gaming and entertainment experience.

Featured Highlights Of PSP Go:

* Sliding 3.8-inch wide LCD display with 480 x 272 pixels resolution (43% lighter than PSP 3000)
* Integrated 16GB flash memory, expandable via Memory Stick Micro (M2) slot (no UMD drive)
* Wi-Fi and Bluetooth connectivity
* New Media Go software application allows users to access and download entertainment content on PlayStation Store via their PCs
* New SensMe channels music application, the mood based music recommendation system that can categorize music content into channels including “Relax,” “Dance” and “Upbeat”

The new amazing PSP Go that arrives in Piano Black and Pearl White colors is scheduled to be available for US$249 and euro 249 beginning October 1, 2009.

Another PSP highlight!

Top 100 Surgical Secrets

2009-06-03T15:30:00.010+08:00

These secrets are 100 of the top board alerts. They summarize the concepts, principles, and most salient details of surgical practice.

1. Clinical determinants of brain death are the loss of the papillary, corneal, oculovestibular, oculocephalic, oropharyngeal, and respiratory reflexes for > 6 hours. The patient should also undergo an apnea test, in which the pCO2 is allowed to rise to at least 60 mmHg without coexistent hypoxia. The patient should be observed for the absence of spontaneous breathing.

2. The estimated risks of HBV, HCV, and HIV transmission by blood transfusion in the United States are 1 in 205,000 for HBV, 1 in 1,935,000 for HCV, and 1 in 2,135,000 for HIV.

3. The most common location of an undescended testis is the inguinal canal.

4. The most common solid renal mass in infancy is a congenital mesoblastic nephroma and in childhood a Wilms' tumor.

5. Ogilvie's syndrome is acute massive dilatation of the cecum and the ascending and transverse colon without organic obstruction.

6. The best screening method for prostate cancer is digital rectal exam combined with serum prostate-specific antigen.

7. The most common histologic type of bladder cancer is transitional cell carcinoma.

8. Carcinoma in situ of the bladder is treated with immunotherapy with intravesical bacillus Calmette-Guérin (BCG).LOLZ.. BCG used for Ca?

9. Localized renal cell carcinoma is treated with surgery (radical nephrectomy).

10.The most common cause of male infertility is varicocele.

11. The most common nonbacterial cause of pneumonia in transplant patients is cytomegalovirus.

12. Chimerism is leukocyte sharing between the graft and the recipient so that the graft becomes a genetic composite of both the donor and the recipient.

13. OKT3 is a mouse monoclonal antibody that binds to and blocks the T-cell CD3 receptor.

14. The most common disease requiring liver transplant is hepatitis C.

15. Cystic hygroma is a congenital malformation with a predilection for the neck. It is a benign lesion that usually presents as a soft mass in the lateral neck.

16. In neuroblastomas, age at presentation is the major prognostic factor. Children younger than 1 year have an overall survival rate > 70%, whereas the survival rate for children older than 1 year is < 35%.
17. The most feared complication of diaphragmatic hernia is persistent fetal circulation.
18. The three most common variants of tracheoesophageal fistula are (1) proximal esophageal atresia with distal tracheoesophageal fistula, (2) isolated esophageal atresia, and (3) tracheo-esophageal fistula with esophageal atresia.
19. Atresia can occur anywhere in the GI tract: duodenal (50%), jejunoileal (45%), or colonic (5%). Duodenal atresia arises from failure of recanalization during the 8th-10th week of gestation; jejunoileal and colonic atresia are caused by an in utero mesenteric vascular accident.
20. The types of aortic dissection are ascending (type A) dissection, which involves only the ascending or both the ascending and descending aorta, and descending dissection (type B), which involves only the descending aorta.

21. A solitary pulmonary nodule is < 3 cm and is discrete on chest radiograph. It is usually surrounded by lung parenchyma.
22. Mediastinal staging is indicated in patients with apparent or documented lung cancer who have (1) known lung cancer with mediastinal nodes > 1 cm accessible by cervical mediastinal exploration, as assessed by CT scan; (2) adenocarcinoma of the lung and multiple mediastinal lymph nodes < 1 cm; (3) central or large (> 5 cm) lung cancers with mediastinal lymph nodes < 1 cm; and (4) lung cancer with risk of thoracotomy and lung resection.
23. The most common causes of aortic stenosis are now congenital anomalies and calcific (degenerative) disease.
24. In mitral regurgitation, the left ventricle ejects blood via two routes: (1) antegrade, through the aortic valve, or (2) retrograde, through the mitral valve. The amount of each stroke volume ejected retrograde into the left atrium is the regurgitant fraction. To compensate for the regurgitant fraction, the left ventricle must increase its total stroke volume. This ultimately produces volume overload of the left ventricle and leads to ventricular dysfunction.
25. The indications for CABG are (1) left main coronary artery stenosis; (2) three-vessel coronary artery disease (70% stenosis) with depressed left ventricular (LV) function or two-vessel coronary artery disease (CAD) with proximal left anterior descending (LAD) involvement; and (3) angina despite aggressive medical therapy.
26. Hibernating myocardium is improved by CABG. Myocardial hibernation refers to the reversible myocardial contractile function associated with a decrease in coronary flow in the setting of preserved myocardial viability. Some patients with global systolic dysfunction exhibit dramatic improvement in myocardial contractility after CABG.
27. The surgical treatment of ulcerative colitis is total colectomy with ileoanal pouch anastomosis.
28. Dieulafoy's ulcer is a gastric vascular malformation with an exposed submucosal artery, usually within 2-5 cm of the gastroesophageal junction. It presents with painless hematemesis, often massive.
29. The role of blind subtotal colectomy in the management of massive lower gastrointestinal bleeding is limited to a small group of patients in whom a specific bleeding source cannot be identified. The procedure is associated with a 16% mortality rate.
30. Colorectal polyps < 2 cm have a 2% risk of containing cancer, 2 cm polyps have a 10% risk, and polyps > 2 cm have a cancer risk of 40%. Sixty percent of villous polyps are > 2 cm, and 77% of tubular polyps are < 1 cm at the time of discovery.
31. Patients with colorectal cancer with lymph node involvement (Dukes' C) should receive chemotherapy postoperatively to treat micrometastases.
32. Goodsall's rule states the location of the internal opening of an anorectal fistula is based on the position of the external opening. An external opening posterior to a line drawn transversely across the perineum originates from an internal opening in the posterior midline. An external opening, anterior to this line, originates from the nearest anal crypt in a radial direction.
Incarcerated inguinal hernia: structures in the hernia sac still have a good blood supply but are stuck in the sac because of adhesions or a narrow neck of the hernia sac. Strangulated inguinal hernia: hernia structures have a compromised blood supply because of anatomic constriction at the neck of the hernia.

33. Incarcerated inguinal hernia: structures in the hernia sac still have a good blood supply but are stuck in the sac because of adhesions or a narrow neck of the hernia sac. Strangulated inguinal hernia: hernia structures have a compromised blood supply because of anatomic constriction at the neck of the hernia.
34. Chvostek's sign is spasm of the facial muscles caused by tapping the facial nerve trunk. Trousseau's sign is carpal spasm elicited by occlusion of the brachial artery for 3 minutes with a blood pressure cuff.
35. The two surgical options for Graves' disease are subtotal thyroidectomy or near-total thyroidectomy.
36. The only biochemical test that is routinely needed to identify patients with unsuspected hyperthyroidism is serum thyroid-stimulating hormone concentration.
37. The surgically correctable causes of hypertension are renovascular hypertension, pheochromocytoma, Cushing's syndrome, primary hyperaldosteronism, coarctation of the aorta, and unilateral renal parenchymal disease.
38. The "triple negative test" or "diagnostic triad" for diagnosing a palpable breast mass includes physical examination, breast imaging, and biopsy.
39. Chest wall radiation is indicated after mastectomy in patients with greater than 5 cm primary cancers, positive mastectomy margins, or more than four positive lymph nodes, all of which are associated with heightened locoregional recurrence rates.
40. Sentinel lymph nodes are the first stop for tumor cells metastasizing through lymphatics from the primary tumor.
41. The most common site of origin of subungual melanomas is the great toe. Amputation at or proximal to the metatarsal phalangeal joint and regional sentinel lymph node biopsy are advised by most authors.
42. Ramus marginalis mandibularis, the lowest branch of the nerve that innervates the depressor muscles of the lower lip, is the most commonly injured facial nerve branch during parotidectomy.
43. Waldeyer's ring is the mucosa of the posterior oropharynx covering a bed of lymphatic tissue that aggregates to form the palatine, lingual, pharyngeal, and tubal tonsils. These structures form a ring around the pharyngeal wall. This may be the site of primary or metastatic tumor.
44. A patient in whom the head and neck examination is completely normal but FNA of a cervical node reveals squamous cancer should have examination of the mouth, pharynx, larynx, esophagus, and tracheobronchial tree under anesthesia (triple endoscopy). If nothing is seen, blind biopsy of the nasopharynx, tonsils, base of tongue, and pyriform sinuses should be done at the same sitting.
45. The microorganisms implicated in atherosclerosis include Chlamydia pneumoniae, Helicobacter pylori, streptococci, and Bacillus typhosus.
46. The cumulative 10-year amputation rate for claudication is 10%.
47. The absolute reduction in risk of stroke is 6% over a 5-year period in asymptomatic patients with > 60% stenosis who undergo carotid endarterectomy plus aspirin versus patients treated with aspirin alone (5.1% versus 11%).
48. Abdominal aortic aneurysm's average expansion rate is 0.4 cm/year.
49. Heparin binds to antithrombin III, rendering it more active.
50. The patient with suspected intermittent claudication should initially be evaluated by obtaining ankle brachial index or segmental limb pressures at rest.
51. Shock is suboptimal consumption of O2 and excretion of CO2 at the cellular level.
52. Nitric oxide is synthesized in vascular endothelial cells by constitutive nitric oxide synthase and inducible NOS, using arginine as the substrate.
53. Saliva has the hightest potassium concentration (20 mEq), followed by gastric secretions (10 mEq), then pancreatic and duodenal secretions (5 mEq).
54. Basal caloric expenditure = 25 kcal/kg/day with a requirement of approximately 1 g protein/kg/day.
55. 6.25 g of protein contains 1 g of nitrogen.
56. Dextrose has 3.4 kcal/g, protein 4 kcal/g, fat 9 kcal/g (20% lipid solution delivers 2 kcal/mL).
57. Maximal glucose infusion rates in parenteral formulas should not exceed 5 mg/kg/min.
58. Refeeding syndrome occurs in moderately to severely malnourished patients (e.g., chronic alcoholism or anorexia nervosa) who, upon presentation with a large nutrient load, develop clinically significant decreases in serum phosphorus, potassium, calcium, and magnesium levels. Hyperglycemia is common secondary to blunted insulin secretion. ATP production is mitigated, and the classic presentation is respiratory failure.
59. Glutamine is the most common amino acid found in muscle and plasma. Levels decrease after surgery and physiologic stress. Glutamine serves as a substrate for rapidly replicating cells (interestingly, it is also the number one metabolic substrate for neoplastic cells), maintains the integrity and function of the intestinal barrier, and protects against free radical damage by maintaing GSH levels. Glutamine is unstable in IV form unless linked as a dipeptide.
60. Fever is caused by activated macrophages that release interleukin-1, tumor necrosis factor, and interferon in response to bacteria and endotoxin. The result is a resetting of the hypothalamic thermoregulatory center.
61. Cardiac output = heart rate x stroke volume; normal CO is 5-6 L/min.
62. SVR = [(MAP - CVP)/CO] x 80; normal SVR is 800-1200 dyne.sec/cm-5.
63. Hypovolemic shock: low CVP and PCWP, low CO and SVO2, high SVR.
64. Cardiogenic shock: high CVP and PCWP, low CO and SVO2, variable SVR.
65. Septic shock: low or normal CVP and PCWP, high CO initially, high SVO2, low SVR.
66. Kehr's sign is concurrent LUQ and left shoulder pain, indicating diaphragmatic irritation from a ruptured spleen or subdiaphragmatic abscess. Anatomically, the diaphragm and the back of the left shoulder enjoy parallel innervation.
67. Rebound tenderness implies peritoneal inflammation and irritation not simply abdominal tenderness.
68. The 5 Ws of post-operative fever are wound (infection), water (UTI), wind (atelectasis, pneumonia), walking (thrombophlebitis), and wonder drugs (drug fevers).
69. Cricothyroidotomy should not be performed in patients <> 80 mmHg; femoral (groin) pulse estimates SBP > 70 mmHg; and carotid (neck) pulse estimates SBP > 60 mmHg.
71. A general rule for crystalloid infusion to replace blood loss is a 3:1 ratio of isotonic crystalloid to blood.
72. Raccoon eyes (periorbital ecchymosis) and Battle's sign (mastoid ecchymosis) are clinical indicators of basilar skull fracture.
73. CPP = MAP - ICP. Some debate exists on the minimum allowable CPP, but consensus indicates that a cerebral perfusion pressure of 50-70 mmHg is necessary.
74. Violation of the platysma defines a penetrating neck wound.
75. Tension pneumothorax is air accumulation in the pleural space eliciting increased intrathoracic pressure and resulting in a kinking of the SVC and IVC that compromises venous return to heart.
76. The most common site of thoracic aortic injury in blunt trauma is just distal to the take-off of the left subclavian artery.
77. The most common manifestation of blunt myocardial injury is arrhythmia.
78. Indications for thoracotomy in a stable patient with hemothorax include an immediate tube thoracostomy output of > 1500 mL and ongoing bleeding of 250 mL/h for 4 consective hours.
79. Beck's triad is hypotension, distended neck veins, and muffled heart sounds.
80. The hepatic artery supplies approximately 30% of blood flow to the liver while the portal vein supplies the remaining 70%. The oxygen delivery, however, is similar for both at 50%.
81. The Pringle maneuver is a manual occlusion of the hepatoduodenal ligament to interrupt blood flow to the liver.
82. Splenectomy significantly decreases IgM levels.
83. 90% of trauma fatalities due to pelvic fractures are due to venous bleeding and bone oozing; only 10% of fatal pelvic bleeding from blunt trauma is arterial (most common site is superior gluteal artery).
84. Intraperitoneal bladder rupture from blunt trauma: operative management; extraperitoneal rupture: observant management.
85. Pseudoaneurysm is a disruption of the arterial wall leading to a pulsatile hematoma contained by fibrous connective tissue (but not all three arterial wall layers, which defines a true aneurysm).
86. The earliest sign of lower extremity compartment syndrome is neurologic in the distribution of the peroneal nerve with numbness in the first dorsal webspace and weak dorsiflexion.
87. Posterior knee dislocations are associated with popliteal artery injuries and are an indication for angiography.
88. Management of suspected navicular fracture despite negative radiography is short-arm cast and repeat x-ray in 2 weeks; at high risk for avascular necrosis.
89. Parkland formula: lactated Ringer's at 4 mL/kg x %TBSA (second- and third-degree only) of burn. Infuse 50% of volume in first 8 hours and the remaining 50% over the subsequent 16 hours.
90. The metabolic rate peaks at 2.5 times the basal metabolic rate in severe burns > 50% TBSA.
91. Gallstones and alcohol abuse are the two main causes of acute pancreatitis.
92. Alcohol abuse accounts for 75% of cases of chronic pancreatitis.
93. Isolated gastric varices and hypersplenism indicate splenic vein thrombosis and are an indication for splenectomy.
94. The treatment for gallstone pancreatitis is cholecystectomy and intraoperative cholangiogram during the same hospital stay once the pancreatitis has subsided.
95. Proton pump inhibitors irreversibly inhibit the parietal cell hydrogen ion pump.
96. Definitive treatment of alkaline reflux gastritis after a Billroth II includes a Roux-en-Y gastro-jejunostomy from a 40-cm efferent jejunal limb.
97. Cushing's ulcer is a stress ulcer found in critically ill patients with central nervous system injury. It is typically single and deep, with a tendency to perforate.
98. Curling's ulcer is a stress ulcer found in critically ill patients with burn injuries.
99. Marginal ulcer is an ulcer found near the margin of gastroenteric anastomosis, usually on the small bowel side.
100. The most common cause of small bowel obstructions is adhesive disease; the second most common cause is hernias.

TUMOURS OF THE PANCREAS

2009-06-02T21:59:00.005+08:00

Let's talk about Pancreatic tumour. There are many types of pancreatic tumour. Although ductal carcinoma of the pancreas is one of the most lethal of all gastrointestinal tumours, 10–15% of tumours of the pancreas (including those of the periampullary region) are not of the same histological type as ductal carcinoma and have a much better prognosis. This group of tumours includes ampullary carcinoma, islet cell tumours of the pancreas and cystic tumours of the pancreas. A tumour of the pancreas should, therefore, not be assumed to carry a poor prognosis. Ok?

Ductal adenocarcinoma of the pancreas is highly malignant and has usually metastasised by the time of diagnosis. Smoking is the only recognised aetiological factor and the disease is uncommon under the age of 40. The disease occurs in the head of the pancreas in 80% of cases. It presents with obstructive jaundice in 70% of cases but may also present with severe upper abdominal pain (which may radiate into the back), weight loss, anorexia, malaise, or rarely, thrombophlebitis migrans.

On examination, there may be cervical lymphadenopathy, an abdominal mass, hepatomegaly or ascites. The gallbladder may be palpable. Courvoisier’s law states that if, in the presence of jaundice, the gallbladder is palpable, then the cause is unlikely to be gallstones. Investigations include basic blood tests and specific diagnosis by ultrasound, CT or MRI. The ERCP may be helpful too, and may also allow therapeutic manoeuvres such as stent insertion (see section on obstructive jaundice).

Most tumours are treated palliatively by insertion of a biliary stent or bypass surgery. Resectional surgery is suitable for 15–20% of patients with a ductal carcinoma but 50–75% of patients with ampullary carcinoma, islet cell tumours or cystic tumours of the pancreas. Five-year survival following curative resection in ductal carcinoma is 10–15% although resection is also associated with good relief of symptoms. For those with ampullary tumours, islet cell tumours or cystic tumours, 5 year survival of 40% can be anticipated.

For tumours of the head of the pancreas or peri-ampullary region, pancreatico-duodenectomy (Whipple’s operation) is the operation of choice. The pylorus-preserving operation is the operation of choice. The mortality rate of pancreatico-duodenectomy is less than 5%.

Whipple’s procedure (partial pancreatoduodenectomy) for carcinoma of the
head of pancreas (shaded).

1st day of our Orthopaedic posting!

2009-06-01T20:11:00.010+08:00

Good luck to my classmate. Jom pi wards dan clinics!

Amik ko..

2009-05-31T19:19:00.002+08:00

A 61-year-old woman presents to the emergency department (ED) after being referred from her primary care provider's (PCP) office for evaluation of tachycardia. She had been seen by her PCP for routine placement of a purified protein derivative (PPD) tuberculin skin test and was incidentally noted to have a pulse of 160 bpm. The patient currently denies any specific complaints other than occasional palpitations. On review of her systems, however, she notes having night sweats; a 110-lb (50-kg) weight loss over the preceding 12 months; and 2-3 months of anxiety, diarrhea, and occasional diplopia. She denies having any fever, chills, chest pain, dyspnea, or swelling in her extremities. She has a past medical history of an unspecified thyroid problem. She does not take any daily medications and has no medication allergies. She has a 50-pack-year smoking history, with occasional alcohol consumption. She had been homeless for a period of time but is currently living in an apartment.

On examination, the patient is awake and fully oriented. She is diaphoretic but in no apparent distress. Her temperature is 97.0°F (36.1°C); her pulse is 160 bpm; her respiratory rate is 24 breaths/min, with an oxygen saturation of 98%; and her blood pressure is 190/117 mm Hg. She has bilateral exophthalmos with exotropia of the right eye. Her visual acuity and extraocular movements are intact. The neck examination reveals a diffuse, nontender goiter, without nodules or thyroid bruits. The heart is tachycardic, intermittently irregular, and without murmurs. The lungs are clear to auscultation bilaterally. The abdomen is nondistended, soft, and nontender, with no palpable masses. There is no edema of the extremities. The neurologic examination reveals normal mentation, intact cranial nerves, intact motor strength and sensation, and normal reflexes. No tremor is noted.The initial laboratory studies reveal complete blood count, electrolytes, renal function, and cardiac marker findings that are all within normal limits. A plain chest radiograph is interpreted as normal.An electrocardiogram (ECG) is obtained.

I'll discuss more about this topic on the next issue..coming with more answers!!!..think it man..

SURGERY: Biliary Tract

2009-05-30T20:27:00.018+08:00

Topic today will be about Biliary tract

GALLSTONES

Gallstones are very common topic and are therefore frequently asked in the exams. Majority of them are asymptomatic and which require no treatment. However, they cause a wide range of clinical problems, depending on their position. They are either made up of cholesterol or pigment (bilirubin breakdown products) or a mixture of the two. Most (75%) gallstones are predominantly cholesterol. Pure pigment stones are rare (<10%) Ninety per cent of gallstones are radiolucent, i.e. they do not show on a plain X-ray (unlike renal calculi, of which 90% are radio-opaque).

Predisposing factors to gallstone formaton include:
1. female
2. sex (three times more common)
3. obesity,
4. age (10% of <50-year-olds have gallstones, and 30% of <70-year-olds),
5. Haemolytic anemia
6. Hyperlipidaemias
7. Crohn’s disease.

Some people appear to have a tendency to form gallstones and are said to have ‘lithogenic bile’. People often refer to the typical gallstone patient as 4F which is fat, female, fertile and forty. Ok? So remember that 4F if u cant remember the risk factors

Complications of gallstones can be divided into 3:
1. In the gallbladder

Chronic cholecystitis
Biliary colic
Acute cholecystitis
Empyema
Biliary peritonitis
Abscess
Mucocele
Carcinoma of gallbladder

2. In the common bile duct

Obstructive jaundice
Cholangitis
Pancreatitis

3. In the gut

Gallstone ileus

BILIARY COLIC

Biliary colic is the pain that associated with irritation of the viscera secondary to cholecystitis and gallstones or in a specific terms caused by gallbladder muscle spasms against a stone stuck in the neck of the gallbladder (Hartmann’s pouch) or the cystic duct. It may account for some of the symptoms for chronic cholecystitis. Unlike intestinal colic, the pain was continuous and not in waves. It is usually felt in the epigastrium or right upper quadrant and may radiate around both costal margins and into the back. The pain can be extremely severe and patients may be sweaty, pale and tachycardic because of it. They may also feel nauseated or vomit. They will usually be unable to get comfortable and will prefer to writhe around rather than stay still. Attacks usually last less than six hours and examination is usually otherwise normal. Differential diagnoses include other causes of severe upper abdominal pain, such as perforated peptic ulcer, pancreatitis, ruptured aneurysm, etc. Management involves giving analgesia, investigation to confirm gallstones (ultrasound) and subsequent cholecystectomy in most cases.

ACUTE CHOLECYSTITIS

History

At early stage acute cholecystitis may appear to be biliary colic, and indeed many attacks of acute cholecystitis probably start with biliary colic! The exact mechanisms of acute cholescystitis are poorly understood but they said that it are caused by chemical inflammation within an obstructed gallbladder. Bacterial infection probably is a secondary event in about one-third of cases and these may be the ones most likely to develop complications.

Patients will typically have symptoms of severe right upper quadrant or epigastric pain. Like biliary colic, this may radiate around the costal margins or into the back. However unlike biliary colic, patients will prefer to lie still and take shallow breaths (this is now a form of local peritonitis, not colic). They will usually have a temperature and tachycardia, and may also have nausea and vomiting.

Physical examination

Murphy’s sign may be positive and is often asked about in short case. It is elicited by pressing in the right upper quadrant under the costal margin. The patient is then asked to breathe in, and winces or gasps with pain as the gallbladder moves down and hits the examiner’s hand. The test should also be performed in the left upper quadrant to exclude nonspecific reactions due to other pathology.

A mass may be present in the right upper quadrant, but if so this is not usually the gallbladder itself but rather a ‘phlegmon’ (i.e. inflamed andadherent omentum and bowel around the gallbladder).

Investigation

The most important confirmatory test is an ultrasound scan. US confirm gallstones, showing thickening and oedema of the gallbladder wall and localise the tender spot to the gallbladder itself. It can also exclude dilatation of the common bile duct and other pathology, such as liver masses.

Image through the long axis of the GB (GB) demonstrates the gallbladder neck (red arrow). GB wall thickness is measured between the gallbladder lumen and the hepatic parenchyma (red arrowheads) with normal thickness <3cm

Only very occasionally is a HIDA scan used to help confirm or exclude cholecystitis. The principle of this test is that HIDA (a radioisotope) is taken up by the liver and excreted into the bile. If the cystic duct is patent, it will fill the gallbladder effectively, excluding cholecystitis.

Management

The treatment of acute cholecystitis is initial resuscitation with intravenous
fluids and antibiotics. The patient will normally be kept nil by mouth or on sips of clear fluids, and initial investigations will be arranged, including basic blood tests such as an FBC (usually the white cell count is raised), U & Es, LFTs and amylase (as acute pancreatitis may be a differential diagnosis).

With conservative treatment approximately 80–90% of cases of acute cholecystitis will settle over the next 24–48 h (i.e. the pain settles, the temperature falls and the patient’s abdomen becomes nontender). In about 10% of cases there will not be a prompt resolution of symptoms and signs, and in these cases surgery is usually advised.

Particularly worrying signs are increasing temperature, tachycardia and the onset of increasing tenderness or the signs of peritonitis. These may indicate infarction of the gallbladder (gangrenous cholecystitis) or perforation, which may produce either a local collection or generalised peritonitis. A gallbladder full of pus (empyema of the gallbladder) usually leads to an unwell patient with the signs of sepsis (fever, tachycardia, hypotension, etc.) as well as pain, and tenderness in the right upper quadrant.

More controversial is the question of what to do with patients who do not absolutely require early surgery. Although conventional management is to allow the acute episode to settle down and to readmit the patient for elective cholecystectomy 6–8 weeks later, many surgeons now prefer cholecystectomy in the acute phase. This allows patients to recover quicker and to be spared further episodes of pain. Laparoscopic cholecystectomy can now be carried out in the acute phase by experienced surgeons.

CHRONIC CHOLECYSTITIS

Chronic cholecystitis is a term used to describe symptoms of upper abdominal pain, indigestion, bloating, burping, nausea and occasional vomiting. Sometimes this symptom complex is called flatulent dyspepsia. The patient may describe the symptoms as being precipitated by fatty food (fats stimulate the release of cholecystokinin, which causes gallbladder contractions). There is usually nothing to find on physical examination.

The main differential diagnoses include
1. peptic ulceration
2. hiatus hernia
3. irritable bowel syndrome.

Because gallstones are so common, it's important not to automatically discribe such symptoms to them simply because that gallstones are present on an US scan. A missed peptic ulcer or irritable bowel syndrome will obviously not be helped by unnecessary cholecystectomy! And the patient will continue to get those symptoms. If the symptoms are thought to be arising from the gallbladder and are significant, then the treatment is cholecystectomy, usually laparoscopic.

Attempting to dissolve gallstones using 'bile salt therapy' might be possible for patients with small, noncalcified stones. It also reserved for those who refuse or unfit for surgery. However bear in mind that this treatment is not very successful.

CHOLANGITIS

Cholangitis is a condition where there is infection within the biliary tract and it is rare unless there is associated obstruction. This is a demonstration of the surgical principle that obstructed tubes tend to get infected, i.e. appendicitis, pyelonephritis, etc. Cholangitis is clinically manifested by Charcot’s triad of pain, jaundice and rigors (rigors means involuntary shaking in association with pyrexia). It requires prompt diagnosis and treatment, otherwise it can have a high mortality. Treatment consists of resuscitaton with fluids and the administration of intravenous antibiotics. If resolution is not rapid, then attempts to produce biliary drainage, endoscopically, radiologically or surgically, are required.

That's all for today! Happy revising!

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