Shyam styleS

COMPUTER & INTERNET (TRICKS & TIPS)

2010-08-17T09:26:00.000-07:00

AUTO PLAY OPTION

1. Go to Start->Run->gpedit.msc
2. Computer Config -> Administrative Template -> System
3. Double click Turn off Autoplay
4. Enable it.

WORLD’S #1 QUICK REFERENCE GUIDE BarCharts, Inc.®

BASIC SHORTCUT KEYS
WORD® SHORTCUT KEYS
EXCEL® SHORTCUT KEYS
F2 Edit the selected cell
Alt + F File menu options in current program
Ctrl + A Select all contents of the page
F5 Go to a specific cell
Alt + E Edit options in current program
Ctrl + B Bold highlighted selection
F7 Spell check selected text and/or document
F1 Universal help (for all programs)
Ctrl + C Copy selected text
F11 Create chart
Ctrl + A Select all text
Ctrl + X Cut selected text
Ctrl + Shift + ; Enter the current time
Ctrl + X Cut selected item
Ctrl + N Open new/blank document
Ctrl + ; Enter the current date
Shift + Del Cut selected item
Ctrl + O Open options
Alt + Shift + F1 Insert new worksheet
Ctrl + C Copy selected item
Ctrl + P Open the print window
Shift + F3 Open the Excel® formula window
Ctrl + Ins Copy selected item
Shift + F5 Bring up search box
Ctrl + F Open find box
Ctrl + V Paste
Ctrl + A Select all contents of worksheet
Ctrl + I Italicize highlighted selection
Shift + Ins Paste
Ctrl + B Bold highlighted selection
Ctrl + K Insert link
Home Go to beginning of current line
Ctrl + I Italicize highlighted selection
Ctrl + U Underline highlighted selection
Ctrl + Home Go to beginning of document
Ctrl + C Copy selected text
Ctrl + V Paste
End Go to end of current line
Ctrl + V Paste
Ctrl + Y Redo the last action performed
Ctrl + End Go to end of document
Ctrl + D Fill
Shift + Home Highlight from current position to beginning of line
Ctrl + Z Undo last action
Ctrl + K Insert link
Shift + End Highlight from current position to end of line
Ctrl + G Find and replace options
Ctrl + F Open find and replace options
Ctrl + Move one word to the left at a time
Ctrl + H Find and replace options
Ctrl + G Open go-to options
Ctrl + Move one word to the right at a time
Ctrl + H Open find and replace options
Ctrl + J Justify paragraph alignment
Ctrl + U Underline highlighted selection
Ctrl + L Align selected text or line to the left
Ctrl + Y Underline selected text
Ctrl + Q Align selected paragraph to the left
MICROSOFT® WINDOWS® SHORTCUT KEYS
Ctrl + 5 Strikethrough highlighted selection
Alt + Tab Switch between open applications
Ctrl + E Align selected text or line to the center
Ctrl + O Open options
Alt +
Shift + Tab
Switch backwards between open
applications
Ctrl + R Align selected text or line to the right
Ctrl + N Open new document
Ctrl + M Indent the paragraph
Ctrl + P Open print dialog box
Alt + Print
Screen Create screen shot for current program
Ctrl + T Hanging indent
Ctrl + S Save
Ctrl + Z Undo last action
Ctrl + D Font options
Ctrl + Alt + Del Reboot/Windows® task manager
Ctrl + F9 Minimize current window
Ctrl + Shift + F Change the font
Ctrl + Esc Bring up start menu
Ctrl + F10 Maximize currently selected window
Ctrl + Shift + > Increase selected font +1
Alt + Esc Switch between applications on taskbar
Ctrl + F6 Switch between open workbooks/windows
Ctrl + ] Increase selected font +1
F2 Rename selected icon
Ctrl + Page up & Page Down Move between Excel® worksheets in the same document
Ctrl + Shift + < Decrease selected font -1 F3 Start find from desktopCtrl + [ Decrease selected font -1 F4 Open the drive selection when browsingCtrl + Tab Move between two or more open Excel® filesCtrl + Shift + * View or hide non printing charactersAlt + = Create formula to sum all of above cellsF5 Refresh contentsCtrl + Move one word to the leftCtrl + ‘ Insert value of above cell into current cellAlt + F4 Close current open programCtrl + Shift + ! Format number in comma formatCtrl + F4 Close window in programCtrl + Move one word to the rightCtrl + Shift + $ Format number in currency formatCtrl + Plus Key Automatically adjust widths of all columns in Windows ExplorerCtrl + Move to beginning of the line or paragraphCtrl + Shift + # Format number in date formatCtrl + Move to the end of the paragraphCtrl + Shift + % Format number in percentage formatAlt + Enter Open properties window of selected iconCtrl + Del Delete word to right of cursorCtrl + Shift + ^ Format number in scientific format or programCtrl + Backspace Delete word to left of cursorCtrl + Shift + @ Format number in time formatShift + F10 Simulate right-click on selected itemCtrl + End Move cursor to end of documentCtrl + Move to next section of textShift + Del Delete programs/files permanentlyCtrl + Home Move cursor to beginning of documentCtrl + Space Select entire column Holding Shift During Bootup Boot safe mode or bypass system filesShift + Space Select entire rowCtrl + Space Reset highlighted text to default fontCtrl + W Close documentCtrl + 1 Single-space lines Holding Shift During Bootup When putting in an audio CD, will prevent CD Player from playingCtrl + 2 Double-space linesCtrl + 5 1.5-line spacing OUTLOOK® SHORTCUT KEYSAlt + S Send the emailCtrl + Alt + 1 Change text to heading 1WINKEY SHORTCUTSCtrl + C Copy selected textCtrl + Alt + 2 Change text to heading 2WINKEY + D Bring desktop to the top of other windowsCtrl + X Cut selected textCtrl + Alt + 3 Change text to heading 3WINKEY + M Minimize all windowsCtrl + P Open print dialog boxF1 Open helpWINKEY + SHIFT + M Undo the minimize done by WINKEY + M and WINKEY + DCtrl + K Complete name/email typed in address barShift + F3 Change case of selected textCtrl + B Bold highlighted selectionWINKEY + E Open Microsoft ExplorerShift + Insert PasteCtrl + I Italicize highlighted selectionWINKEY + Tab Cycle through open programs on taskbarCtrl + U Underline highlighted selectionF4 Repeat last action performed (Word 2000+)WINKEY + F Display the Windows® Search/Find featureCtrl + R Reply to an emailF7 Spell check selected text and/or documentWINKEY +CTRL + F Display the search for computers windowCtrl + F Forward an emailShift + F7 Activate the thesaurusCtrl + N Create a new email F12 Save asWINKEY + F1 Display the Microsoft® Windows® helpCtrl + Shift + A Create a new appointment to your calendarCtrl + S SaveWINKEY + R Open the run windowCtrl + Shift + O Open the outboxShift + F12 SaveWINKEY + Pause /Break Open the system properties windowCtrl + Shift + I Open the inboxAlt + Shift + D Insert the current dateCtrl + Shift + K Add a new taskAlt + Shift + T Insert the current timeWINKEY + U Open utility managerCtrl + Shift + C Create a new contactCtrl + Shift+ J Create a new journal entryCtrl + W Close documentWINKEY + L Lock the computer (Windows XP® & later)INCREASE BROADBAND:

this ones simple:
this is for broad band connections. I didn’t try it on dial up but might work for dial up.
1.make sure your logged on as actually "Administrator". do not log on with any account that just has administrator privileges.
2. start - run - type gpedit.msc
3. expand the "local computer policy" branch
4. expand the "administrative templates" branch
5. expand the "network branch"
6. Highlight the "QoS Packet Scheduler" in left window
7. in right window double click the "limit reservable bandwidth" setting
8. on setting tab check the "enabled" item
9. where it says "Bandwidth limit %" change it to read 0
reboot if you want to but not necessary on some systems your all done. Effect is immediate on some systems. some need re-boot. I have one machine that
needs to reboot first, the others didn't. Don't know why this is.

CATCH HACKERS

Hackers cover their tracks. Experienced hackers cover them more thorougly, but amateur hackers sometimes leave things behind. Don't expect them to leave any really big evidence behind; expect more of little things here and there you might find surprising. For example, if you're writing a term paper and a black hat hacker accidently saved it when he took a paragraph out- that's suspicious. Where did that paragraph go? Well, for one thing, now you know he was in that area. Check the folders surrounding the file- you might find something.

Tip 2: Decipher between the type of hackers that are attacking you. Experienced hackers will have a more in depth look around when they penetrate your system. They won't touch much because they know that that won't add too much to their knowledge. But if you know a hacker's been in, and some files are messed with, and you have a log of someone guessing passwords to a file or something of that sort, its probably some newbie who's just starting out. These are the easiest hackers to catch. They usually get so caught up in thoughts like "I'm in!" that they forget the basics, such as work behind a proxy.

My friend was setting up a webserver once. His first time too, and he wasn't to anxious to set up some good software to protect against hackers and viruses. He didn't put up one IDS, and before you know it, the obvious happened. But this time, a newbie had struck. The nice log files showed, bluntly across the screen, multiple instances of a foreign IP address that stood out. Some stupid newbie had tried to login as "uucp" on my friend's XP computer, with a password of "uucp." Well, that's great, but he also had tried the same user/pass combination three times, enough to get himself logged nicely. Even a semi-brainless user with some form of neurological system knows that uucp isn't a default XP account. Again, excitement toiled this hacker's brain, and maybe if he hadn't done that, along with a few other stupid things, he wouldn't have gotten caught. What other things did he do? Well, lets see. He opened 35 instances of MS-DOS. He tried to clean the printer's heads, and he edited a .gif in notepad. Then he uninstalled a few programs and installed some html editor, and replaced four files with the words "14P."

He might as well have posted his phone number. In a few days, we had tracked him down to a
suburban town in Ohio. We let him go, not pressing any charges, because he had done nothing really damaging and had provided me with an example of a moron for this guide.

Tip 3: Don't go crazy if you lose data. Chances are, if it was that important, you would have backed it up anyway. Most hackers nowadays wish they were back in 1989 when they could use a Black Box and having a Rainbow Book actually meant something. Most hackers aren't black hat, they are white hat, and some even grey hat. But in the end, most hackers that are in systems aren't satisfied by looking around. From past experiences, I have concluded that many hackers like to remember where've they been. So, what do they do? They either press delete here and there, or copy some files onto their systems. Stupid hackers (yes, there are plenty of stupid hackers) send files to e-mail addresses. Some free email companies will give you the IP of a certain e-mail address's user if you can prove that user has been notoriously hacking you. But most of the time, by the time you get the e-mail id it's been unused for weeks if not months or years, and services like hotmail have already deleted it.

Tip 4: Save information! Any information that you get from a log file (proxy server IP, things like "14P", e-mail addresses that things were sent to, etc.) should be saved to a floppy disk (they're not floppy anymore, I wish I could get out of the habit of calling them that) incase there's a next time. If you get another attack, from the same proxy, or with similar e-mail addresses (e.g: one says Blackjack 123@something.whatever and the other says Black_jack_45@something.znn.com ) you can make an assumption that these hackers are the same people. In that case, it would probably be worth the effort to resolve the IP using the proxy and do a traceroute. Pressing charges is recommended if this is a repeat offender.

Tip 5: Don't be stupid. If you've been hacked, take security to the next level. Hackers do talk about people they've hacked and they do post IPs and e-mail addresses. Proof? Take a look at Defcon Conventions. I've never gone to one, but I've seen the photos. The "Wall of Shame"-type of boards I've seen have IPs and e-mail addresses written all over them in fat red, dry-erase ink. Don't be the one to go searching the Defcon website and find your e-mail address posted on the Wall of Shame board!

Tip 6: Don't rely on luck. Chances are, sometime or another, you're going to be targeted for an attack. Here you can rely on luck. Maybe they'll forget? Maybe they don't know how to do it? If you think this way, a surprise is going to hit your face very hard. Another way you could stupidly rely on luck is by saying this: It's probably just a whitehat. On the contrary, my friend, it's probably just a blackhat. A blackhat with knowledge stored in his head, ready to be used as an ax. It's your data. You take the chance

CHANGING IP

1)Get to a command prompt. (START, run, cmd).
2)Type "ipconfig /release" (without the quotes).
3)Type "ipconfig /renew" (without the quotes).
4)Windows (second option)
5)Get to a command prompt. (START, run, cmd).
6)Type "ipconfig /release" (without the quotes).
7)Shut down computer.
8)Turn off computer.
9)Turn off all ethernet hubs/switches.
10)Turn off cable/DSL modem.
11)Leave off overnight.
11)Turn everthing back on

FOLDER WALLPAPER

Goto Control pannel > Folder Options > View tab
there find a way to enable show all hidden files (including the system files)
(i hope you know this much)

Now which ever folder you want to set a background to, open that folder.
there should be a desktop.ini, if its noot there, copy from any other folder.
Now open that desktop.ini file, delete everything if you have copied from any other folder ( but if it was there itself, leave whatever's written there only) and paste the following text in it

[{BE098140-A513-11D0-A3A4-00C04FD706EC}]
IconArea_Image=

like

[{BE098140-A513-11D0-A3A4-00C04FD706EC}]
IconArea_Image=D:\My Documents\My Pictures\spaceball.gif
7/24/07 ?.The HKV.?™
^^^
If you cannot find any other desktop.ini, (this is a very rare case)
then just type the above text in a notepad file & save it as desktop.ini in that folder.
Then goto Start > Run
type CMD and hit enter.
Command prompt will open up.
Type attrib (but dont press enter yet)
now drag the desktop.ini you've just created from that folder into that command prompt window.
then type +s +h +r
now hit enter.

NAMELESS FOLDER

1)Right Click on the desktop.Make a new folder

2)Now rename the folder with a space(U have to hold ALT key and type 0160).

3)Now u have a folder with out a name.

4)Right click on the folder>properties>customize. Click on change icon.

5)Scroll a bit, u should find some empty spaces, Click on any one of them.click ok Thats it,now u can store ur personal data without any 3rd party tools

NET SPEED INCREASE

HEY HERE A TRICK TO IMPROVE UR NET SPEED
Go to desktop->My computer-(right click on)->manage->->Device manager-> now u see a window of - Device manager

then go to Ports->Communication Port(double click on it and Open).

after open u can see a Communication Port properties.

go the Port Setting:----

and now increase ur "Bits per second" to 128000.

and "Flow control" change 2 Hardware.

U WILL NOTICE AN IMMEDIATE RESULT....if not restart.then its definate.

INTERNET SPEED 2

Click Start then Run and type "gpedit.msc" without quotes.

This opens the "group policy editor" and go to: "Local Computer Policy"

Then "Computer Configuration" Then "Administrative Templates"

Then select "Network" then "QOS Packet Scheduler"

After that select "Limit Reservable Bandwidth".
Double click on Limit Reservable bandwidth. It will say it is not configured, but the truth is under the 'Explain' tab i.e.” By default, the Packet Scheduler limits the system to 20 percent of the bandwidth of a connection, but you can use this setting to override the default."
So the trick is to ENABLE reservable bandwidth, then set it to ZERO. This will allow the system to reserve nothing, rather than the default 20%.

CREATE LOGON MESSAGE

Click Start, click Run, type regedit, and then click OK.In the Registry Editor, drill down to the following key:
HKEY_LOCAL_MACHINE\SOFTWARE\Microsoft\Windows NT\CurrentVersion\WinlogonRight-click LegalNoticeCaption, click Modify, type My Windows XP Machine, and then click OK.Right-click LegalNoticeText, click Modify, and then type your message.Close the editor and your new message will appear at every log on.This tip applies to computers that are part of a domain. For stand-alone or peer-to-peer networks,
the custom screen appears just before the Welcome screen

CHANGE TITLE BAR OF WINDOWS MEDIA PLAYER

1.Start Regedit
2.Go to HKEY_CURRENT_USER\Software\Policies\Microsoft
\WindowsMediaPlayer (create a new key named WindowsMediaPlayer if its not der)
3.Create a string value of TitleBar
4.Give it a value of whatever you want to appear in the title bar

IMPROVE THE SPEED OF YOUR MOZILA FIREFOX BROWSER

1. First in the URL bar, Type “about:config”. This will bring up a list
of commands and variables you can edit.
2. The second step is to put “network.http.pipelining” in the filter
and change the value to “true”.
3. After that you will want to put “network.http.proxy.pipelining” in
the filter.
Like the last one, make that value set to “true” also.
4. Next, locate “network.http.pipelining.maxrequests” and change the
value to some number higher, say 10,20 or even 30, it would make up to
10,20 or 30 requests at once.
5. The last step is to right click anywhere and select “New” then
“Integer”. Name it “nglayout.initialpaint.delay” and make its value
“0?. This will make the browser respond faster on the information of
the websites it receives.
6. Close out FireFox (make sure FireFox is closed by viewing the Task
Manager) and restart it and enjoy the new mega speed

RAM CLEANING

U may recognize that ur system gets slower and slower when playing and working a lot with ur pc. That's cause ur RAM is full of remaining progress pieces u do not need any more.

So create a new text file on ur desktop and call it "RAMcleaner" Then open the text file and

Type

FreeMem=Space(128000000)
in this file and save it as RAMcleaner.vbs [ You may choose the "All Files" option when u save it ]

Run the file and ur RAM may be cleaned

Then go to 'TASK MANAGER'-'PROCESSES' Then u see full the full process get 'o' 'o'

Ya ur RAM is clean nw Experiece the speed

Remove shortcut arrow from desktop icons

Here's how you can remove those shortcut arrows from your desktop icons in Windows XP.

1. Start regedit.
2. Navigate to HKEY_CLASSES_ROOT\lnkfile
3. Delete the IsShortcut registry value.

You may need to restart Windows XP.

RUN COMMANDS

You can access all these programs by going through START/RUN or Simply Click Windows Key+R

* SQL Client Configuration - cliconfg
* System Configuration Editor - sysedit
* System Configuration Utility - msconfig
* System File Checker Utility (Scan Immediately)- sfc /scannow
* System File Checker Utility (Scan Once At Next Boot)- sfc /scanonce
* System File Checker Utility (Scan On Every Boot) - sfc /scanboot
* System File Checker Utility (Return to Default Setting)- sfc /revert
* System File Checker Utility (Purge File Cache)- sfc /purgecache
* System File Checker Utility (Set Cache Size to size x)-sfc/cachesize=x
* System Information - msinfo32.
* Task Manager – taskmgr
* System Properties - sysdm.cpl
* Task Manager – taskmgr
* TCP Tester - tcptest
* Telnet Client - telnet
* Tweak UI (if installed) - tweakui
* User Account Management- nusrmgr.cpl
* Utility Manager - utilman
* Windows Address Book - wab
* Windows Address Book Import Utility - wabmig
* Windows Backup Utility (if installed)- ntbackup
* Windows Explorer - explorer
* Windows Firewall- firewall.cpl
* Windows Magnifier- magnify
* Windows Management Infrastructure - wmimgmt.msc
* Windows Media Player - wmplayer
* Windows Messenger - msmsgs
* Windows Picture Import Wizard (need camera connected)- wiaacmgr
* Windows System Security Tool – syskey
* Windows Update Launches - wupdmgr
* Windows Version (to show which version of windows)- winver
* Windows XP Tour Wizard - tourstart
* Wordpad - write
* Password Properties - password.cpl
* Performance Monitor - perfmon.msc
* Phone and Modem Options - telephon.cpl
* Phone Dialer - dialer
* Pinball Game - pinball
* Power Configuration - powercfg.cpl
* Printers and Faxes - control printers
* Printers Folder – printers
* Private Character Editor - eudcedit
* Quicktime (If Installed)- QuickTime.cpl
* Real Player (if installed)- realplay
* Regional Settings - intl.cpl
* Registry Editor - regedit
* Registry Editor - regedit32
* Remote Access Phonebook - rasphone
* Remote Desktop - mstsc
* Removable Storage - ntmsmgr.msc
* Removable Storage Operator Requests - ntmsoprq.msc
* Resultant Set of Policy (XP Prof) - rsop.msc
* Scanners and Cameras - sticpl.cpl
* Scheduled Tasks - control schedtasks
* Security Center - wscui.cpl
* Services - services.msc
* Shared Folders - fsmgmt.msc
* Shuts Down Windows - shutdown
* Sounds and Audio - mmsys.cpl
* Spider Solitare Card Game - spider
* Malicious Software Removal Tool - mrt
* Microsoft Access (if installed) - access.cpl
* Microsoft Chat - winchat
* Microsoft Excel (if installed) - excel
* Microsoft Frontpage (if installed)- frontpg
* Microsoft Movie Maker - moviemk
* Microsoft Paint - mspaint
* Microsoft Powerpoint (if installed)- powerpnt
* Microsoft Word (if installed)- winword
* Microsoft Syncronization Tool - mobsync
* Minesweeper Game - winmine
* Mouse Properties - control mouse
* Mouse Properties - main.cpl
* Nero (if installed)- nero
* Netmeeting - conf
* Network Connections - control netconnections
* Network Connections - ncpa.cpl
* Network Setup Wizard - netsetup.cpl
* Notepad - notepad
* Nview Desktop Manager (If Installed)- nvtuicpl.cpl
* Object Packager - packager
* ODBC Data Source Administrator- odbccp32.cpl
* On Screen Keyboard - osk
* Opens AC3 Filter (If Installed) - ac3filter.cpl
* Outlook Express - msimn
* Paint – pbrush
* Keyboard Properties - control keyboard
* IP Configuration (Display Connection Configuration) - ipconfi/all
* IP Configuration (Display DNS Cache Contents)- ipconfig /displaydns
* IP Configuration (Delete DNS Cache Contents)- ipconfig /flushdns
* IP Configuration (Release All Connections)- ipconfig /release
* IP Configuration (Renew All Connections)- ipconfig /renew
* IP Configuration(RefreshesDHCP&Re-RegistersDNS)-ipconfig/registerdns
* IP Configuration (Display DHCP Class ID)- ipconfig/showclassid
* IP Configuration (Modifies DHCP Class ID)- ipconfig /setclassid
* Java Control Panel (If Installed)- jpicpl32.cpl
* Java Control Panel (If Installed)- javaws
* Local Security Settings - secpol.msc
* Local Users and Groups - lusrmgr.msc
* Logs You Out Of Windows - logoff.....
* Accessibility Controls - access.cpl
* Accessibility Wizard - accwiz
* Add Hardware - Wizardhdwwiz.cpl
* Add/Remove Programs - appwiz.cpl
* Administrative Tools control - admintools
* Adobe Acrobat (if installed) - acrobat
* Adobe Designer (if installed)- acrodist
* Adobe Distiller (if installed)- acrodist
* Adobe ImageReady (if installed)- imageready
* Adobe Photoshop (if installed)- photoshop
* Automatic Updates - wuaucpl.cpl
* Bluetooth Transfer Wizard – fsquirt
* Calculator - calc
* Certificate Manager - certmgr.msc
* Character Map - charmap
* Check Disk Utility - chkdsk
* Clipboard Viewer - clipbrd
* Command Prompt - cmd
* Component Services - dcomcnfg
* Computer Management - compmgmt.msc
* Control Panel - control
* Date and Time Properties - timedate.cpl
* DDE Shares - ddeshare
* Device Manager - devmgmt.msc
* Direct X Control Panel (If Installed)- directx.cpl
* Direct X Troubleshooter- dxdiag
* Disk Cleanup Utility- cleanmgr
* Disk Defragment- dfrg.msc
* Disk Management- diskmgmt.msc
* Disk Partition Manager- diskpart
* Display Properties- control desktop
* Display Properties- desk.cpl
* Display Properties (w/Appearance Tab Preselected)- control color
* Dr. Watson System Troubleshooting Utility- drwtsn32
* Driver Verifier Utility- verifier
* Event Viewer- eventvwr.msc
* Files and Settings Transfer Tool- migwiz
* File Signature Verification Tool- sigverif
* Findfast- findfast.cpl
* Firefox (if installed)- firefox
* Folders Properties- control folders
* Fonts- control fonts
* Fonts Folder- fonts
* Free Cell Card Game- freecell
* Game Controllers- joy.cpl
* Group Policy Editor (XP Prof)- gpedit.msc
* Hearts Card Game- mshearts
* Help and Support- helpctr
* HyperTerminal- hypertrm
* Iexpress Wizard- iexpress
* Indexing Service- ciadv.msc
* Internet Connection Wizard- icwconn1
* Internet Explorer- iexplore
* Internet Setup Wizard- inetwiz
* Internet Properties- inetcpl.cpl

SET UR NAME ON TASK BAR

Open Control Panel -> Regional and Language Options -> Customize ->Time
here u can see A.M. and P.M. change it with u r name.

VIRTUAL MEMORY

Right click my computer-properties-Advanced-performance-setting-Advanced-change-
custom size (here u can allocate u r virtual memory) and set -apply-ok

virtual memory (actually memory multiply with 3) you can set the maximum size

Parents wedding

2010-06-22T06:43:00.000-07:00

Useful link for student nurses

2010-06-17T07:59:00.001-07:00

http://nursingcrib.com/ ,
http://healthlibrary.stanford.edu/resources/bodysystems/cardio_other.html#otherheart .

U can find disease conditions, care plans, case studies, books and jobs thru this link. just use it if you need......

Respiratory diseases

2010-06-17T02:39:00.000-07:00

Respiratory diseases are diseases that affect the air passages, including the nasal passages, the bronchi and the lungs. They range from acute infections, such as pneumonia and bronchitis, to chronic conditions such as asthma and chronic obstructive pulmonary disease. These include diseases of the lung, pleural cavity, bronchial tubes, trachea, upper respiratory tract and of the nerves and muscles of breathing.
Respiratory disease is responsible for over 10% of hospitalizations and over 16% of deaths in Canada. The study of respiratory disease is known as pulmonology. A doctor who specializes in respiratory disease is known as a pulmonologist, a chest medicine specialist, a respiratory medicine specialist, a respirologist or a thoracic medicine specialist.
Respiratory diseases can be classified in many different ways
• by the organ involved
• by the pattern of symptoms
• by the cause of the disease
A. Obstructive lung diseases – are diseases of the lung where the bronchial tubes become narrowed making it hard to move air in and especially out of the lung.
B. Restrictive lung diseases – (also known as interstitial lung diseases) are a category of respiratory disease characterized by a loss of lung compliance, causing incomplete lung expansion and increased lung stiffness. E.g. in infant respiratory distress syndrome (IRDS)
C. Respiratory tract infections – Infections can affect any part of the respiratory system. They are traditionally divided into upper respiratory tract infections and lower respiratory tract infections.
D. Upper respiratory tract infections - The most common upper respiratory tract infection is the common cold however, infections of specific organs of the upper respiratory tract such as sinusitis, tonsillitis, otitis media, pharyngitis and laryngitis are also considered upper respiratory tract infections.
E. Lower respiratory tract infection - The most common lower respiratory tract infection in is pneumonia, a lung infection. Pneumonia is usually caused by bacteria, particularly Streptococcus pneumoniae in Western countries. Worldwide, tuberculosis is an important cause of pneumonia. Other pathogens such as viruses and fungi can cause pneumonia for example severe acute respiratory syndrome and pneumocystis pneumonia. A pneumonia may develop complications such as a lung abscess, a round cavity in the lung caused by the infection or an empyema, the spread of the infection to the pleural cavity.
F. Respiratory Tumors – Tumours of the respiratory system are either malignant or benign.
1. Malignant tumors, or cancers of the respiratory system, particularly lung cancers, are a major health problem responsible for 15% of all cancer diagnoses and 29% of all cancer deaths. The majority of respiratory system cancers are attributable to smoking tobacco.
The major types of respiratory system cancer are:
• Small cell lung cancer
• Non-small cell lung cancer
o Adenocarcinoma
o Large cell undifferentiated carcinoma
• Other lung cancers (carcinoid, Kaposi’s sarcoma, melanoma)
• Lymphoma
• Head and neck cancer
• Mesothelioma, usually caused by exposure to asbestos dust.
In addition, since many cancers spread via the bloodstream and the entire cardiac output passes through the lungs, it common for cancer metastases to occur the lung. Breast cancer may invade directly through local spread, and through lymph node metastases. After metastasis to the liver, colon cancer frequently metastasizes to the lung. Prostate cancer, germ cell cancer and renal cell carcinoma may also metastasize to the lung.
Treatment of respiratory system cancer depends on the type of cancer. Surgery (usually removal of part of the lung, a lobectomy or an entire lung, a pneumonectomy), chemotherapy and radiotherapy are all used. The chance of surviving lung cancer depends on the cancer stage at the time the cancer is diagnosed and is only about 14-17% overall. In the case of metastases to the lung, treatment can occasionally be curative but only in certain, rare circumstances.
2. Benign tumors are relatively rare causes of respiratory disease. Examples of benign tumors are:
• Pulmonary hamartoma
• Congenital malformations such as pulmonary sequestration and congenital cystic adenomatoid malformation (CCAM).
G. Pleural cavity diseases - diseases include empyema and mesothelioma which are mentioned above.
• A collection of fluid in the pleural cavity is known as a pleural effusion. This may be due to fluid shifting from the bloodstream into the pleural cavity due to conditions such as congestive heart failure and cirrhosis. It may also be due to inflammation of the pleura itself as can occur with infection, pulmonary embolus, tuberculosis, mesothelioma and other conditions.
• A pneumothorax is a hole in the pleura covering the lung allowing air in the lung to escape into the pleural cavity. The affected lung “collapses” like a deflated balloon. A tension pneumothorax is a particularly severe form of this condition where the air in the pleural cavity cannot escape, so the pneumothorax keeps getting bigger until it compresses the heart and blood vessels, leading to a life threatening situation.
H. Pulmonary vascular diseases
• Pulmonary embolism, a blood clot that forms in a vein, breaks free, travels through the heart and lodges in the lungs (thromboembolism). Large pulmonary emboli are fatal, causing sudden death. A number of other substances can also embolise to the lungs but they are much more rare: fat embolism (particularly after bony injury), amniotic fluid embolism (with complications of labour and delivery), air embolism (iatrogenic).
• Pulmonary arterial hypertension, elevated pressure in the pulmonary arteries. It can be idiopathic or due to the effects of another disease, particularly COPD. This can lead to strain on the right side of the heart, a condition known as cor pulmonale.
• Pulmonary edema, leakage of fluid from capillaries of the lung into the alveoli (or air spaces). It is usually due to congestive heart failure.
• Pulmonary hemorrhage, inflammation and damage to capillaries in the lung resulting in blood leaking into the alveoli. This may cause blood to be coughed up. Pulmonary hemorrhage can be due to auto-immune disorders such as Wegener’s Granulomatosis and Goodpasture’s syndrome.
I. Disorders of breathing mechanics
The brain co-ordinates breathing and sends messages via nerves to the muscles of respiration. The muscles produce the movements of breathing. Disorders of the brain’s control of breathing, the nerves or the muscles of respiration can affect the respiratory system. Common disorders of breathing mechanics are:
• Obstructive sleep apnea
• Central sleep apnea
• Amyotrophic lateral sclerosis
• Guillan-Barre syndrome
• Myasthenia gravis
Obesity is often associated with sleep apnea and can cause either an obstructive or a restrictive pattern on spirometry. Obesity reduces the movement of the chest wall which can, in extreme cases, result in the obesity-hypoventilation syndrome, a cause of respiratory failure.
POTENTIAL NURSING DIAGNOSIS FOR CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) AND ASTHMA
1. Ineffective airway clearance
2. Impaired gas exchange
3. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs
POTENTIAL NURSING DIAGNOSIS FOR PNEUMONIA
1. Ineffective airway clearance
2. Impaired gas exchange
3. Risk for (spread) infection
4. Activity intolerance
5. Acute pain
6. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs
7. Risk for deficient fluid volume
8. Risk for imbalanced nutrition less than body requirements
POTENTIAL NURSING DIAGNOSIS FOR LUNG CANCER: POSTOPERATIVE CARE
1. Impaired gas exchange
2. Ineffective airway clearance
3. Acute pain
4. Fear/ Anxiety
5. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs
POTENTIAL NURSING DIAGNOSIS FOR PNEUMOTHORAX/ HEMOTHORAX
1. Ineffective breathing pattern
2. Trauma/ Suffocation
3. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs
POTENTIAL NURSING DIAGNOSIS FOR RADICAL NECK SURGERY: LARYNGECTOMY (POSTOPERATIVE CARE)
1. Ineffective airway clearance
2. Risk for aspiration
3. Impaired verbal communication
4. Impaired skin or tissue integrity
5. Impaired oral mucus membrane
6. Acute pain
7. Imbalanced nutrition less than body requirements
8. Disturbed body image / Ineffective role performance
9. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs
POTENTIAL NURSING DIAGNOSIS FOR VENTILATORY ASSISTANCE (MECHANICAL)
1. Ineffective breathing pattern/ Impaired spontaneous ventilation
2. Ineffective airway clearance
3. Impaired verbal communication
4. Fear/ anxiety
5. Impaired oral mucus membrane
6. Imbalanced nutrition less than body requirements
7. Risk for infection
8. Risk for dysfunctional ventilatory weaning response
9. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs
POTENTIAL NURSING DIAGNOSIS FOR PULMONARY TUBERCULOSIS (PTB)
1. Risk for (spread/ reactivation) infection
2. Ineffective airway clearance
3. Risk for impaired gas exchange
4. Imbalanced nutrition, less than body requirements
5. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs

Cardiovascular diseases (CVDs)

2010-06-17T02:37:00.000-07:00

Cardiovascular diseases (CVDs) are a group of disorders of the heart and blood vessels and include:
• Coronary heart disease – disease of the blood vessels supplying the heart muscle
• Cerebrovascular disease – disease of the blood vessels supplying the brain
• Peripheral arterial disease – disease of blood vessels supplying the arms and legs
• Rheumatic heart disease – damage to the heart muscle and heart valves from rheumatic fever, caused by streptococcal bacteria
• Congenital heart disease – malformations of heart structure existing at birth.
• Deep vein thrombosis and pulmonary embolism – blood clots in the leg veins, which can dislodge and move to the heart and lungs.
Heart attacks and strokes are usually acute events and are mainly caused by a blockage that prevents blood from flowing to the heart or brain. The most common reason for this is a build-up of fatty deposits on the inner walls of the blood vessels that supply the heart or brain. Strokes can also be caused by bleeding from a blood vessel in the brain or from blood clots.
FACTS ABOUT CARDIOVASCULAR DISEASES
• CVDs are the number one cause of death globally: more people die annually from CVDs than from any other cause;
• An estimated 17.5 million people died from CVDs in 2005, representing 30% of all global deaths. Of these deaths, an estimated 7.6 million were due to coronary heart disease and 5.7 million were due to stroke.
• Over 80% of CVD deaths take place in low- and middle-income countries and occur almost equally in men and women;
• By 2015, almost 20 million people will die from CVDs, mainly from heart disease and stroke. These are projected to remain the single leading causes of death.
CAUSES OF CARDIOVASCULAR DISEASES
• The causes of CVDs are well established and well known. The most important causes of heart disease and stroke are unhealthy diet, physical inactivity and tobacco use. These are called ‘modifiable risk factors’.
• The effects of unhealthy diet and physical inactivity may show up in individuals as raised blood pressure, raised blood glucose, raised blood lipids, and overweight and obesity; these are called ‘intermediate risk factors’.
• The major modifiable risk factors are responsible for about 80% of coronary heart disease and cerebrovascular disease.
• There are also a number of underlying determinants of chronic diseases, or, if you like, "the causes of the causes". These are a reflection of the major forces driving social, economic and cultural change – globalization, urbanization, and population ageing. Other determinants of CVDs are poverty and stress.
COMMON SYMPTOMS OF CARDIOVASCULAR DISEASES
• Often, there are no symptoms of the underlying disease of the blood vessels. A heart attack or stroke may be the first warning of underlying disease.
• Symptoms of a heart attack include: pain or discomfort in the centre of the chest; pain or discomfort in the arms, the left shoulder, elbows, jaw, or back. In addition the person may experience difficulty in breathing or shortness of breath; feeling sick or vomiting; feeling light-headed or faint; breaking into a cold sweat; and becoming pale.
• Women are more likely to have shortness of breath, nausea, vomiting, and back or jaw pain.
• The most common symptom of a stroke is sudden weakness of the face, arm, or leg, most often on one side of the body. Other symptoms include sudden onset of: numbness of the face, arm, or leg, especially on one side of the body; confusion, difficulty speaking or understanding speech; difficulty seeing with one or both eyes; difficulty walking, dizziness, loss of balance or coordination; severe headache with no known cause; and fainting or unconsciousness.
• People experiencing these symptoms should seek medical care immediately.
POTENTIAL NURSING DIAGNOSIS FOR SEVERE HYPERTENSION:
1. Risk for decreased cardiac output
2. Activity intolerance
3. Acute headache pain
4. Imbalanced nutrition more than body requirements
5. Ineffective coping
6. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs
POTENTIAL NURSING DIAGNOSIS FOR CHRONIC HEART FAILURE (CHF)
1. Decreased Cardiac output
2. Activity intolerance
3. Excess fluid volume
4. Risk for impaired gas exchange
5. Risk for impaired skin integrity
6. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs
POTENTIAL NURSING DIAGNOSIS FOR ANGINA (CORONARY ARTERY DISEASE)
1. Acute pain
2. Risk for decreased cardiac output
3. Anxiety
4. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs

POTENTIAL NURSING DIAGNOSIS FOR MYOCARDIAL INFARCTION
1. Acute pain
2. Activity intolerance
3. Anxiety/ Fear
4. Risk for decreased cardiac output
5. Ineffective tissue perfusion
6. Risk for excess fluid volume
7. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs
POTENTIAL NURSING DIAGNOSIS FOR DYSRHYTHMIAS (INCLUDING DIGITALIS TOXICITY)
1. Risk for decreased cardiac output
2. Risk for poisoning, digitalis toxicity
3. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs
POTENTIAL NURSING DIAGNOSIS FOR CARDIAC SURGERY: POSTOPERATIVE CARE – CORONARY ARTERY BYPASS GRAFT (CABG), MINIMALLY INVASIVE DIRECT CORONARY ARTERY BYPASS (MIDCAB), CARDIOMYOPLASTY, VALVE REPLACEMENT
1. Risk for decreased cardiac output
2. Acute pain
3. Ineffective role performance
4. Risk for ineffective breathing pattern
5. Impaired skin integrity
6. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs
POTENTIAL NURSING DIAGNOSIS FOR THROMBOPHLEBITIS: DEEP VEIN THROMBOSIS (INCLUDING PULONARY EMBOLI CONSIDERATIONS)
1. Ineffective tissue perfusion
2. Acute pain
3. Impaired gas exchange (in presence of pulmonary embolus)
4. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs.

Hormones of the Reproductive System

2010-06-17T02:36:00.000-07:00

Hormones of the Reproductive System

Females
The ovaries of sexually-mature females secrete:
• a mixture of estrogens of which 17β-estradiol is the most abundant (and most potent).
• progesterone.
Estrogens
Estrogens are steroids. They
• are primarily responsible for the conversion of girls into sexually-mature women.
o development of breasts
o further development of the uterus and vagina
o broadening of the pelvis
o growth of pubic and axillary hair
o increase in adipose (fat) tissue
• participate in the monthly preparation of the body for a possible pregnancy
• participate in pregnancy if it occurs
Estrogens also have non-reproductive effects.
• They antagonize the effects of the parathyroid hormone, minimizing the loss of calcium from bones and thus helping to keep bones strong.
• They promote blood clotting.
Progesterone
Progesterone is also a steroid. It has many effects in the body, some having nothing to do with sex and reproduction. Here we shall focus on the role of progesterone in the menstrual cycle and pregnancy [Link to a special page on progesterone].
How estrogens and progesterone achieve their effects
Steroids like estrogens and progesterone are small, hydrophobic molecules that are transported in the blood bound to a serum globulin.
• In "target" cells, i.e., cells that change their gene expression in response to the hormone, they bind to receptor proteins located in the cytoplasm and/or nucleus.
• The hormone-receptor complex enters the nucleus (if it formed in the cytoplasm) [View] and
• binds to specific sequences of DNA, called the estrogen (or progesterone) response elements
• Response elements are located in the promoters of genes.
• The hormone-receptor complex acts as a transcription factor (often recruiting other transcription factors to help) which
• turns on (sometimes off) transcription of those genes.
• Gene expression in the cell produces the response.

Regulation of Estrogen and Progesterone
The synthesis and secretion of estrogens is stimulated by follicle-stimulating hormone (FSH), which is, in turn, controlled by the hypothalamic gonadotropin releasing hormone (GnRH).
Hypothalamus → GnRH → Pituitary → FSH → Follicle → Estrogens
High levels of estrogens suppress the release of GnRH (bar) providing a negative-feedback control of hormone levels.
It works like this: Secretion of GnRH depends on certain neurons in the hypothalamus which express a gene (KiSS-1) encoding a protein of 145 amino acids. From this are cut several short peptides collectively called kisspeptin. These are secreted and bind to G-protein-coupled receptors on the surface of the GnRH neurons stimulating them to release GnRH. However, high levels of estrogen (or progesterone or testosterone) inhibit the secretion of kisspeptin and suppress further production of those hormones.
Progesterone production is stimulated by luteinizing hormone (LH), which is also stimulated by GnRH.
Hypothalamus → GnRH → Pituitary → LH → Corpus luteum → Progesterone
Elevated levels of progesterone control themselves by the same negative feedback loop used by estrogen (and testosterone).
The Menstrual Cycle
About every 28 days, some blood and other products of the disintegration of the inner lining of the uterus (the endometrium) are discharged from the uterus, a process called menstruation. During this time a new follicle begins to develop in one of the ovaries. After menstruation ceases, the follicle continues to develop, secreting an increasing amount of estrogen as it does so.
• The rising level of estrogen causes the endometrium to become thicker and more richly supplied with blood vessels and glands.
• A rising level of LH causes the developing egg within the follicle to complete the first meiotic division (meiosis I), forming a secondary oocyte.
• After about two weeks, there is a sudden surge in the production of LH.
• This surge in LH triggers ovulation: the release of the secondary oocyte into the fallopian tube.
• Under the continued influence of LH, the now-empty follicle develops into a corpus luteum (hence the name luteinizing hormone for LH).
• Stimulated by LH, the corpus luteum secretes progesterone which
o continues the preparation of the endometrium for a possible pregnancy
o inhibits the contraction of the uterus
o inhibits the development of a new follicle
• If fertilization does not occur (which is usually the case),
o the rising level of progesterone inhibits the release of GnRH which, in turn,
o inhibits further production of progesterone.
• As the progesterone level drops,
o the corpus luteum begins to degenerate;
o the endometrium begins to break down, its cells committing programmed cell death (apoptosis);
o the inhibition of uterine contraction is lifted, and
o the bleeding and cramps of menstruation begin.
Pregnancy
Fertilization of the egg takes place within the fallopian tube. As the fertilized egg passes down the tube, it undergoes its first mitotic divisions. By the end of the week, the developing embryo has become a hollow ball of cells called a blastocyst. At this time, the blastocyst reaches the uterus and embeds itself in the endometrium, a process called implantation. With implantation, pregnancy is established.
The blastocyst has two parts:
• the inner cell mass, which will become the baby, and
• the trophoblast, which will
o develop into the placenta and umbilical cord
o and begin to secrete human chorionic gonadotropin (HCG).
HCG is a glycoprotein. It is a dimer of
• the same alpha subunit (of 92 amino acids) used by TSH, FSH, and LH and
• a unique beta subunit (of 145 amino acids).
HCG behaves much like FSH and LH with one crucial exception: it is NOT inhibited by a rising level of progesterone. Thus HCG prevents the deterioration of the corpus luteum at the end of the fourth week and enables pregnancy to continue beyond the end of the normal menstrual cycle.
Because only the implanted trophoblast makes HCG, its early appearance in the urine of pregnant women provides the basis for the most widely used test for pregnancy (which can provide a positive signal even before menstruation would have otherwise begun).
As pregnancy continues, the placenta becomes a major source of progesterone, and its presence is essential to maintain pregnancy. Mothers at risk of giving birth too soon can be given a synthetic progestin to help them retain the fetus until it is full-term.
Birth
Toward the end of pregnancy,
• The placenta releases large amounts of CRH which stimulates the pituitary glands of both mother and her fetus to secrete
• ACTH, which acts on their adrenal glands causing them to release the estrogen precursor dehydroepiandrosterone sulfate (DHEAS).
• This is converted into estrogen by the placenta.
• The rising level of estrogen causes the smooth muscle cells of the uterus to
o synthesize connexins and form gap junctions. Gap junctions connect the cells electrically so that they contract together as labor begins.
o express receptors for oxytocin.
• Oxytocin is secreted by the posterior lobe of the pituitary as well as by the uterus.
• Prostaglandins are synthesized in the placenta and uterus.
• The normal inhibition of uterine contraction by progesterone is turned off by several mechanisms while
• both oxytocin and prostaglandins cause the uterus to contract and labor begins.
Three or four days after the baby is born, the breasts begin to secrete milk.
• Milk synthesis is stimulated by the pituitary hormone prolactin (PRL), and
• its release from the breast is stimulated by oxytocin.
• Milk contains an inhibitory peptide. If the breasts are not fully emptied, the peptide accumulates and inhibits milk production. This autocrine action thus matches supply with demand.
Other Hormones
• Relaxin
As the time of birth approaches in some animals (e.g., pigs, rats) , this polypeptide has been found to:
o relax the pubic ligaments
o soften and enlarge the opening to the cervix.
Relaxin is found in pregnant humans but at higher levels early in pregnancy than close to the time of birth. Relaxin promotes angiogenesis, and in humans it probably plays a more important role in the development of the interface between the uterus and the placenta that it does in the birth process.
• Activins, Inhibins, Follistatin.
These proteins are synthesized within the follicle. Activins and inhibins bind to follistatin. Activins increase the action of FSH; inhibins, as their name suggests, inhibit it. How important they are in humans remains to be seen. However the important role that activin and follistatin play in the embryonic development of vertebrates justifies mentioning them here.
Oral contraceptives: the "pill"
The feedback inhibition of GnRH secretion by estrogens and progesterone provides the basis for the most widely-used form of contraception. Dozens of different formulations of synthetic estrogens or progestins (progesterone relatives) — or both — are available. Their inhibition of GnRH prevents the mid-cycle surge of LH and ovulation. Hence there is no egg to be fertilized.
Usually the preparation is taken for about three weeks and then stopped long enough for normal menstruation to occur.
The main side-effects of the pill stem from an increased tendency for blood clots to form (estrogen enhances clotting of the blood).
RU-486
RU-486 (also known as mifepristone) is a synthetic steroid related to progesterone. Unlike the synthetic progestins used in oral contraceptives that mimic the actions of progesterone, RU-486 is a progesterone antagonist; that is, it blocks the action of progesterone. It does this by binding more tightly to the progesterone receptor than progesterone itself but without the normal biological effects:
• The RU-486/receptor complex is not active as a transcription factor.
• Thus genes that are turned on by progesterone are turned off by RU-486.
• The proteins needed to establish and maintain pregnancy are no longer synthesized.
• The endometrium breaks down.
• The embryo detaches from it and can no longer make chorionic gonadotropin (HCG).
• Consequently the corpus luteum ceases its production of progesterone.
• The inhibition on uterine contraction is lifted.
• Soon the embryo and the breakdown products of the endometrium are expelled.
These properties of RU-486 have caused it to be used to induce abortion of an unwanted fetus. In practice, the physician assists the process by giving a synthetic prostaglandin (e.g., misoprostol [Cytotec®]) 36–48 hours after giving the dose of RU-486. Use of RU-486 is generally limited to the first seven weeks of pregnancy.
RU-486 has been used for many years in some countries. However, the controversies surrounding abortion in the United States kept it from being authorized for use here until September 2000.
Menopause
The menstrual cycle continues for many years. But eventually, usually between 42 and 52 years of age, the follicles become less responsive to FSH and LH. They begin to secrete less estrogen. Ovulation and menstruation become irregular and finally cease. This cessation is called menopause.
With levels of estrogen now running one-tenth or less of what they had been, the hypothalamus is released from their inhibitory influence (bar). As a result it now stimulates the pituitary to increased activity. The concentrations of FSH and LH in the blood rise to ten or more times their former values. These elevated levels may cause a variety of unpleasant physical and emotional symptoms.
Hormone replacement therapy (HRT)
Many menopausal women elect to take a combination of estrogen and progesterone after they cease to make their own. The benefits are:
• reduction in the unpleasant symptoms of the menopause
• a reduction in the loss of calcium from bones and thus a reduction in osteoporosis and the fractures that accompany it.
It was also believed that HRT reduced the risk of cardiovascular disease. However, a recent study of 16,000 menopausal women was stopped 3 years early when it was found that, in fact, HRT increased (albeit only slightly) not decreased the incidence of cardiovascular disease.
Perhaps synthetic selective estrogen response modulators or SERMs (raloxifene is an example) will provide the protective effects without the harmful ones. Stay tuned.
Environmental estrogens
Some substances that find their way into the environment, such as
• DDE, a breakdown product of the once widely-used insecticide DDT,
• DDT itself (still used in some countries (e.g., Mexico), and
• PCBs, chemicals once used in a wide variety of industrial applications
can bind to the estrogen (and androgen) receptors and mimic (weakly) the effects of the hormone. This has created anxiety that they may be responsible for harmful effects such as cancer and low sperm counts.
However, there is as yet little evidence to support these worries.
• No epidemiological relationship has been found between the incidence of breast cancer and the levels of these compounds in the body.
• As for laboratory studies that found a synergistic effect of two of these substances on receptor binding (findings that created the great alarm), these have not been replicated in other laboratories, and the authors of the original report have since withdrawn it as invalid.
________________________________________
Males
The principal androgen (male sex hormone) is testosterone. This steroid is manufactured by the interstitial (Leydig) cells of the testes. Secretion of testosterone increases sharply at puberty and is responsible for the development of the so-called secondary sexual characteristics (e.g., beard) of men.
Testosterone is also essential for the production of sperm.
Link to diagram showing location and structure of the testes.

Production of testosterone is controlled by the release of luteinizing hormone (LH) from the anterior lobe of the pituitary gland, which is in turn controlled by the release of GnRH from the hypothalamus. LH is also called interstitial cell stimulating hormone (ICSH).
Hypothalamus → GnRH → Pituitary → LH → Testes → Testosterone
The level of testosterone is under negative-feedback control: a rising level of testosterone suppresses the release of GnRH from the hypothalamus. This is exactly parallel to the control of estrogen secretion in females. [Look back]
Males need estrogen, too!
In 1994, a man was described who was homozygous for a mutation in the gene encoding the estrogen receptor. A single nonsense mutation had converted a codon (CGA) for arginine early in the protein into a STOP codon (TGA). Thus no complete estrogen receptor could be synthesized.
This man was extra tall, had osteoporosis and "knock-knees", but was otherwise well. His genetic defect confirms the important role that estrogen has in both sexes for normal bone development.
It is not known whether this man (or any of the few other men who have been found with the same disorder) is fertile or not. However, an article in the 4 December 1997 issue of Nature reports that male mice whose estrogen receptor gene has been "knocked out" are sterile.
Anabolic steroids
A number of synthetic androgens are used for therapeutic purposes. These drugs promote an increase in muscle size with resulting increases in strength and speed. This has made them popular with some athletes, e.g., weight lifters, cyclists, runners, swimmers, professional football players.
Usually these athletes (females as well as males) take doses far greater than those used in standard therapy. Such illicit use carries dangers (besides being banned from an event because of a positive drug test): acne, a decrease in libido, and — in males — testicle size and sperm counts to name a few.
Genetic abnormalities of gonadal function.
Many things can go wrong with sexual development in both males and females; fortunately rarely. Let's look only at a few that clearly result from the inheritance of single-gene mutations.
• Inherited mutations in both copies of the gene encoding the GnRH receptor result in failure to develop at puberty.
• Mutations in the gene encoding the LH receptor prevent normal sexual development in both sexes.
• Mutations in the gene encoding the FSH receptor block development of the gonads in both males and females.
• Mutations in any of the genes encoding the enzymes for synthesis and metabolism of testosterone interfere with normal sexual function in males.
• A similar spectrum of disorders in males can be caused by mutations in the genes encoding the androgen receptor.

Migraine

2010-06-17T02:34:00.000-07:00

Migraine

Migraine is a neurological syndrome characterized by altered bodily perceptions, severe headaches, and nausea. Physiologically, the migraine headache is a neurological condition more common to women than to men.[1][2] The word migraine was borrowed from Old French migraigne (originally as "megrim", but respelled in 1777 on a contemporary French model). The French term derived from a vulgar pronunciation of the Late Latin word hemicrania, itself based on Greek hemikrania, from Greek roots for "half" and "skull".[3]
The typical migraine headache is unilateral (affecting one half of the head) and pulsating, lasting from 4 to 72 hours;[2] symptoms include nausea, vomiting, photophobia (increased sensitivity to light), and phonophobia (increased sensitivity to sound).[4][5][6] Approximately one-third of people who suffer migraine headache perceive an aura—unusual visual, olfactory, or other sensory experiences that are a sign that the migraine will soon occur.[7]
Initial treatment is with analgesics for the headache, an antiemetic for the nausea, and the avoidance of triggering conditions. The cause of migraine headache is unknown; the most common theory is a disorder of the serotonergic control system.
There are migraine headache variants, some originate in the brainstem (featuring intercellular transport dysfunction of calcium and potassium ions) and some are genetically disposed.[8] Studies of twins indicate a 60 to 65 percent genetic influence upon their propensity to develop migraine headache.[9][10] Moreover, fluctuating hormone levels indicate a migraine relation: 75 percent of adult patients are women, although migraine affects approximately equal numbers of prepubescent boys and girls; propensity to migraine headache is known to disappear during pregnancy, although in some women migraines may become more frequent during pregnancy.

Management
Conventional treatment focuses on three areas: trigger avoidance, symptomatic control, and prophylactic pharmacological drugs. Patients who experience migraines often find that the recommended migraine treatments are not 100% effective at preventing migraines, and sometimes may not be effective at all. Pharmacological treatments are considered effective if they reduce the frequency or severity of migraine attacks by 50%.[50]
Children and adolescents are often first given drug treatment, but the value of diet modification should not be overlooked. The simple task of starting a diet journal to help modify the intake of trigger foods like hot dogs, chocolate, cheese and ice cream could help alleviate symptoms.[31]
For patients who have been diagnosed with recurring migraines, migraine abortive medications can be used to treat the attack, and may be more effective if taken early, losing effectiveness once the attack has begun. Treating the attack at the onset can often abort it before it becomes serious, and can reduce the near-term frequency of subsequent attacks.[citation needed]
Paracetamol or non-steroidal anti-inflammatory drug (NSAIDs)
The first line of treatment is over-the-counter abortive medication.
• Regarding non-steroidal anti-inflammatory drugs, a randomized controlled trial found that naproxen can abort about one third of migraine attacks, which was 5% less than the benefit of sumatriptan.[51]
• Paracetamol (known as acetaminophen in North America) benefited over half of patients with mild or moderate migraines in a randomized controlled trial.[52]
• Simple analgesics combined with caffeine may help.[53] During a migraine attack, emptying of the stomach is slowed, resulting in nausea and a delay in absorbing medication. Caffeine has been shown to partially reverse this effect. Excedrin is an example of an aspirin with caffeine product. Caffeine is recognized by the U.S. Food and Drug Administration as an Over The Counter Drug (OTC) treatment for migraine when compounded with aspirin and paracetamol.[54] Even by itself, caffeine can be helpful during an attack,[55][56] despite the fact that in general migraine-sufferers are advised to limit their caffeine intake.[56]
Patients themselves often start off with paracetamol, aspirin, ibuprofen, or other simple analgesics that are useful for tension headaches. OTC drugs may provide some relief, although they are typically not effective for most sufferers.
In all, the U.S. Food and Drug Administration has approved three OTC products specifically for migraine: Excedrin Migraine, Advil Migraine, and Motrin Migraine Pain. Excedrin Migraine, as mentioned above, is a combination of aspirin, acetaminophen, and caffeine. Both Advil Migraine and Motrin Migraine Pain are straight NSAIDs, with ibuprofen as the only active ingredient.[57]
Analgesics combined with antiemetics
Antiemetics by mouth may help relieve symptoms of nausea and help prevent vomiting, which can diminish the effectiveness of orally taken analgesia. In addition some antiemetics such as metoclopramide are prokinetics and help gastric emptying which is often impaired during episodes of migraine. In the UK there are three combination antiemetic and analgesic preparations available: MigraMax (aspirin with metoclopramide), Migraleve (paracetamol/codeine for analgesia, with buclizine as the antiemetic) and paracetamol/metoclopramide (Paramax in UK).[58] The earlier these drugs are taken in the attack, the better their effect.
Some patients find relief from taking other sedative antihistamines which have anti-nausea properties, such as Benadryl which in the US contains diphenhydramine (but a different non-sedative product in the UK).
Serotonin agonists
Main article: triptans
Sumatriptan and related selective serotonin receptor agonists are excellent for severe migraines or those that do not respond to NSAIDs[51] or other over-the-counter drugs.[52] Triptans are a mid-line treatment suitable for many migraineurs with typical migraines. They may not work for atypical or unusually severe migraines, transformed migraines, or status (continuous) migraines.
Selective serotonin reuptake inhibitors (SSRIs) are not approved by the U.S. Food and Drug Administration (FDA) for treatment of migraines, but have been found to be effective by clinical consensus.[50]
Antidepressants
Tricyclic antidepressants have been long established as highly efficacious prophylactic treatments.[50] These drugs, however, may give rise to undesirable side effects, such as insomnia, sedation or sexual dysfunction. SSRIs antidepressants are less established than tricyclics for migraines prophylaxis. Despite the absence of FDA approval for migraine treatment, antidepressants are widely prescribed.[50] In addition to tricyclics and SSRIs, the anti-depressant nefazodone may also be beneficial in the prophylaxis of migraines due to its antagonistic effects on the 5-HT2A[59] and 5-HT2C receptors[60][61] It has a more favorable side effect profile than amitriptyline, a tricyclic antidepressant commonly used for migraine prophylaxis. Anti-depressants offer advantages for treating migraine patients with comorbid depression.[50]
Ergot alkaloids
Until the introduction of sumatriptan in 1991, ergot derivatives (see ergoline) were the primary oral drugs available to abort a migraine once it is established.
Ergot drugs can be used either as a preventive or abortive therapy, though their relative expense and cumulative side effects suggest reserving them as an abortive rescue medicine. However, ergotamine tartrate tablets (usually with caffeine), though highly effective, and long lasting (unlike triptans), have fallen out of favour due to the problem of ergotism. Oral ergotamine tablet absorption is reliable unless the patient is nauseated. Anti-nausea administration is available by ergotamine suppository (or Ergostat sublingual tablets made until circa 1992). Ergot drugs themselves can be so nauseating it is advisable for the sufferer to have something at hand to counteract this effect when first using this drug. Ergotamine-caffeine 1/100 mg fixed ratio tablets (like Cafergot, Ercaf, etc.) are much less expensive per headache than triptans, and are commonly available in Asia and Romania (Cofedol). They are difficult to obtain in the USA. Ergotamine-caffeine can't be regularly used to abort evening or night onset migraines due to debilitating caffeine interference with sleep. Pure ergotamine tartrate is highly effective for evening-night migraines, but is rarely or never available in the USA. Dihydroergotamine (DHE), which must be injected or inhaled, can be as effective as ergotamine tartrate, but is much more expensive than $2 USD Cafergot tablets.
Steroids
Based on a recent meta analysis a single dose of IV dexamethasone, when added to standard treatment, is associated with a 26% decrease in headache recurrence.[62]
Other agents
If over-the-counter medications do not work, or if triptans are unaffordable, the next step for many doctors is to prescribe Fioricet or Fiorinal, which is a combination of butalbital (a barbiturate), paracetamol (in Fioricet) or acetylsalicylic acid (more commonly known as aspirin and present in Fiorinal), and caffeine. While the risk of addiction is low, butalbital can be habit-forming if used daily, and it can also lead to rebound headaches. Barbiturate-containing medications are not available in many European countries.
Amidrine, Duradrin, and Midrin is a combination of acetaminophen, dichloralphenazone, and isometheptene often prescribed for migraine headaches. Some studies have recently shown that these drugs may work better than sumatriptan for treating migraines.[63]
Antiemetics may need to be given by suppository or injection where vomiting dominates the symptoms.
Recently it has been found that calcitonin gene related peptides (CGRPs) play a role in the pathogenesis of the pain associated with migraine as triptans also decrease its release and action. CGRP receptor antagonists such as olcegepant and telcagepant are being investigated both in vitro and in clinical studies for the treatment of migraine.[64]
[edit] Status migrainosus
Status migrainosus is characterized by migraine lasting more than 72 hours, with not more than four hours of relief during that period. It is generally understood that status migrainosus has been refractory to usual outpatient management upon presentation.
Treatment of status migrainosus consists of managing comorbidities (i. e. correcting fluid and electrolyte abnormalities resulting from anorexia and nausea/vomiting often accompanying status migr.), and usually administering parenteral medication to "break" (abort) the headache.
Although the literature is full of many case reports concerning treatment of status migrainosus, first line therapy consists of intravenous fluids, metoclopramide, and triptans or DHE.[65]
[edit] Herbal treatment
The herbal supplement feverfew (more commonly used for migraine prevention, see below) is marketed by the GelStat Corporation as an OTC migraine abortive, administered sublingually (under the tongue) in a mixture with ginger.[66] An open-label study (funded by GelStat) found some tentative evidence of the treatment's effectiveness,[67] but no scientifically sound study has been done. Cannabis, in addition to prevention, is also known to relieve pain during the onset of a migraine.

Heart diseases

2010-06-17T02:13:00.001-07:00

Heart disease
Heart disease or cardiopathy is an umbrella term for a variety of different diseases affecting the heart. As of 2007, it is the leading cause of death in the United States,[1][2] England, Canada and Wales,[3] killing one person every 34 seconds in the United States alone.

Types of heart disease
Coronary heart disease
Main article: Coronary heart disease
Coronary heart disease refers to the failure of the coronary circulation to supply adequate circulation to cardiac muscle and surrounding tissue. Coronary heart disease is most commonly equated with Coronary artery disease although coronary heart disease can be due to other causes, such as coronary vasospasm.[5]
Coronary artery disease is a disease of the artery caused by the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium. Angina pectoris (chest pain) and myocardial infarction (heart attack) are symptoms of and conditions caused by coronary heart disease.
Over 459,000 Americans die of coronary heart disease every year[6]. In the United Kingdom, 101,000 deaths annually are due to coronary heart disease.[7]
Cardiomyopathy
Cardiomyopathy literally means "heart muscle disease" (Myo= muscle, pathy= disease) It is the deterioration of the function of the myocardium (i.e., the actual heart muscle) for any reason. People with cardiomyopathy are often at risk of arrhythmia and/or sudden cardiac death.
• Extrinsic cardiomyopathies – cardiomyopathies where the primary pathology is outside the myocardium itself. Most cardiomyopathies are extrinsic, because by far the most common cause of a cardiomyopathy is ischemia. The World Health Organization calls these specific cardiomyopathies[citation needed]:
o Alcoholic cardiomyopathy
o Coronary artery disease
o Congenital heart disease
o Nutritional diseases affecting the heart
o Ischemic (or ischaemic) cardiomyopathy
o Hypertensive cardiomyopathy
o Valvular cardiomyopathy – see also Valvular heart disease below
o Inflammatory cardiomyopathy – see also Inflammatory heart disease below
o Cardiomyopathy secondary to a systemic metabolic disease
o Myocardiodystrophy
• Intrinsic cardiomyopathies – weakness in the muscle of the heart that is not due to an identifiable external cause.
o Dilated cardiomyopathy (DCM) – most common form, and one of the leading indications for heart transplantation. In DCM the heart (especially the left ventricle) is enlarged and the pumping function is diminished.
o Hypertrophic cardiomyopathy (HCM or HOCM) – genetic disorder caused by various mutations in genes encoding sarcomeric proteins. In HCM the heart muscle is thickened, which can obstruct blood flow and prevent the heart from functioning properly.
o Arrhythmogenic right ventricular cardiomyopathy (ARVC) – arises from an electrical disturbance of the heart in which heart muscle is replaced by fibrous scar tissue. The right ventricle is generally most affected.
o Restrictive cardiomyopathy (RCM) – least common cardiomyopathy. The walls of the ventricles are stiff, but may not be thickened, and resist the normal filling of the heart with blood.
o Noncompaction Cardiomyopathy – the left ventricle wall has failed to properly grow from birth and such has a spongy appearance when viewed during an echocardiogram.
Cardiovascular disease
Cardiovascular disease is any of a number of specific diseases that affect the heart itself and/or the blood vessel system, especially the veins and arteries leading to and from the heart. Research on disease dimorphism suggests that women who suffer with cardiovascular disease usually suffer from forms that affect the blood vessels while men usually suffer from forms that affect the heart muscle itself. Known or associated causes of cardiovascular disease include diabetes mellitus, hypertension, hyperhomocysteinemia and hypercholesterolemia.
Types of cardiovascular disease include:
• Atherosclerosis
Ischaemic heart disease
• Ischaemic heart disease – another disease of the heart itself, characterized by reduced blood supply to the organs.
Heart failure
Heart failure, also called congestive heart failure (or CHF), and congestive cardiac failure (CCF), is a condition that can result from any structural or functional cardiac disorder that impairs the ability of the heart to fill with or pump a sufficient amount of blood throughout the body. Therefore leading to the heart and body's failure.
• Cor pulmonale, a failure of the right side of the heart.
Hypertensive heart disease
Hypertensive heart disease is heart disease caused by high blood pressure, especially localised high blood pressure. Conditions that can be caused by hypertensive heart disease include:
• Left ventricular hypertrophy
• Coronary heart disease
• (Congestive) heart failure
• Hypertensive cardiomyopathy
• Cardiac arrhythmias
Inflammatory heart disease
Inflammatory heart disease involves inflammation of the heart muscle and/or the tissue surrounding it.
• Endocarditis – inflammation of the inner layer of the heart, the endocardium. The most common structures involved are the heart valves.
• Inflammatory cardiomegaly
• Myocarditis – inflammation of the myocardium, the muscular part of the heart.
Valvular heart disease
Valvular heart disease is disease process that affects one or more valves of the heart. There are four major heart valve which may be affected by valvular heart disease, including the tricuspid and aortic valves in the right side of the heart, as well as the mitral and aortic valves in the left side of the heart.

Hypertension Treatment

2010-06-17T02:12:00.000-07:00

Hypertension
Treatment
Lifestyle modifications
The first line of treatment for hypertension is the same as the recommended preventative lifestyle changes such as the dietary changes, physical exercise, and weight loss, which have all been shown to significantly reduce blood pressure in people with hypertension.[55] If hypertension is high enough to justify immediate use of medications, lifestyle changes are still recommended in conjection with medication.
Biofeedback
Biofeedback devices can be used alone or in conjunction with lifestyle changes and/or medications to reduce hypertension. One example of Biofeedback is Resperate, a portable, battery-operated personal therapeutic medical device, sold over the counter in the United States. However, claims of efficacy for this particular device are not supported by scientific studies. Testimonials are used to promote such products, while no real evidence exists that the use of

Medications
Main article: Antihypertensive drugs
There are many classes of medications for treating hypertension, together called antihypertensives, which — by varying means — act by lowering blood pressure. Reduction of the blood pressure by 5–6 mmHg can decrease the risk of stroke by 40%, decrease the risk of heart disease by 15–20%, and reduce the likelihood of dementia, heart failure, and death.
The aim of treatment should be reduce blood pressure to <140/90 mmHg for most individuals, and lower individuals with diabetes or kidney disease (some medical professionals recommend keeping levels below 120/80 mmHg).[56] Each drug reduces systolic blood pressure by about 5–10 mmHg, so often multiple drugs are combined to achieve the goal blood pressure.
Commonly used prescription drugs include:[5]
• ACE inhibitors such as captopril, enalapril, fosinopril (Monopril), lisinopril (Zestril), quinapril, ramipril (Altace)
• Angiotensin II receptor antagonists may be used where ACE inhibitors are not tolerated: e.g., telmisartan (Micardis, Pritor), irbesartan (Avapro), losartan (Cozaar), valsartan (Diovan), candesartan (Amias), olmesartan (Benicar, Olmetec)
• Calcium channel blockers such as nifedipine (Adalat)[57] amlodipine (Norvasc), diltiazem, verapamil
• Diuretics: e.g., bendroflumethiazide, chlorthalidone, hydrochlorothiazide (also called HCTZ).
Other less commonly used prescription drugs include:
• Diuretics such a furosemide or low-dosages of spironolactone
• Alpha blockers such as prazosin, or terazosin. Doxazosin has been shown to the increase risk of heart failure, and to be less effective than a diuretics.[58]
• Beta blockers such as atenolol, labetalol, metoprolol (Lopressor, Toprol-XL), propranolol. Whilst once were first line agents, now they are less commonly used because they increase the risk of diabetes.[59]
• Direct renin inhibitors such as aliskiren (Tekturna).[60]

Anti-diabetic drug

2010-06-17T02:09:00.000-07:00

Anti-diabetic drug

Anti-diabetic drugs treat diabetes mellitus by lowering glucose levels in the blood. With the exceptions of insulin, exenatide, and pramlintide, all are administered orally and are thus also called oral hypoglycemic agents or oral antihyperglycemic agents. There are different classes of anti-diabetic drugs, and their selection depends on the nature of the diabetes, age and situation of the person, as well as other factors.
Diabetes mellitus type 1 is a disease caused by the lack of insulin. Insulin must be used in Type I, which must be injected or inhaled.
Diabetes mellitus type 2 is a disease of insulin resistance by cells. Treatments include (1) agents which increase the amount of insulin secreted by the pancreas, (2) agents which increase the sensitivity of target organs to insulin, and (3) agents which decrease the rate at which glucose is absorbed from the gastrointestinal tract.
Several groups of drugs, mostly given by mouth, are effective in Type II, often in combination. The therapeutic combination in Type II may include insulin, not necessarily because oral agents have failed completely, but in search of a desired combination of effects. The great advantage of injected insulin in Type II is that a well-educated patient can adjust the dose, or even take additional doses, when blood glucose levels measured by the patient, usually with a simple meter, as needed by the measured amount of sugar in the blood.
Contents
• 1 Insulin
• 2 Secretagogues
o 2.1 Sulfonylureas
o 2.2 Meglitinides
• 3 Sensitizers
o 3.1 Biguanides
o 3.2 Thiazolidinediones
• 4 Alpha-glucosidase inhibitors
• 5 Peptide analogs
o 5.1 Incretin mimetics
 5.1.1 Glucagon-like peptide (GLP) analogs and agonists
 5.1.2 Gastric inhibitory peptide (GIP) analogs
o 5.2 DPP-4 inhibitors
o 5.3 Amylin analogues
• 6 Experimental agents
• 7 Alternative medicine
• 8 Notes
• 9 References

Insulin
Insulin is usually given subcutaneously, either by injections or by an insulin pump. Research is underway of other routes of administration. In acute care settings, insulin may also be given intravenously. There are several types of insulin, characterized by the rate which they are metabolized by the body.
Secretagogues
Sulfonylureas
Sulfonylureas were the first widely used oral hypoglycemic medications. They are insulin secretagogues, triggering insulin release by direct action on the KATP channel of the pancreatic beta cells. Eight types of these pills have been marketed in North America, but not all remain available. The "second-generation" drugs are now more commonly used. They are more effective than first-generation drugs and have fewer side effects. All may cause weight gain.
Sulfonylureas bind strongly to plasma proteins. Sulfonylureas are only useful in Type II diabetes, as they work by stimulating endogenous release of insulin. They work best with patients over 40 years old, who have had diabetes mellitus for under ten years. They can not be used with type I diabetes, or diabetes of pregnancy. They can be safely used with metformin or -glitazones. The primary side effect is hypoglycemia.
Typical reductions in A1C values for second generation sulfonylureas are 1.0-2.0%.
• First-generation agents
o tolbutamide (Orinase)
o acetohexamide (Dymelor)
o tolazamide (Tolinase)
o chlorpropamide (Diabinese)
• Second-generation agents
o glipizide (Glucotrol)
o glyburide (Diabeta, Micronase, Glynase)
o glimepiride (Amaryl)
o gliclazide (Diamicron)
Meglitinides
Meglitinides help the pancreas produce insulin and are often called "short-acting secretagogues." They act on the same potassium channels as sulfonylureas, but at a different binding site.[1] By closing the potassium channels of the pancreatic beta cells, they open the calcium channels, hence enhancing insulin secretion.[2]
They are taken with or shortly before meals to boost the insulin response to each meal. If a meal is skipped, the medication is also skipped.
Typical reductions in A1C values are 0.5-1.0%.
• repaglinide (Prandin)
• nateglinide (Starlix)
Adverse reactions include weight gain and hypoglycemia.
Sensitizers
Insulin sensitizers address the core problem in Type II diabetes—insulin resistance. Among oral hypoglycemic agents, insulin sensitizers are the largest category.[3]
Biguanides
Main article: Biguanide
Biguanides reduce hepatic glucose output and increase uptake of glucose by the periphery, including skeletal muscle. Although it must be used with caution in patients with impaired liver or kidney function, metformin, a biguanide, has become the most commonly used agent for type 2 diabetes in children and teenagers. Amongst common diabetic drugs, metformin is the only widely used oral drug that does not cause weight gain.
Typical reductions in A1C values for metformin is 1.5-2.0%.
• metformin (Glucophage). Metformin may be the best choice for patients who also have heart failure.[4] Should be temporarily discontinued before any radiographic procedure involving intravenous iodinated contrast as patients are at an increased risk of lactic acidosis.
• phenformin (DBI): used from 1960s through 1980s, withdrawn due to lactic acidosis risk.[5]
• buformin: also withdrawn due to lactic acidosis risk.[6]
Metformin is usually the first-line medication used for treatment of type-2 diabetes. It is generally prescribed at initial diagnosis in conjunction with exercise and weight loss as opposed to in the past, where Metformin was prescribed after diet and exercise had failed. Initial dosing is 500 mg once daily, then if need be increased to 500 mg twice daily up to 1000 mg twice daily. It is also available in combination with other oral diabetic medications.
There is an extended release formulation available, but it is typically reserved for patients experiencing GI side effects.
Thiazolidinediones
Main article: Thiazolidinedione
Thiazolidinediones (TZDs), also known as "glitazones," bind to PPARγ, a type of nuclear regulatory protein involved in transcription of genes regulating glucose and fat metabolism. These PPARs act on Peroxysome Proliferator Responsive Elements (PPRE [1]). The PPREs influence insulin sensitive genes, which enhance production of mRNAs of insulin dependent enzymes. The final result is better use of glucose by the cells.
Typical reductions in A1C values are 1.5-2.0%.
• rosiglitazone (Avandia)
• pioglitazone (Actos)
• troglitazone (Rezulin): used in 1990s, withdrawn due to hepatitis and liver damage risk.[7]
As a result of multiple retrospective studies, there is a concern about rosiglitazone's safety, although it is established that the group, as a whole, has beneficial effects on diabetes. The greatest concern is an increase in the number of severe cardiac events in patients taking it. The ADOPT study showed that initial therapy with drugs of this type may prevent the progression of disease,[8] as did the DREAM trial.[9]
Concerns about the safety of rosiglitazone arose when a retrospective meta-analysis was published in the New England Journal of Medicine.[10] There have been a significant number of publications since then, and a Food and Drug Administration panel[11] voted, with some controversy, 20:3 that available studies "supported a signal of harm," but voted 22:1 to keep the drug on the market. The meta-analysis was not supported by an interim analysis of the trial designed to evaluate the issue, and several other reports have failed to conclude the controversy. This weak evidence for adverse effects has reduced the use of rosiglitazone, despite its important and sustained effects on glycemic control.[12] Safety studies are continuing.
In contrast, at least one large prospective study, PROactive 05, has shown that pioglitazone may decrease the overall incidence of cardiac events in people with type II diabetes who have already had a heart attack.[13]
Alpha-glucosidase inhibitors
Alpha-glucosidase inhibitors are "diabetes pills" but not technically hypoglycemic agents because they do not have a direct effect on insulin secretion or sensitivity. These agents slow the digestion of starch in the small intestine, so that glucose from the starch of a meal enters the bloodstream more slowly, and can be matched more effectively by an impaired insulin response or sensitivity. These agents are effective by themselves only in the earliest stages of impaired glucose tolerance, but can be helpful in combination with other agents in type 2 diabetes.
Typical reductions in A1C values are 0.5-1.0%.
• miglitol (Glyset)
• acarbose (Precose/Glucobay)
These medications are rarely used in the United States because of the severity of their side effects (flatulence and bloating). They are more commonly prescribed in Europe. They do have the potential to cause weight loss by lowering the amount of sugar metabolized.
Research has shown the culinary mushroom Maitake (Grifola frondosa) has a hypoglycemic effect,[14][15][16][17][18][19] possibly due to the fact the mushroom naturally acts as an alpha-glucosidase inhibitor.[20]
Peptide analogs

Overview of insulin secretion
Incretin mimetics
Incretins are insulin secretagogues. The two main candidate molecules that fulfill criteria for being an incretin are Glucagon-like peptide-1 (GLP-1) and Gastric inhibitory peptide (aka glucose-dependent Insulinotropic peptide or GIP). Both GLP-1 and GIP are rapidly inactivated by the enzyme dipeptidyl peptidase-4 (DPP-4).
Glucagon-like peptide (GLP) analogs and agonists
GLP agonists bind to a membrane GLP receptor.[2] As a consequence of this, insulin release from the pancreatic beta cells is increased. Endogenous GLP has a half life of only a few minutes; thus an analogue of GLP would not be practical.
• Exenatide (also Exendin-4, marketed as Byetta) is the first GLP-1 agonist approved for the treatment of type 2 diabetes. Exenatide is not an analogue of GLP, but rather a GLP agonist.[21][22] Exenatide has only 53% homology with GLP, which increases its resistance to degradation by DPP-4 and extends its half-life.[23] Typical reductions in A1C values are 0.5-1.0%.
• Liraglutide, a once daily human analogue (97% homology), is being developed by Novo Nordisk under the brand name Victoza. The product was approved by the European Medicines Agency (EMEA) on July 3, 2009, and by the U.S. Food and Drug Administration (FDA) on January 25, 2010.[24][25][26][27][28][29]
• Taspoglutide is presently in Phase III Clinical Trials with Hoffman-La Roche.
These agents may also cause a decrease in gastric motility, responsible for the common side effect of nausea, and is probably the mechanism by which weight loss occurs.
Gastric inhibitory peptide (GIP) analogs
• None are FDA approved
DPP-4 inhibitors
Dipeptidyl peptidase-4 (DPP-4) inhibitors increase blood concentration of the incretin GLP-1 (glucagon-like peptide-1) by inhibiting its degradation by dipeptidyl peptidase-4 (DPP-4).
Typical reductions in A1C values are 0.5-1.0%.
Examples are:
• vildagliptin (Galvus) EU Approved 2008.
• sitagliptin (Januvia) FDA approved Oct 2006.
• saxagliptin (Onglyza) FDA Approved July 2009.
Amylin analogues
Amylin agonist analogues slow gastric emptying and suppress glucagon. They have all the incretins actions except stimulation of insulin secretion. As of 2007, pramlintide is the only clinically available amylin analogue. Like insulin, it is administered by subcutaneous injection. The most frequent and severe adverse effect of pramlintide is nausea, which occurs mostly at the beginning of treatment and gradually reduces. Typical reductions in A1C values are 0.5-1.0%.
Experimental agents
Many other potential drugs are currently in investigation by pharmaceutical companies. Some of these are simply newer members of one of the above classes, but some work by novel mechanisms. For example, at least one compound that enhances the sensitivity of glucokinase to rising glucose is in the stage of animal research. Others are undergoing phase I/II studies.
• PPARα/γ ligands (muraglitazar and tesaglitazar - development stopped due to adverse risk profile, aleglitazar - under clinical development)
• SGLT2 (sodium-dependent glucose transporter 2) inhibitors increase urinary glucose.
• FBPase (fructose 1,6-bisphosphatase) inhibitors decrease gluconeogenesis in the liver.
Alternative medicine
A recent review article presents the profiles of plants with hypoglycaemic properties, reported in the literature from 1990 to 2000 and states that "Medical plants play an important role in the management of diabetes mellitus especially in developing countries where resources are meager."[30]
The first registered use of anti-diabetic drugs was as herbal extracts used by Indians in the Amazon Basin for the treatment of type 2 diabetes, and today promoted as vegetable insulin although not formally an insulin analog.[31] The major recent development was done in Brazil around Myrcia sphaerocarpa and other Myrcia species.[32] The usual treatment is with concentrated (root) Myrcia extracts, commercialized as "Pedra hume de kaá". Phytochemical analysis of the Myrcia extracts reported kinds of flavanone glucosides (myrciacitrins) and acetophenone glucosides (myrciaphenones), and inhibitory activities on aldose reductase and alpha-glucosidase.[33]
Walnut leaf can significantly reduce fasting blood glucose levels in rats with alloxan-induced diabetes, and rats thus treates show some evidence of regeneration of the beta cells.[34] Garlic also significantly reduces fasting blood glucose levels in rats with alloxan-induced diabetes.[35]
At least two studies have shown that cinnamon can act significantly reducing some effects of diabetes. One study on people used fine ground cassia (Cinnamomum aromaticum) for oral consumption. Another study used an extract (MHCP) on laboratory rats. The study on people published in 2003 conducted in the Department of Human Nutrition, NWFP Agricultural University, Peshawar, Pakistan concluded "that the inclusion of cinnamon in the diet of people with type 2 diabetes will reduce risk factors associated with diabetes and cardiovascular diseases."[36] The study on laboratory rats at Department of Biochemistry, Biophysics and Molecular Biology, Iowa State University published in 2001 used purified hydroxychalcone (MHCP) from cinnamon. Part of the study's conclusion stated that "the MHCP is fully capable of mimicking insulin" and recommended further studies.[37][38] The Food and Drug Administration has not yet evaluated the use of cinnamon for the management of diabetes. It should be noted that the spice sold as cinnamon is often obtained from C. verum (true cinnamon), not C. aromaticum (cassia).
Research has shown the Maitake mushroom (Grifola frondosa) has a hypoglycemic effect, and may be beneficial for the management of diabetes.[14][15][16][17][18][19] The reason Maitake lowers blood sugar is due to the fact the mushroom naturally acts as an alpha glucosidase inhibitor.[2] Other mushrooms like Reishi,[39][40] Agaricus blazei,[41][42][43][44] Agrocybe cylindracea[45] and Cordyceps[46][47][48][49][50] have been noted to lower blood sugar levels to a certain extent, although the mechanism is currently unknown.
Cinnamon
Though not yet evaluated by the Food and Drug Administration, at least two studies have shown that cinnamon can act significantly reducing some effects of diabetes. One study on people used fine ground cinnamon (Cinnamomum cassia) for oral consumption. Another study used an extract (MHCP) on laboratory rats.
The study on people published in 2003 conducted in the Department of Human Nutrition, NWFP Agricultural University, Peshawar, Pakistan concluded:
The results of this study demonstrate that intake of 1, 3, or 6 g of cinnamon per day reduces serum glucose, triglyceride, LDL cholesterol, and total cholesterol in people with type 2 diabetes and suggest that the inclusion of cinnamon in the diet of people with type 2 diabetes will reduce risk factors associated with diabetes and cardiovascular diseases.[51]
The study on laboratory rats at Department of Biochemistry, Biophysics and Molecular Biology, Iowa State University published in 2001 used purified hydroxychalcone from cinnamon. The extract was named "MHCP". Part of the study's conclusion stated that "the MHCP is fully capable of mimicking insulin" and recommended further studies.[52][53]
Other studies have failed to reproduce these results, and, because large doses of cinnamon are not innocuous, some experts advise against treatment of diabetes with cinnamon.[54]
Chromium and vanadium
Chromium - Cholesterol and triglycerides are risk factors in heart disease and diabetes, and studies show that chromium lowers levels of total cholesterol, LDL cholesterol, and triglycerides.[55][56][57][58] Chromium supplements such as chromium picolinate have been shown to improve glucose tolerance in people with type 2 diabetes,[59][60][61] although other studies have not replicated this result.[62] A meta analysis of these trials concluded that chromium supplements had no beneficial effect on healthy people, but that there might be an improvement in glucose metabolism in diabetics, although the authors stated that the evidence for this effect remains weak.[63]
Vanadium - A form of vanadium, vanadyl sulfate, seems to improve glucose control in people with type 2 diabetes.[64][65][66][67][68]
A pilot study has also found evidence that Tai Chi and Qigong reduce the severity of type 2 diabetes.[69]
Benfotiamine, a pro-vitamin of vitamin B1 which has been in use in Europe as an over-the-counter medicine for alcoholic neuropathy for the past half century with no significant side-effects or toxicity, has recently been found to block the major metabolic pathways by which excess blood glucose in the body is transformed into the advanced glycation endproducts (AGEs) which cause diabetic complications.[70] Studies have shown that taking oral benfotiamine can prevent diabetic retinopathy,[71] diabetic neuropathy,[72] and diabetic nephropathy[73] independently of any affect on the blood sugar levels of the patient. In theory, taking benfotiamine might allow patients to be less scrupulous in trying to normalize blood sugar levels and thus free them from the danger of hypoglycemia and the stress of stringent blood sugar monitoring, while still protecting them against the negative effects of hyperglycemia. Research is ongoing to establish the full significance of benfotiamine in the treatment of diabetes.
Traditional plant treatments for diabetes
A study was made of the effects on glucose homeostasis in normal and streptozotocin (induced) diabetic mice of eleven plants that have been used as traditional treatments for diabetes. The mice were given diets containing dried leaves from the following plants: agrimony (Agrimonia eupatoria), alfalfa (Medicago sativa), blackberry (Rubus fructicosus), celandine (Chelidonium majus), eucalyptus (Eucalyptus globulus), lady's mantle (Alchemilla vulgaris), and lily of the valley (Convallaria majalis); seeds of coriander (Coriandrum sativum); dried berries of juniper (Juniperus communis); bulbs of garlic (Allium sativum) and roots of liquorice (Glycyrhizza glabra). The study concluded that "The results suggest that certain traditional plant treatments for diabetes, namely agrimony, alfalfa, coriander, eucalyptus and juniper, can retard the development of streptozotocin diabetes in mice".[74]
Mushrooms
Research has shown the Maitake mushroom (Grifola frondosa) has a hypoglycemic effect, and may be beneficial for the management of diabetes.[14][15][16][17][18][19] The reason Maitake lowers blood sugar is due to the fact the mushroom naturally acts as an alpha glucosidase inhibitor.[75] Other mushrooms like Reishi,[39][40] Agaricus blazei,[41][42][43][76] Agrocybe cylindracea[77] and Cordyceps[46][47][48][49][50] have been noted to lower blood sugar levels to a certain extent, although the mechanism is currently unknown.
Aloe vera Oral administration of aloe vera might be a useful adjunct for lowering blood glucose in diabetic patients as well as for reducing blood lipid levels in patients with hyperlipidaemia[citation needed]. Ten controlled clinical trials were found to reach that conclusion in four independent literature searches. However, caveats reported in each study led the researchers to conclude that aloe vera's clinical effectiveness was not yet sufficiently defined in 1999.[78]

Huntington's disease -clinical research

2010-06-17T02:07:00.000-07:00

Huntington's disease clinical research
There are different therapies under investigation for Huntington's disease. Huntington's disease is a is a genetic neurological disorder characterized after onset by uncoordinated, jerky body movements and a decline in some mental abilities for which there is no cure or effective treatments. Animal models help in the ongoing investigations using intrabody therapy, gene silencing, or stem cell implants, but all are at their first steps. Several clinical trials of various compounds are also in development. Many of these trials use the unified Huntington's disease rating scale (UHDRS) developed by the Huntington's Study Group.[1] This provides an overall rating system based on motor, behavioral, cognitive, and functional assessments, backed up by a reference database of previous results provided by HSG for reference.[2] Another avenue of research is understanding the physical mechanics of protein folding, HD is one of several targets of the folding@home project,[3] one of the largest distributed computing systems on the World Wide Web.
Contents
• Animal models
• Intrabody therapy
• Gene silencing
• Stem cell treatments
• Pharmacological
Animal models

A laboratory mouse
Appropriate animal models are critical for understanding the fundamental mechanisms causing the disease and for supporting the early stages of drug development. Neurochemically-induced mice or monkeys were first available,[5][6] but they did not mimic the progressive features of the disease. After the HD gene was discovered, transgenic animals exhibiting HD were generated by inserting a CAG repeat expansion into the genome, of mice (strain R6/2),[7][8]), Drosophila fruit flies,[9] and more recently monkeys.[10] Expression without insertion of a DNA repeat in nematode worms also produced a valuable model.[11]
Intrabody therapy
Genetically-engineered intracellular antibody fragments called intrabodies have shown therapeutic results, by inhibiting mHtt aggregation, in Drosophila models. This was achieved using an intrabody called C4 sFv, a single chain variable fragment which binds to the end of mHtt within a cell. This therapy prevented larval and pupal mortality (without therapy 77% died) and delayed neurodegeneration in the adult, significantly increasing their lifespan.[14] Intrabodies have shown promise as a useful tool for drug discovery, and may potentially be used as a therapy for HD and other neurodegenerative disorders caused by protein mis-folding or abnormal protein interactions.
Gene silencing
As HD has been conclusively linked to a single gene, gene silencing is potentially possible. Researchers have investigated using gene knockdown of mHTT as a potential treatment. Using a mouse model, siRNA therapy achieved a 60% reduction in expression of mHTT and progression of the disease was stalled.[17] However, this study used the human form of the mHTT protein in mice, and was therefore only able to directly target the mHTT, leaving endogenous, wild-type mouse Htt gene expression unaffected. From a practical standpoint, it would be difficult in humans to use siRNA to target the mutant form while leaving the normal copy unaffected. The precise function of Hyy is unknown, but in mice, complete deletion of the Htt gene is lethal. Thus, using RNA interference to treat HD could have unexpected effects unless knock-down of the normal Htt protein can be avoided. Other issues include problems delivering the siRNA to the appropriate target tissue, off-target effects of siRNA, and toxicity from shRNA over-expression. Another study showed that mouse models already in late stages of the disease recovered motor function after expression of mHTT was stopped.
Stem cell treatments
Main article: Stem cell treatments
Stem cell implants are a stem cell treatment where damaged neurons are replaced by transplantation of stem cells (or possibly neural stem cells—a type of somatic [adult] stem cell) into affected regions of the brain. Hypothetically, embryonic stem cells can be differentiated into neuronal precursors in vitro, and transplanted into damaged areas of the brain to generate replacement neurons; if enough damaged neurons can be replaced and develop the correct synaptic connectivity, symptoms could be alleviated. This treatment would not prevent further neuronal damage, so it would have to be an ongoing treatment. Experiments have yielded some positive results in animal models, but stem cell treatment for HD remains highly speculative and has not been tested in clinical trials.
Pharmacological
As of August 2008, several trials of various compounds are in development or ongoing,[22] a few at the point of testing on larger numbers of people, known as phase III of clinical trials. Substances that have shown promise in initial experiments include dopamine receptor blockers, select dopamine antagonists, such as creatine and CoQ10, the antibiotic Minocycline, antioxidant-containing foods and nutrients, and antidepressants, including selective serotonin reuptake inhibitors such as sertraline, fluoxetine, and paroxetine. A recent study suggested strong association between specific single nucleotide polymorphisms alleles and CAG expansion also provides an opportunity of personalized therapeutics in HD where the clinical development of only a small number of allele-specific targets may be sufficient to treat up to 88% of the HD patient population.

DIALYSIS

2010-06-17T02:06:00.000-07:00

DIALYSIS

What is dialysis?
The kidneys are responsible for filtering waste products from the blood. Dialysis is a procedure that is a substitute for many of the normal duties of the kidneys. The kidneys are two organs located on either side of the back of the abdominal cavity. Dialysis can allow individuals to live productive and useful lives, even though their kidneys no longer work adequately. In the United States, there are over 200,000 people who use dialysis techniques on an ongoing basis.
Dialysis helps the body by performing the functions of failed kidneys. The kidney has many roles. An essential job of the kidney is to regulate the body's fluid balance. It does this by adjusting the amount of urine that is excreted on a daily basis. On hot days, the body sweats more. Thus, less water needs to be excreted through the kidneys. On cold days, the body sweats less. Thus, urine output needs to be greater in order to maintain the proper balance within the body. It is the kidney's job to regulate fluid balance by adjusting urine output.
Another major duty of the kidney is to remove the waste products that the body produces throughout the day. As the body functions, the cells use energy. The operation of the cells produces waste products that must be removed from the body. When these waste products are not removed adequately, they build up in the body. An elevation of waste products, as measured in the blood, is called "azotemia." When waste products accumulate they, cause a sick feeling throughout the body called "uremia."
When do patients require dialysis?

Patients usually require dialysis when the waste products in their body become so high that they start to become sick from them. The level of the waste products usually builds up slowly. Doctors measure several blood chemical levels to help decide when dialysis is necessary. The two major blood chemical levels that are measured are the "creatinine level" and the "blood urea nitrogen" (BUN) level. As these two levels rise, they are indicators of the decreasing ability of the kidneys to cleanse the body of waste products.
Doctors use a urine test, the "creatinine clearance," to measure the level of kidney function. The patient saves urine in a special container for one full day. The waste products in the urine and in the blood are estimated by measuring the creatinine. By comparing the blood and urine level of this substance, the doctor has an accurate idea of how well the kidneys are working. This result is called the creatinine clearance. Usually, when the creatinine clearance falls to 10-12 cc/minute, the patient needs dialysis.
The doctor uses other indicators of the patient's status to decide about the need for dialysis. If the patient is experiencing a major inability to rid the body of excess water, or is complaining of problems with the heart, lungs, or stomach, or difficulties with taste or sensation in their legs, dialysis may be indicated even though the creatinine clearance has not fallen to the 10-12 cc/minute level.

What types of dialysis are there?

There are two main types of dialysis: "hemodialysis" and "peritoneal dialysis." Hemodialysis uses a special type of filter to remove excess waste products and water from the body. Peritoneal dialysis uses a fluid that is placed into the patient's stomach cavity through a special plastic tube to remove excess waste products and fluid from the body.
During Hemodialysis, blood passes from the patient's body through a filter in the dialysis machine, called a "dialysis membrane." For this procedure, the patient has a specialized plastic tube placed between an artery and a vein in the arm or leg (called a "gortex graft"). Sometimes, a direct connection is made between an artery and a vein in the arm. This procedure is called a "Cimino fistula." Needles are then placed in the graft or fistula, and blood passes to the dialysis machine, through the filter, and back to the patient. In the dialysis machine, a solution on the other side of the filter receives the waste products from the patient.
Peritoneal dialysis uses the patients own body tissues inside of the belly (abdominal cavity) to act as the filter. The intestines lie in the abdominal cavity, the space between the abdominal wall and the spine. A plastic tube called a "dialysis catheter" is placed through the abdominal wall into the abdominal cavity. A special fluid is then flushed into the abdominal cavity and washes around the intestines. The intestinal walls act as a filter between this fluid and the blood stream. By using different types of solutions, waste products and excess water can be removed from the body through this process.

What does the patient do during dialysis?

Hemodialysis

Treatment for hemodialysis takes place in a hemodialysis unit. This is a special building that is equipped with machines that perform the dialysis treatment. Special equipment adds the proper materials to purified water for the dialysis machines. The dialysis unit is also the place where patients can receive dietary counseling and help with social needs.
Patients generally go to the dialysis unit three times a week for treatment. For example, the schedule is either on Monday, Wednesday, and Friday or Tuesday, Thursday, and Saturday. Before treatment, patients weigh themselves so that excess fluid accumulated since the last dialysis session can be measured. Patients then go to assigned chairs that are like lounge chairs. The area of the graft or fistula (the connection between the artery and vein), is cleaned thoroughly. Two needles are then inserted into the graft or fistula. One takes the blood to the machine where it is cleaned. The other needle allows blood that is returning to the patient to go back into the patient's body.
Treatments last from 2 ½ to 4 ½ hours. During this time, the dialysis staff checks the patient's blood pressure frequently and adjusts the dialysis machine to ensure that the proper amount of fluid is being removed from the patients body. Patients can read, watch television, sleep, or do other work during treatment.
Peritoneal Dialysis

Peritoneal dialysis requires the patient to play a more active role in their dialysis treatment. Of primary importance is the patient's responsibility for maintaining a clean surface on the abdomen, where treatment is administered, in order to prevent infection.
In this process, the patient weighs herself/himself to determine the fluid to be used. The patient then puts on a mask and cleans the peritoneal catheter site. Fluid that has been allowed to stay in the peritoneal cavity is drained back into the plastic bag that originally contained the fluid. The patient then disconnects this bag and connects a new bag of solution that is allowed to drain into the peritoneal cavity. Once the fluid is in the body, the new bag is rolled up and placed in the patient's underwear until the next treatment. This procedure usually takes 30 minutes to accomplish and must be done four to five times a day.
As an alternative to this treatment, some patients on peritoneal dialysis use a machine called a "cycler." This cycler is used every night. Five to six bags of dialysis fluid is used on the cycler and the machine automatically changes the fluid while the patient sleeps.

What are the advantages of the different types of dialysis?

Each of the two types of dialysis, hemodialysis and peritoneal dialysis, has advantages and disadvantages. It is up to the patient to decide which of these procedures is best by considering her/his life style, other medical conditions, support systems, and how much responsibility and participation in the treatment program he/she desires. Each patient must view the two types of dialysis procedures from her/his own perspective.
Regardless of which type of dialysis is chosen , patients have certain responsibilities such as following a diet program, watching their fluid intake and taking special vitamins and other medicines to control blood pressure and calcium and phosphorus balance.
For many patients, the major advantage of hemodialysis is minimal participation in the treatment. However, patients are required to adhere to a specific schedule and travel to the dialysis unit. Hemodialysis also requires stricter diet control and fluid control than peritoneal dialysis.
For those patients preferring more independence, peritoneal dialysis allows for more flexible scheduling and can be performed at home. The patient still must undergo a certain amount of dialysis each day, but can alter the exact timing of the dialysis procedure. On the other hand, peritoneal dialysis must be done every day of the week.
The major problem with peritoneal dialysis is infection. The patient has a plastic tube that goes from the peritoneal cavity to the outside of the body and this is a potential site for the entry of bacteria into the body. Great emphasis is placed on cleanliness and technique during the training sessions.

Indications and contraindications of dialysis

Indications for Dialysis -In Chronic Renal Failure
In patients with chronic renal failure factors to be considered before initiating dialysis should include comorbid conditions and patient preference. Timing of therapy is dictated by serum chemistries and symptoms.
A) Absolute indications
Uremic Pericarditis
Uremic Encephalopathy or Neuropathy
Pulmonary edema (unresponsive to diuretics)
Severe Hypertension
Severe hyperkalemia
Intractable acidosis
Severe Bleeding diathesis
Persistent gastrointestinal symptoms
S.Creatinine more than 12 mg/dl, BUN more than 100 mg/dl
B) Relative indications
Mild encephalopathy or neuropathy
Severe edema (unresponsive to diuretics)
Progressive gastrointestinal symptoms
Recurrent GI “itis”: stomatitis, gastritis, dudenitis, pancreatitis
Ascitis without hepatic disease
Anemia refractor to Erythropoietin
Mild Bleeding diathesis
Pruritus
Infectious complications
Depression
C) Early indications
Decrease ideal body weight
Decrease in muscle mass (decrease s creatinine or its clearance)
Decrease in s.albumin to less than 4 g/l
GFR less than 15 ml/min (by I iothalamate)
S. Creatinine >10 mg/dl and bun >100 mg /dl
Decrease in s.transferrin
Low total cholesterol
Growth retardation in children
D) Specific indications for peritoneal dialysis
Patients with cardiovascular or hemodynamic instability
Hemodialysis patients with vascular access failure or can not be created (e.g. diabetic patients)
High risk of anti coagulation
Patients in the older age group (over 65) and small children
Severe hemodialysis-related symptoms or disequilibrium
Social reason
Indications for Dialysis other than chronic renal failure
1-Acute renal failure
2-Poisons and Drug intoxication
3-Hypercalcaemia
4-Hyperuricemia
5-Hypothermia
6-Metabolic alkalosis (special dialysis solution required)

Dialyzable drugs and Poisons (partial list)
a) Barbiturates : Phenobarbital -Pentobarbital -Amobarbital
b) Alcohol's : Methanol -Ethanol -Ethylene glycol -Isopropanol
c) Analgesics : Acetylsalicylic acid -Methylsalicylate
d) Metals : Calcium -Potassium -Sodium -Lithium
e) Endogenous toxins : Uric acid -Uremic toxins -Hyperosmolar state
f) Halides : Bromide
e) Miscellaneous : Theophylline -Mannitol -Radiocontrast -Thiocynate -
Boric acid -Aniline
NB 1) Dialysis for poisoning should be considered only when supportive measures are ineffective or there is impending irreversible organ toxicity.
2) Hemoperfusion is required in some cases

Factors to be considered in determine drug’s dialyzability:
1) Dialysis related factors:
Dialyzer membrane characteristics
Surface area
Blood flow rate
Dialysate flow rate
Degree of ultrafitration
Duration of dialysis

2) Drug related factors :
Availability of the drug in the plasma
Drug pharmacokinetic characteristics
Drug molecular weight (<500 cross the membrane more readily)
Drug solubility (water soluble are dialyzable than lipid soluble)

Factors Determinants for Dialysis
Factors determining the mode of chronic dialysis should include medical and non medical factors which have an impact on the treatment modality. Physicians have the responsibility to discuss the therapeutic options and offer their advice and recommendations about the choices. In general renal transplantation should be recommended as the preferred mode of renal replacement therapy in whom surgery and immunosupression is safe and feasible.
Medical Factors
1. Age
2. Comorbid medical illnesses
3. Patient survival
4. Patient rehabilitation
5. Quality of life
Non Medical Factors
1. Government-imposed Economic limitations
2. Physician and Patient bias
3. Resource availability
4. Social ,Religious ,Cultural mores
5. Availability of transplantation
6. Family support
7. Cost , race , sex , reimbursement

Contraindications of Dialysis therapy
Principally there is no absolute contraindication to dialysis therapy. Advanced age in and of itself is not a contraindication to dialysis therapy. Many elderly are physiologically equivalent to young patients.
Relative contraindications to dialysis therapy
1. Advanced malignancy (except multiple myeloma)
2. Alzheimer’s disease
3. Multi-infarct dementia
4. Hepatorenal syndrome
5. Advanced liver cirrhosis with encephalopathy
6. Hypotension unresponsive to pressors
7. Terminal illness
8. Organic brain syndrome
Contraindication for Peritoneal dialysis
Absolute
1. Peritoneal fibrosis
2. Pleuroperitoneal leak
Relative Major
1. Chronic Ostomies
2. Severe hypercatabolic state
3. Fresh aortic prosthesis
4. Recent Abdominal surgery
5. Recent Thoracic surgery
6. Extensive Abdominal adhesions
7. Quadriplegia
8. Blindness
9. Physical handicaps
10. Mental Retardation
Relative Minor
1. Polycystic Kidney disease
2. Diverticulosis
3. Obesity
4. Peripheral vascular disease
5. Hyperlipidemia
6. Social

Introduction
Background
Chronic renal failure (CRF) requiring dialysis or transplantation is known as end-stage renal disease (ESRD). In the United States, diabetic nephropathy is the most common and hypertension the second most common cause. Along with glomerulonephritis, these cause approximately 75% of all adult cases. Certain geographic areas have a high incidence of HIV nephropathy. Genetic kidney disease such as polycystic kidney disease is a common cause in young adults.1
Patients with end-stage renal disease (ESRD) are commonly encountered in the ED with problems related to the metabolic complications of their renal disease or dialysis complications. Various problems related to vascular access in patients on hemodialysis and to abdominal catheters in patients using continuous ambulatory peritoneal dialysis (CAPD) are also common. Patients who have undergone renal transplantation may experience a variety of transplant-related conditions.
Patients with chronic renal failure often present to the ED with an unrelated condition. In these cases, the level of renal function may have important implications for diagnosis and treatment.
Pathophysiology
All major organ systems are affected by renal failure. Prevalence of symptoms is a function of the glomerular filtration rate (GFR), which averages 120 mL/min in a healthy adult. As the GFR falls to less than approximately 20% of normal, symptoms of uremia may begin to occur. They almost are invariably present when the GFR decreases to less than 10% of normal. Measuring GFR requires a timed urine collection as well as measurement of serum creatinine. However, it can be accurately estimated from a patient's age, weight, gender, and serum creatinine level. Online calculators are available to automate the calculation.2

Signs and symptoms of renal failure are due to overt metabolic derangements resulting from inability of failed kidneys to regulate electrolyte, fluid, and acid-base balance; they are also due to accumulation of toxic products of amino acid metabolism in the serum. Signs and symptoms include the following:
Systemic signs

Malaise, weakness, and fatigue are very common.
Gastrointestinal signs

GI disturbances include anorexia, nausea, vomiting, and hiccups. Peptic ulcer disease and symptomatic diverticular disease are common in patients with CRF.
Neurological signs

Peripheral neuropathy and restless legs syndrome are the most common neurologic complications of CRF. Seizures may occur due to uremia, and the prevalence of stroke is increased.
Hematologic signs

Anemia is inevitable in CRF because of loss of erythropoietin production. Abnormalities in white cell and platelet functions lead to increased susceptibility to infection and easy bruising.
Dermatologic signs

Pruritus is a common dermatologic complication assumed to be secondary to accumulation of toxic pigments (urochromes) in the dermis.
Metabolic/endocrine signs

Volume overload occurs when salt and water intake exceeds losses and excretion. This causes congestive heart failure (CHF) and exacerbates hypertension. Hyperkalemia is the most common immediately life-threatening metabolic complication of renal failure and may develop suddenly when GFR is severely reduced. Anion gap acidosis results from decreased hydrogen ion excretion and may exacerbate hyperkalemia. Hypocalcemia is potentially life threatening and results from loss of vitamin D and increased parathyroid hormone levels. Hypermagnesemia also may occur.

Cardiac signs

Volume overload may cause CHF and pulmonary edema. Hypertension contributes to cardiovascular disease. Dyslipidemia is a primary risk factor for cardiovascular disease and a common complication of ESRD. Uremia may also lead to pericardial effusion and, in rare cases, pericardial tamponade. Cardiovascular mortality is 10-20 times higher in dialysis patients than in the normal population.

Vascular signs

Vascular access complications are similar to those seen in any patient with a vascular surgical procedure (eg, bleeding, local or disseminated intravascular infections, vessel [graft] occlusion).
Dialysis catheters

A peritoneal dialysis catheter subjects patients to the risks of peritonitis and local infection. The catheter acts as a foreign body and provides a portal of entry for pathogens from the external environment.
Infection/immunologic

Patients who have received renal transplants may experience recurrent renal failure due to rejection or other graft complications. In addition, chronic immunosuppression makes them prone to infection.
Frequency
United States
The government of the United States funds treatment of end-stage renal disease (ESRD) universally for US citizens. As a consequence, the population of patients receiving dialysis or who have had a renal transplant in the United States is large. During 2004, the last year with complete data availability, 104,364 patients (approximately 0.03% of the US population) began renal replacement therapy, an adjusted incidence rate of 339 per 1,000,000. As of 2005, more than 485,000 patients were receiving treatment for ESRD in the United States. As a result, patients with ESRD are encountered on a regular basis in US emergency departments.
International
Resources allocated for treatment of ESRD vary throughout the world, and the treatments are expensive. Untreated ESRD is rapidly fatal, and treatment is too expensive for most individuals to purchase privately. Consequently, very few patients with ESRD are encountered in countries where ESRD treatment is not funded by the government.

The morbidity and mortality of dialysis patients is much higher in the United States compared with most other countries. This is probably a consequence of selection bias. Due to liberal criteria for receiving government-funded dialysis in the United States and rationing (both medical and economic) in most other countries, US patients receiving dialysis are on the average older and sicker than those in other countries.
Mortality/Morbidity
Patients in renal failure are prone to all of the complications of any underlying condition, such as diabetes and hypertension. In addition, renal failure causes a variety of metabolic and physiologic derangements.
• The most common cause of sudden death in patients with end-stage renal disease (ESRD) is hyperkalemia, which is often encountered in patients after missed dialysis or dietary indiscretion. Serum potassium also rises when the serum is acidemic, even though total body potassium is unchanged. Hyperkalemia is usually asymptomatic and should be treated empirically when suspected and when arrhythmia or cardiovascular compromise is present.
• Iatrogenic complications related to fluid administration (fluid overload) or medications are frequently encountered in patients in renal failure.
• Cardiovascular mortality is 10-20 times higher in dialysis patients than in the normal population.
• Anemia results in fatigue, reduced exercise capacity, decreased cognition, and impaired immunity.
• Renal transplant patients are prone to infection, especially in the immediate post-transplant period.
Race
Etiology of end-stage renal disease (ESRD) differs among racial groups primarily because of the prevalence of predisposing conditions, such as diabetes and hypertension. In populations with problematic access and utilization of primary medical care for treatment of predisposing conditions, ESRD often is encountered in relatively young patients. While the costs of treatment for ESRD are borne by the entire population (through government funding), relatively inexpensive preventive treatments often are funded poorly. Diseases such as diabetes and hypertension are much less likely to lead to renal failure when appropriately treated. The cost of primary care for these conditions is far lower than for dialysis or transplantation, yet primary care remains poorly funded, while ESRD treatment is reimbursed completely by the government. This conundrum is reflective of the often illogical and capricious nature of health care spending in the United States.

In the United States, racial and ethnic discrepancies in ESRD exist, with 2006 rates in the African American and Native American populations 3.6 and 1.8 times greater, respectively, than the rate among whites, and the rate in the Hispanic population 1.5 times higher than that of non-Hispanics.3
Sex
Presentation and treatment of chronic renal failure (CRF) and end-stage renal disease (ESRD) do not differ significantly between men and women. Differences in causes of renal failure are related to the types of underlying conditions prevalent in men and women.
Age
While the etiology of CRF differs among age groups, the presentations and nature of complications are similar. Young children with ESRD often are treated with transplantation rather than dialysis because of a relatively greater long-term benefit compared to that of adults, and due to difficulties related to vascular access for dialysis.
Clinical
History
Renal failure produces no symptoms early in the course of the disease. At this stage, symptoms of the underlying illness may bring the patient to medical attention and renal insufficiency is noted on laboratory testing.
• Chronic renal failure (CRF) potentially affects all organ systems. History for the presenting disorder is similar to that encountered when the same disorder exists in patients without renal failure.
• The following presentations are seen frequently in CRF. Moreover, some problems are unique to patients with CRF/ESRD; many of these are related to treatments, such as dialysis or transplantation.
• Electrolyte abnormalities include life-threatening hyperkalemia, which is usually asymptomatic.
o Dilutional hyponatremia may cause mental status changes or seizures.
o Hypocalcemia or hypermagnesemia may cause weakness and life-threatening dysrhythmias.
o Neuromuscular irritability is seen with hypocalcemia and may present as tetany or paresthesia.
o Hypermagnesemia causes neuromuscular depression with weakness and loss of reflexes.
o Acidosis may present as shortness of breath due to the work of breathing from compensatory hyperpnea.
• Pericarditis and asymptomatic pericardial effusion are common in patients with ESRD. Cardiac tamponade may occur but is rare. Presentation of pericarditis and tamponade are typical, with pleuritic chest pain being the most common presentation.
o Tamponade presents as fatigue, weakness, syncope, or dyspnea.
o Hypotension is usually present, and, if advanced, frank shock and cardiovascular collapse occur.
• Hypotension with postural weakness or syncope may occur as a complication of fluid shifts from dialysis or from any other cause. Sepsis is a serious cause of hypotension.
• Myocardial ischemia or infarction is common in patients with ESRD; consider this diagnosis in hypotensive patients along with other conditions, such as GI bleeding.
• Dialysis dysequilibrium syndrome is a common neurologic complication seen in dialysis patients.
o Syndrome is characterized by weakness, dizziness, headache, and in severe cases, mental status changes. Diagnosis is one of exclusion.
o A prime characteristic of the syndrome is that it is nonfocal.
• Peritonitis is common in patients being treated with continuous ambulatory peritoneal dialysis (CAPD), occurring approximately once per patient year. Patients present with abdominal pain, which may be mild, or complain of a cloudy effluent. Fever often is absent.
• Infection at the catheter exit site manifests as expected local pain, erythema, warmth, and/or fluctuance.
• Other abdominal conditions, such as appendicitis, pancreatitis, or diverticulitis, should be considered when patients present with abdominal pain, especially if signs and symptoms are localized.
• Vascular access problems include infections, which are usually manifest with typical signs and symptoms such as local pain, redness, warmth, or fluctuance. Fever may be present without local signs.
o Clotting of the vascular access presents as loss of normal bruit or thrill. There may be signs or symptoms of distal limb ischemia.
o Patients may present after dialysis or minor trauma with bleeding from their vascular access. Bleeding usually can be controlled with elevation and firm but nonocclusive pressure. In the immediate postdialysis period, protamine may be needed to reverse the effect of heparin (routinely used in dialysis to prevent clotting). Life-threatening bleeding may occur.
Physical
• Chronic renal failure (CRF) produces no specific physical findings.
• Patients with an arteriovenous fistula or graft should have the site examined regularly. Abnormal findings include loss of palpable thrill, overlying erythema, or active bleeding from the incisional wound of a newly placed fistula or graft.
• Physical findings of chronic renal failure complications generally are those expected with the specific complication and do not differ from those encountered when the condition occurs in patients with normal renal function.
• Certain complications are very common in renal failure.
• CAPD-associated peritonitis
o Abdominal pain and tenderness usually are generalized and relatively mild.
o Localized pain and tenderness suggest a local process, such as incarcerated hernia or appendicitis.
o Severe generalized peritonitis may be due to a perforated viscus as in any other patient.
• Transplant-related problems: Pain and tenderness over a transplanted kidney may be due to infection (pyelonephritis), obstruction (stone or extrinsic compression), or graft rejection.
• Vascular access aneurysms or pseudoaneurysms : These present as localized swelling, which may be pulsatile, and are often chronic. A rapid increase in size may indicate active bleeding.
Causes
Once chronic renal failure (CRF) has occurred, treatment options and complications are largely independent of the cause.
• In terms of broad categories of disease, glomerulonephritis and interstitial nephritis are the most common causes of CRF in adults and children.
• Chronic upper urinary tract infection causes CRF in all age groups.
• CRF also is encountered in children because of congenital anomalies such as chronic hydronephrosis, which is caused by anatomic defects that obstruct urine flow or allow reflux from the bladder (vesicoureteral reflux).
• Kidneys may be congenitally hypoplastic.
• Hereditary nephropathies also exist.
• In adults, diabetic and hypertensive nephropathies are the most common specific causes of CRF.
• Polycystic disease, renal vascular disease, and analgesic nephropathy also are common.
• In certain geographic areas, HIV-related renal disease is becoming common.
• Certain diseases such as some of the types of glomerulonephritis tend to recur in transplanted kidneys. In these cases, dialysis is the preferred treatment option.
• Consider renal transplant patients to be mildly to moderately immunosuppressed.
o In the immediate posttransplant period or during a rejection episode, intensive immunosuppression puts patients at considerable risk of infection, including disseminated viral infections such as herpes zoster.
o Degree of immunosuppression is less late in the posttransplant course when corticosteroids alone may be used.

Glycogen storage disease type II (Pompe Disease)

2010-06-17T02:05:00.000-07:00

Glycogen storage disease type II (Pompe Disease)

Glycogen storage disease type II (also called Pompe disease or acid maltase deficiency) is an autosomal recessive metabolic disorder[1] which damages muscle and nerve cells throughout the body. It is caused by an accumulation of glycogen in the lysosome due to deficiency of the lysosomal acid alpha-glucosidase enzyme. It is the only glycogen storage disease with a defect in lysosomal metabolism, and the first glycogen storage disease to be identified, in 1932.
The build-up of glycogen causes progressive muscle weakness (myopathy) throughout the body and affects various body tissues, particularly in the heart, skeletal muscles, liver and nervous system.
Glycogen storage disease type II
Classification and external resources
ICD-10
E74.0

ICD-9
271.0

OMIM
232300

DiseasesDB
5296

eMedicine
med/908 ped/1866

MeSH
D006009

Variants
Pompe disease has historically been divided into three forms defined by age of onset and progression of symptoms (see below). More recently there has been a trend to divide the disease into two groups: infantile onset (involving the massive enlargement of the heart) and late onset (no heart enlargement).[citation needed]
Infantile, or early onset, is noticed shortly after birth. Symptoms include severe lack of muscle tone, weakness, an enlarged liver (hepatomegaly), and an enlarged heart (cardiomegaly).[citation needed] Mental function is not affected. Development appears normal for the first weeks or months but slowly declines as the disease progresses. Swallowing may become difficult and the tongue may protrude and become enlarged. Most children die from respiratory or cardiac complications before 2 years of age.[citation needed]
Juvenile onset symptoms appear in early to late childhood and include progressive weakness of respiratory muscles in the trunk, diaphragm and lower limbs, as well as exercise intolerance. Intelligence is normal.[citation needed]
Adult onset symptoms also involve generalized muscle weakness and wasting of respiratory muscles in the trunk, lower limbs, and diaphragm. Many patients report respiratory distress, headache at night or upon waking, diminished deep tendon reflexes, and proximal muscle weakness, such as difficulty in climbing stairs. Intellect is not affected. A small number of adult patients live without major symptoms or limitations.[citation needed]
Pompe's disease is one of the infiltrative causes of restrictive cardiomyopathy.[citation needed]

Treatment
Cardiac and respiratory complications are treated symptomatically. Physical and occupational therapy may be beneficial for some patients. Alterations in diet may provide temporary improvement but will not alter the course of the disease.[citation needed] Genetic counseling can provide families with information regarding risk in future pregnancies.
On April 28, 2006 the US Food and Drug Administration approved a biologics license application (BLA) for Myozyme (alglucosidase alfa, rhGAA),[2] the first treatment for patients with Pompe disease. This was based on enzyme replacement therapy work pioneered by Drs Arnold Reuser and Ans van der Ploeg at Erasmus University, Rotterdam.[3] Myozyme falls under the FDA Orphan Drug designation and was approved under a priority review.
The currently approved Myozyme is manufactured by Genzyme Corp. in Cambridge, Massachusetts, USA. Its development was a complex process. Genzyme first partnered with Pharming Group NV who had managed to produce acid alpha-glucosidase from the milk of transgentic rabbits. They also partnered with a second group based at Duke University using Chinese hamster ovary cells. In 2001 it acquired Novazyme which was also working on this enzyme. Genzyme also had its own product (Myozyme) under development. In November 2001 Genzyme chief executive Henri Termeer organised a systematic comparison of the various potential drugs in transgenic mice. It was found that Myozyme was the most efficatious and easiest to manufacture. Work on the other products was then discontinued.
The FDA has approved Myozyme for administration by intravenous infusion of solution into a vein. The safety and efficacy of Myozyme were assessed in two separate clinical trials in 39 infantile-onset patients with Pompe disease ranging in age from 1 month to 3.5 years at the time of the first infusion. Myozyme costs an average of $300,000 a year, and must be taken for the patients' entire life. The treatment is not without side effects which include fever, cardiac failure, pneumonia, respiratory failure and rarely shock. Some insurers have refused to pay for it.[4] The treatment is better at stabilizing the clinical condition than reversing the pathological changes that have already occurred. Early diagnosis leads to better outcomes.
On August 14, 2006, Health Canada approved Myozyme for the treatment of Pompe disease. On June 14, 2007 the Canadian Common Drug Review issued their recommendations regarding public funding for Myozyme therapy. Their recommendation was to provide funding to treat a very small subset of Pompe patients (Infants less one year of age with Cardiomyopathy).[5] The vast majority of developed countries are providing access to therapy for all diagnosed Pompe patients.[6]
In June 2007 it was reported that ZyStor Therapeutics was in the process of developing an enzyme replacement therapy for Pompe disease by leveraging their glycosylation independent lysosomal targeting technology (GILT).[7]
Prognosis
The prognosis for individuals with Pompe disease varies according to the onset and severity of symptoms. Without treatment the disease is particularly lethal in infants and young children.
Myozyme (alglucosidase alfa), which helps break down glucose, is a combined form of the human enzyme acid alpha-glucosidase, and is also currently being used to replace the missing enzyme. In a study[8] which included the largest cohort of patients with Pompe disease treated with enzyme replacement therapy (ERT) to date findings showed that Myozyme treatment clearly prolongs ventilator-free survival and overall survival in patients with infantile-onset Pompe disease as compared to an untreated historical control population. Furthermore, the study demonstrated that initiation of ERT prior to 6 months of age, which could be facilitated by newborn screening, shows great promise to reduce the mortality and disability associated with this devastating disorder.
On December 13, 2007, Genzyme released the initial results of its Late Onset Treatment Study (LOTS). The study was undertaken to evaluate the safety and efficacy of Myozyme in juvenile and adult patients with Pompe disease. LOTS was a randomized, double-blind, placebo-controlled study that enrolled 90 patients at eight primary sites in the United States and Europe. Participants received either Myozyme or a placebo every other week for 18 months. The average age of study participants was 44 years. The primary efficacy endpoints of the study sought to determine the effect of Myozyme on functional endurance as measured by the six-minute walk test and to determine the effect of Myozyme on pulmonary function as measured by percent predicted forced vital capacity.
The results showed that, at 18 months, patients treated with Myozyme increased their distance walked in six minutes by an average of approximately 30 meters as compared with the placebo group (P=0.0283; Wilcoxon test). The placebo group did not show any improvement from baseline. The average baseline distance walked in six minutes in both groups was approximately 325 meters. Percent predicted forced vital capacity in the group of patients treated with Myozyme increased by 1 percent at 18 months. In contrast, it declined by approximately 3 percent in the placebo group (P=0.0026; Wilcoxon test). The average baseline percent predicted forced vital capacity in both groups was approximately 55 percent.
The results for both efficacy endpoints were consistent across various prospectively defined subgroups.

Epidemiology

Glycogen storage disease type II has an autosomal recessive pattern of inheritance.
The disorder is estimated to occur in about 1 in 40,000 births. Worldwide there are thought to be about 5,000 to 10,000 suffers of this disease.
It has an autosomal recessive inheritance pattern. This means the defective gene is located on an autosome, and two copies of the gene—one from each parent—are required to be born with the disorder. As with all cases of autosomal recessive inheritance, children have a 1 in 4 chance of inheriting the disorder when both parents carry the defective gene, and although both parents carry one copy of the defective gene, they are usually not affected by the disorder.

History
The disease is named after Johann Pompe, who characterized it in 1932.[9][10] Pompe described accumulation of glycogen in muscle tissue in some cases of a previously unknown disorder. This accumulation was difficult to explain as the enzymes involved in the usual metabolism of glucose and glycogen were all present and functioning.
The basis for the disease remained a puzzle until Christian de Duve's discovery of lysosomes in 1955 for which he won the Nobel Prize in 1974. His co-worker Henri G. Hers realised in 1965 that the deficiency of a lysosomal enzyme (alpha glucosidase) for the breakdown of glycogen could explain the symptoms of Pompe disease. This discovery lead to establishing the concept of lysosomal storage diseases of which 49 have been described (to date).
Despite recognizing the basis for the disease treatment proved difficult. Administration of the enzyme lead to its uptake by the liver and not the muscle cells where it is needed. Despite this work at Erasmus MC University Medical Center, Rotterdam began in the '70s. In the early 1990s two Dutch scientists, Arnold Reuser and Ans van der Ploeg a PhD student, had the idea that phosphorylated enzyme would be taken via by the mannose-6-phosphate receptors in lysosomes thus allowing the enzyme to be targeted. Using alpha-glucosidase containing phosphorylated mannose residues they were able to show that an increase in the enzyme's activity in the muscles.[11] The increases reported - 43% increase in skeletal muscle and 70% in the heart - were likely to be clinically significant.
They cloned the acid alpha-glucosidase gene and then made the first mouse model of Pompe's disease. A second model was developed by Yuan-Tsong Chen and colleagues at Duke University using the quail. (Dr. Chen is the director of the Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.) The results of the work at Dukes were impressive with one treated animal recovering to the point of being able to fly again.[12]
This was followed by production of alpha-glucosidase in Chinese hamster ovary (CHO) cells and in the milk of transgenic rabbits.[13] This work eventually culminated in the start of clinical trials with the first clinical trial including 4 babies taking place at Erasmus MC Sophia Children’s Hospital in 1999. This was organised by Pharming in the Netherlands. A second trial in 2001 organised by Dr Chen and Synpac, a Taiwan-based company, used enzyme grown in CHO cells[14] (陳垣崇) while he was at Duke University. Both trials were successful.
Genzyme which had an existing enzyme replacement therapy for Gaucher's disease became involved at this point. They developed a product of their own for Pompe's disease also grown in CHO cells. This is now marketed as Myozyme.
Much of the funding for research in this field was provided by the Association of Glycogen Storage Disorders. This association was founded by a Scotsman - Kevin O’Donnell - whose son Calum aged eight months died from Pompe's disease in 1993. A grant from the AGSD-UK in 1996 funded the work that showed that replacement treatment could work. A second fund-raising group was formed in 1999 - the International Pompe Association.
John Crowley became involved in the fund-raising efforts in 1998 after two of his children were diagnosed with Pompe's. He joined the company Novazyme in 1999 which was working on enzyme replacement treatment for Pompe's. Novazyme was sold to Genzyme in 2001 for over US$100 million.

[hide]
v • d • e
Inborn error of carbohydrate metabolism: monosaccharide metabolism disorders (including glycogen storage diseases) (E73-74, 271)

Sucrose, transport
(extracellular) Disaccharide catabolism Lactose intolerance • Sucrose intolerance

Monosaccharide transport Glucose-galactose malabsorption • Inborn errors of renal tubular transport (Renal glycosuria) • Fructose malabsorption

Hexose → glucose
Monosaccharide catabolism fructose: Essential fructosuria • Fructose intolerance
galactose/galactosemia : GALK deficiency • GALT deficiency/GALE deficiency

Glucose ⇄ glycogen
Glycogenesis
GSD type 0, glycogen synthase • GSD type IV, Andersen's, branching

Glycogenolysis
extralysosomal: GSD type V, McArdle, muscle glycogen phosphorylase/GSD type VI, Hers', liver glycogen phosphorylase • GSD type III, Cori's, debranching
lysosomal/LSD: GSD type II, Pompe's, glucosidase

Glucose ⇄ CAC
Glycolysis
MODY 2 • GSD type VII, Tarui's, phosphofructokinase • Triosephosphate isomerase deficiency • Pyruvate kinase deficiency

Pyruvate catabolism PDHA • Fumarase deficiency

Gluconeogenesis
PCD • Fructose bisphosphatase deficiency • GSD type I, von Gierke, glucose 6-phosphatase

Pentose phosphate pathway
Glucose-6-phosphate dehydrogenase deficiency • Pentosuria

Other Hyperoxaluria (Primary hyperoxaluria)

Procedures

2010-06-17T02:01:00.001-07:00

Central Venous Line
A central venous catheter ("central line", "CVC", "central venous line" or "central venous access catheter") is a catheter placed into a large vein in the neck (internal jugular vein), chest (subclavian vein) or groin (femoral vein). It is used to administer medication or fluids, obtain blood tests (specifically the "mixed venous oxygen saturation"), and directly obtain cardiovascular measurements such as the central venous pressure. Certain medications, such as inotropes and amiodarone, are preferably given through a central line.
Types
There are several types of central venous catheters
Tunneled catheter
This type of catheter is inserted into a vein at one location (neck, chest or groin), and tunneled under the skin to a separate exit site, where it emerges from underneath the skin. It is held in place by a Dacron cuff, just underneath the skin at the exit site. The exit site is typically located in the chest, making the access ports less visible than if they were to directly protrude from the neck. Passing the catheter under the skin helps to prevent infection and provides stability.
Implanted port

Implanted port
A port is similar to a tunneled catheter but is left entirely under the skin. Medicines are injected through the skin into the catheter. Some implanted ports contain a small reservoir that can be refilled in the same way. After being filled, the reservoir slowly releases the medicine into the bloodstream. An implanted port is less obvious than a tunneled catheter and requires very little daily care. It has less impact on a person's activities than a PICC line or a tunneled catheter. Surgically implanted infusion port placed below the clavicle (infraclavicular fossa), catheter threaded into the right atrium through large vein. Accessed via non-coring "Huber" needle through the skin. May need to use topical anesthetic prior to accessing port. Used for medications, chemotherapy, TPN, and blood. Easy to maintain for home-based therapy.
PICC line
A peripherally inserted central catheter, or PICC line (pronounced "pick"), is a central venous catheter inserted into a vein in the arm rather than a vein in the neck or chest.
Technical description

Triluminal catheter
Dependent on its use, the catheter is monoluminal, biluminal or triluminal, dependent on the actual number of tubes or lumens (1, 2 and 3 respectively). Some catheters have 4 or 5 lumens, depending on the reason for their use.
The catheter is usually held in place by a suture or staple and an occlusive dressing. Regular flushing with saline or a heparin-containing solution keeps the line patent and prevents thrombosis. Certain lines are impregnated with antibiotics, silver-containing substances (specifically silver sulfadiazine) and/or chlorhexidine to reduce infection risk.
Specific types of long-term central lines are the Hickman catheters, which require clamps to make sure the valve is closed, and Groshong catheters, which have a valve that opens as fluid is withdrawn or infused and remains closed when not in use. Hickman and Groshong lines need more specific measures to prevent infection. Hence, they are inserted into the jugular vein but then tunneled under the skin to maximize the distance a pathogen would need to travel to enter the bloodstream. Hickman lines also have a "cuff" under the skin, again to prevent bacterial migration.[citation needed]
Indications and uses
Indications for the use of central lines include
• Monitoring of the central venous pressure (CVP) in acutely ill patients to quantify fluid balance
• Long-term Intravenous antibiotics
• Long-term Parenteral nutrition especially in chronically ill patients
• Long-term pain medications
• Chemotherapy
• Drugs that are prone to cause phlebitis in peripheral veins (caustic), such as:
o Calcium chloride
o Chemotherapy
o Hypertonic saline
o Potassium chloride
o Amiodarone
• Plasmapheresis
• Dialysis
• Frequent blood draws
• Frequent or persistent requirement for intravenous access
• Need for intravenous therapy when peripheral venous access is impossible
o Blood
o Medication
o Rehydration
Central venous catheters usually remain in place for a longer period of time, especially when the reason for their use is longstanding (such as total parenteral nutrition in a chronically ill patient). For such indications, a Hickman line, a PICC line or a portacath may be considered because of their smaller infection risk. Sterile technique is highly important here, as a line may serve as a porte d'entrée (place of entry) for pathogenic organisms, and the line itself may become infected with organisms such as Staphylococcus aureus and coagulase-negative Staphylococci.[citation needed]
Insertion

Triple lumen in jugular vein
The skin is cleaned, and local anesthetic applied if required. The location of the vein is then identified by landmarks or with the use of a small ultrasound device. A hollow needle is advanced through the skin until blood is aspirated; the color of the blood and the rate of its flow help distinguish it from arterial blood (suggesting that an artery has been accidentally punctured).[citation needed]
The Seldinger technique is then employed to insert the line. This means that a blunt guidewire is passed through the needle, and the needle is then removed. A dilating device may be passed over the guidewire to slightly enlarge the tract, and the central line itself is then passed over the guidewire, which is then removed. All the lumens of the line are aspirated (to ensure that they are all positioned inside the vein) and flushed.[citation needed]
For jugular and subclavian lines, a chest X-ray is typically performed to ensure the line is positioned inside the superior vena cava and, in the case of insertion through the subclavian vein, that there is no resultant pneumothorax.
Complications
Central line insertion may cause a number of complications. The benefit expected from their use therefore needs to outweigh the risk of those complications.
Pneumothorax
Pneumothorax (for central lines placed in the chest); the incidence is thought to be higher with subclavian vein catheterization. In catheterization of the internal jugular vein, the risk of pneumothorax can be minimized by the use of ultrasound guidance. For experienced clinicians, the incidence of pneumothorax is about 1%. Some official bodies, e.g. the National Institute for Health and Clinical Excellence (UK), recommend the routine use of ultrasonography to minimize complications
Infection
All catheters can introduce bacteria into the bloodstream, but CVCs are known for occasionally causing Staphylococcus aureus and Staphylococcus epidermidis sepsis. Infection risks were initially thought to be less in jugular lines, but this only seems to be the case if the patient is obese
If a patient with a central line develops signs of infection, blood cultures are taken from both the catheter and from a vein elsewhere in the body. If the culture from the central line grows bacteria much earlier (>2 hours) than the other site, the line is the likely source of the infection. Quantitative blood culture is even more accurate, but this is not widely available
Generally, antibiotics are used, and occasionally the catheter will have to be removed. In the case of bacteremia from Staphylococcus aureus, removing the catheter without administering antibiotics is not adequate as 38% of such patients may still develop endocarditis.
In a clinical practice guideline, the American Centers for Disease Control and Prevention recommends against routine culturing of central venous lines upon their removal. The guideline makes a number of further recommendations to prevent line infections.
To prevent infection, stringent cleaning of the catheter insertion site is advised. Povidone-iodine solution is often used for such cleaning, but chlorhexidine appears to be twice as good as iodine. Routine replacement of lines makes no difference in preventing infection.
Other complications
Rarely, small amounts of air are sucked into the vein as a result of the negative intrathoracic pressure.[citation needed] If these air bubbles obstruct blood vessels, this is known as an air embolism.
Hemorrhage (bleeding) and formation of a hematoma (bruise) is slightly more common in jugular venous lines than in others.
Arrhythmia may occur during the insertion process when the wire comes in contact with the endocardium. It typically resolved when the wire is pulled back.

Arterial catheter
An arterial line, or art-line, is a thin catheter inserted into an artery. It is most commonly used in intensive care medicine to monitor the blood pressure real-time (rather than by intermittent measurement), and to obtain samples for arterial blood gas measurements. It is not generally used to administer medication.
An arterial line is usually inserted in the wrist (radial artery); but can also be inserted into the elbow (brachial artery), groin (femoral artery), foot (dorsalis pedis artery).

Insertion is often painful; however an anesthetic such as Lidocaine can be used to make the insertion more tolerable, but this can make insertion more difficult.
______________________________________________________________________________

Implantable Cardioverter Defibrillator (ICD) Insertion
The heart's electrical conduction system

The heart is, in the simplest terms, a pump made up of muscle tissue. Like all pumps, the heart requires a source of energy in order to function. The heart's pumping energy comes from an indwelling electrical conduction system.
An electrical stimulus is generated by the sinus node (also called the sinoatrial node, or SA node), which is a small mass of specialized tissue located in the right atrium (right upper chamber) of the heart.
The sinus node generates an electrical stimulus regularly at 60 to 100 times per minute under normal conditions. This electrical stimulus travels down through the conduction pathways (similar to the way electricity flows through power lines from the power plant to your house) and causes the heart's chambers to contract and pump out blood.
The right and left atria (the two upper chambers of the heart) are stimulated first and contract a short period of time before the right and left ventricles (the two lower chambers of the heart).
The electrical impulse travels from the sinus node to the atrioventricular (AV) node, where it stops for a very short period, then continues down the conduction pathways via the "bundle of His" into the ventricles. The bundle of His divides into right and left pathways to provide electrical stimulation to both ventricles.
Reasons for the Procedure
A pacemaker may be inserted in order to provide stimulation for a faster heart rate when the heart is beating too slowly, and when other treatment methods, such as medication, have not improved the heart rate.
An ICD may be inserted in order to provide fast pacing (ATP), cardioversion (small shock), or defibrillation (larger shock) when the heart beats too fast.
Problems with the heart rhythm may cause difficulties because the heart is unable to pump an adequate amount of blood to the body. If the heart rate is too slow, the blood is pumped too slowly.
If the heart rate is too fast or too irregular, the heart chambers are unable to fill up with enough blood to pump out with each beat. When the body does not receive enough blood, symptoms such as fatigue, dizziness, fainting, and/or chest pain may occur.
Some examples of rhythm problems for which a pacemaker or ICD might be inserted include:
• atrial fibrillation - occurs when the atria beat irregularly and too fast
• ventricular fibrillation - occurs when the ventricles beat irregularly and too fast
• bradycardia - occurs when the heart beats too slow
• tachycardia - occurs when the heart beats too fast
• heart block - occurs when the electrical signal is delayed after leaving the SA node; there are several types of heart blocks, and each one has a distinctive ECG tracing
There may be other reasons for your physician to recommend a pacemaker or ICD insertion.
Risks of the Procedure
Possible risks of pacemaker or ICD insertion include, but are not limited to, the following:
• bleeding from the incision or catheter insertion site
• damage to the vessel at the catheter insertion site
• infection of the incision or catheter site
• pneumothorax - air becomes trapped in the pleural space causing the lung to collapse
If you are pregnant or suspect that you may be pregnant, you should notify your physician. If you are lactating, or breastfeeding, you should notify your physician.
Patients who are allergic to or sensitive to medications or latex should notify their physician.
For some patients, having to lie still on the procedure table for the length of the procedure may cause some discomfort or pain.
There may be other risks depending upon your specific medical condition. Be sure to discuss any concerns with your physician prior to the procedure.

Before the Procedure
• Your physician will explain the procedure to you and offer you the opportunity to ask any questions that you might have about the procedure.
• You will be asked to sign a consent form that gives your permission to do the test. Read the form carefully and ask questions if something is not clear.
• You will need to fast for a certain period of time prior to the procedure. Your physician will notify you how long to fast, usually overnight.
• If you are pregnant or suspect that you are pregnant, you should notify your physician.
• Notify your physician if you are sensitive to or are allergic to any medications, iodine, latex, tape, or anesthetic agents (local and general).
• Notify your physician of all medications (prescription and over-the-counter) and herbal supplements that you are taking.
• Notify your physician if you have heart valve disease, as you may need to receive an antibiotic prior to the procedure.
• Notify your physician if you have a history of bleeding disorders or if you are taking any anticoagulant (blood-thinning) medications, aspirin, or other medications that affect blood clotting. It may be necessary for you to stop some of these medications prior to the procedure.
• Your physician may request a blood test prior to the procedure to determine how long it takes your blood to clot. Other blood tests may be done as well.
• You may receive a sedative prior to the procedure to help you relax. If a sedative is given, you will need someone to drive you home afterwards.
• The upper chest may be shaved or clipped prior to the procedure.
• Based upon your medical condition, your physician may request other specific preparation.
During the Procedure

Chest X-ray with Implanted Pacemaker
A pacemaker or implanted cardioverter defibrillator may be performed on an outpatient basis or as part of your stay in a hospital. Procedures may vary depending on your condition and your physician's practices.
Generally, a pacemaker or ICD insertion follows this process:
1. You will be asked to remove any jewelry or other objects that may interfere with the procedure.
2. You will be asked to remove your clothing and will be given a gown to wear.
3. You will be asked to empty your bladder prior to the procedure.
4. An intravenous (IV) line will be started in your hand or arm prior to the procedure for injection of medication and to administer IV fluids, if needed.
5. You will be placed in a supine (on your back) position on the procedure table.
6. You will be connected to an electrocardiogram (ECG or EKG) monitor that records the electrical activity of the heart and monitors the heart during the procedure using small, adhesive electrodes. Your vital signs (heart rate, blood pressure, breathing rate, and oxygenation level) will be monitored during the procedure.
7. Large electrode pads will be placed on the front and back of the chest.
8. You will receive a sedative medication in your IV before the procedure to help you relax. However, you will likely remain awake during the procedure.
9. The pacemaker or ICD insertion site will be cleansed with antiseptic soap.
10. Sterile towels and a sheet will be placed around this area.
11. A local anesthetic will be injected into the skin at the insertion site.
12. Once the anesthetic has taken effect, the physician will make a small incision at the insertion site.
13. A sheath, or introducer, is inserted into a blood vessel, usually under the collarbone. The sheath is a plastic tube through which the pacer/ICD lead wire will be inserted into the blood vessel and advanced into the heart.
14. It will be very important for you to remain still during the procedure so that the catheter placement will not be disturbed and to prevent damage to the insertion site.
15. The lead wire will be inserted through the introducer into the blood vessel. The physician will advance the lead wire through the blood vessel into the heart.
16. Once the lead wire is inside the heart, it will be tested to verify proper location and that it works. There may be one, two, or three lead wires inserted, depending on the type of device your physician has chosen for your condition. Fluoroscopy, (a special type of x-ray that will be displayed on a TV monitor), may be used to assist in testing the location of the leads.
17. Once the lead wire has been tested, an incision will be made close to the location of the catheter insertion (just under the collarbone). You will receive local anesthetic medication before the incision is made.
18. The pacemaker/ICD generator will be slipped under the skin through the incision after the lead wire is attached to the generator. Generally, the generator will be placed on the non-dominant side. (If you are right-handed, the device will be placed in your upper left chest. If you are left-handed, the device will be placed in your upper right chest).
19. The ECG will be observed to ensure that the pacer is working correctly.
20. The skin incision will be closed with sutures, adhesive strips, or a special glue.
21. A sterile bandage/dressing will be applied.
After the Procedure
In the hospital
After the procedure, you may be taken to the recovery room for observation or returned to your hospital room. A nurse will monitor your vital signs for a specified period of time.
You should immediately inform your nurse if you feel any chest pain or tightness, or any other pain at the incision site.
After the specified period of bed rest has been completed, you may get out of bed. The nurse will assist you the first time you get up, and will check your blood pressure while you are lying in bed, sitting, and standing. You should move slowly when getting up from the bed to avoid any dizziness from the period of bedrest.
You will be able to eat or drink once you are completely awake.
The insertion site may be sore or painful, but pain medication may be administered if needed.
Your physician will visit with you in your room while you are recovering. The physician will give you specific instructions and answer any questions you may have.
Once your blood pressure, pulse, and breathing are stable and you are alert, you will be taken to your hospital room or discharged home.
If the procedure is performed on an outpatient basis, you may be allowed to leave after you have completed the recovery process. However, if there are concerns or problems with your ECG, you may stay in the hospital for an additional day (or longer) for monitoring of the ECG.
You should arrange to have someone drive you home from the hospital following your procedure.
At home
You should be able to return to your daily routine within a few days. Your physician will tell you if you will need to take more time in returning to your normal activities. In addition, you should not do any lifting or pulling on anything for a few weeks. You may be instructed not to lift your arms above your head for a period of time.
You will most likely be able to resume your usual diet, unless your physician instructs you differently.
It will be important to keep the insertion site clean and dry. Your physician will give you specific bathing instructions.
Your physician will give you specific instructions about driving. If you had an ICD, you will not be able to drive until your physician gives you approval. Your physician will explain these limitations to you, if they are applicable to your situation.
You will be given specific instructions about what to do if your ICD discharges a shock. For example, you may be instructed to dial 911 or go to the nearest emergency room in the event of a shock from the ICD.
Ask your physician when you will be able to return to work. The nature of your occupation, your overall health status, and your progress will determine how soon you may return to work.
Notify your physician to report any of the following:
• fever and/or chills
• increased pain, redness, swelling, or bleeding or other drainage from the insertion site
• chest pain/pressure, nausea and/or vomiting, profuse sweating, dizziness and/or fainting
• palpitations
Your physician may give you additional or alternate instructions after the procedure, depending on your particular situation.

Foley catheter

Foley catheters are flexible (usually latex) tubes that are passed through the urethra during urinary catheterization and into the bladder to drain urine. They are retained by means of a balloon at the tip which is inflated with sterile water. The balloons typically come in two different sizes: 5 cc and 30 cc. They are commonly made in silicone rubber or natural rubber.
The relative size of a Foley catheter is described using French units (F).[1] The most common sizes are 10 F to 28 F. 1 F is equivalent to 0.33 mm = .013" = 1/77" of diameter. Thus the size in French units is roughly equal to the circumference of the catheter in millimetres.

Side view diagram of male urinary tract with Foley catheter in place to drain urine. A balloon near the tip holds the catheter in place.
Foley catheter (F/Ch. 24) positioned in a male; balloon blocked and outlet plug put on.
Foley catheters come in several sub-types. Coudé (French for elbowed) catheters have a 45° bend at the tip to allow easier passage through an enlarged prostate. Council tip catheters have a small hole at the tip which allows them to be passed over a wire. 3-way catheters are used primarily after bladder, prostate cancer or prostate surgery. They have a third arm or bell that allows an irrigant to pass to the tip of the catheter through a small separate channel into the bladder. This serves to wash away blood and small clots through the primary arm that drains into a collection device. This prevents larger clots, which might plug the catheter, from forming. The second, or inflation, arm has a small plastic valve that allows for the introduction or removal of sterile water through a very small channel to inflate or deflate the retaining balloon.
Foley catheters can also be used to "ripen" the cervix, to allow the induction of labour. The catheter is inserted behind the cervical wall and inflated. The remaining length of the catheter is gently pulled and taped to the inside of the woman's leg. The inflated balloon applies pressure to the cervix, like the baby's head would prior to labour, causing it to dilate. Over time the catheter is adjusted and re-taped to maintain pressure on the cervix. When the cervix has dilated sufficiently, the catheter simply drops out.
They were designed by Frederic Foley, a surgeon working in Boston, Massachusetts, in the 1930s, when he was a medical student
His original design was adopted by C. R. Bard, Inc. of Murray Hill, New Jersey, who manufactured the first prototypes and named them in honor of the surgeon.
A major problem with Foley catheters is that they have a tendency to contribute to urinary tract infections (UTI). This occurs because bacteria can travel up the catheters to the bladder where the urine can become infected. To combat this, the industry is moving to antibiotic coated catheters. This has been helpful, but it has not completely solved this major problem. An additional problem is that Foley catheters tend to become coated over time with a biofilm that can keep them from properly draining the bladder. This increases the degree of static urine left in the bladder, which further contributes to the problem of urinary tract infections. When a Foley catheter becomes clogged, it must be flushed or replaced. Thus keeping Foley Catheters from clogging may help reduce UTIs as well.
When Foley catheters are used
Foley catheters are used during the following situations:
• On patients who are anesthesized or sedated for surgery or other medical care
• On comatose patients
• On some incontinent patients
• On patients whose prostate is enlarged to the point that urine flow from the bladder is cut off. The catheter is kept in until the problem is resolved.
• On patients with acute urinary retention.
• On patients who are unable due to paralysis or physical injury to use either standard toilet facilities or urinals.
• Following urethral surgeries
• Following uretectomy
• Sometimes before Furosemide administration
Alternative treatments
• For obstructed prostates due to BPH: The Spanner Prostatic stent

Lumbar puncture

A patient undergoes a lumbar puncture at the hands of a neurologist. The reddish-brown swirls on the patient's back are tincture of iodine (an antiseptic).
In medicine, a lumbar puncture (colloquially known as a spinal tap) is a diagnostic and at times therapeutic procedure that is performed in order to collect a sample of cerebrospinal fluid (CSF) for biochemical, microbiological, and cytological analysis, or very rarely as a treatment ("therapeutic lumbar puncture") to relieve increased intracranial pressure.

Indications
The most common purpose for a lumbar puncture is to collect cerebrospinal fluid in a case of suspected meningitis, since there is no other reliable tool with which meningitis, a life-threatening but highly treatable condition, can be excluded. Young infants commonly require lumbar puncture as a part of the routine workup for fever without a source, as they have a much higher risk of meningitis than older persons and do not reliably show signs of meningeal irritation (meningismus). In any age group, subarachnoid hemorrhage, hydrocephalus, benign intracranial hypertension and many other diagnoses may be supported or excluded with this test.
Lumbar punctures may also be done to inject medications into the cerebrospinal fluid ("intrathecally"), particularly for spinal anesthesia or chemotherapy.It may also be used to detect the presence of malignant cells in the CSF,as in carcinomatous meningitis or medulloblastoma. Lumbar punctures can be unpleasant for some people, due to increased sensitivity when the needle is inserted to collect the cerebrospinal fluid.
Contraindications
Lumbar puncture should not be performed when idiopathic (unidentified cause) increased intracranial pressure (ICP) is present. The exception is therapeutic use of lumbar puncture to relieve ICP. Ideally, a CT scan should be performed prior to lumbar puncture to rule out space occupying lesions. Ophthalmoscopy for papilledema should also be performed prior to any LP to check for ICP. Also, lumbar puncture should not be attempted when there is coagulopathy, abnormal respiratory pattern,hypertension with bradycardia and deteriorating consciousness or when there are decreased levels of platelets in the blood (less than 50 x 109/L). Lumbar puncture in cases of vertebral deformities (scoliosis or kyphosis) is also contraindicated in hands of an unexperienced physician.[1][2]

Procedure

Spinal needles used in lumbar puncture.
In performing a lumbar puncture, first the patient is usually placed in a left (or right) lateral position with his/her neck bent in full flexion and knees bent in full flexion up to his/her chest, approximating a fetal position as much as possible. It is also possible to have the patient sit on a stool and bend his/her head and shoulders forward. The area around the lower back is prepared using aseptic technique. Once the appropriate location is palpated, local anaesthetic is infiltrated under the skin and then injected along the intended path of the spinal needle. A spinal needle is inserted between the lumbar vertebrae L3/L4 or L4/L5 and pushed in until there is a "give" that indicates the needle is past the dura mater. The needle is again pushed until there is a second 'give' that indicates the needle is now past the arachnoid mater, and in the subarachnoid space. The stylet from the spinal needle is then withdrawn and drops of cerebrospinal fluid are collected. The opening pressure of the cerebrospinal fluid may be taken during this collection by using a simple column manometer. The procedure is ended by withdrawing the needle while placing pressure on the puncture site. In the past, the patient would often be asked to lie on his/her back for at least six hours and be monitored for signs of neurological problems, though there is no scientific evidence that this provides any benefit. The technique described is almost identical to that used in spinal anesthesia, except that spinal anesthesia is more often done with the patient in a sitting position.
The upright seated position is advantageous in that there is less distortion of spinal anatomy which allows for easier withdrawal of fluid. It is preferred by some practitioners when a lumbar puncture is performed on an obese patient where having them lie on their side would cause a scoliosis and unreliable anatomical landmarks. On the other hand, opening pressures are notoriously unreliable when measured on a seated patient and therefore the left or right lateral (lying down) position is preferred if an opening pressure needs to be measured.
Patient anxiety during the procedure can lead to increased CSF pressure, especially if the person holds their breath, tenses their muscles or flexes their knees too tightly against their chest. Diagnostic analysis of changes in fluid pressure during lumbar puncture procedures requires attention both to the patient's condition during the procedure and to their medical history.[
Reinsertion of the stylet may decrease the rate of post lumbar puncture headaches.

Thoracocentesis or Pleural Tap
Thoracentesis (pronounced /ˌθɔrəsɨnˈtiːsɨs/) (also known as thoracocentesis or pleural tap) is an invasive procedure to remove fluid or air from the pleural space for diagnostic or therapeutic purposes. A cannula, or hollow needle, is carefully introduced into the thorax, generally after administration of local anesthesia. The procedure was first described in 1852.
The recommended location varies depending upon the source. It is critical that the patient holds their breath to avoid piercing the lung. Some sources recommend the midaxillary line, in the ninth intercostal space.

Chest X-ray showing a left-sided pleural effusion (right side of image). This can be treated with thoracentesis.

The illustration shows a person having thoracentesis. The person sits upright and leans on a table. Excess fluid from the pleural space is drained into a bag.

Indications
This procedure is indicated when unexplained fluid accumulates in the chest cavity outside the lung. In more than 90% of cases analysis of pleural fluid yields clinically useful information. If a large amount of fluid is present, then this procedure can also be used therapeutically to remove that fluid and improve patient comfort and lung function.
The most common causes of pleural effusions are cancer, congestive heart failure, pneumonia, and recent surgery. In countries where tuberculosis is common, this is also a common cause of pleural effusions.
When cardiopulmonary status is compromised (i.e. when the fluid or air has its repercussions on the function of heart and lungs), due to air (significant pneumothorax), fluid (pleural fluid) or blood (hemothorax) outside the lung, then this procedure is usually replaced with tube thoracostomy, the placement of a large tube in the pleural space.
Contraindications
An uncooperative patient or a coagulation disorder that can not be corrected are absolute contraindications.
Relative contraindications include cases in which the site of insertion has known bullous disease (e.g. emphysema), use of positive end-expiratory pressure (PEEP, see mechanical ventilation) and only one functioning lung (due to diminished reserve). The aspiration should not exceed 1L as there is a risk of development of pulmonary edema.
Complications
Major complications are pneumothorax (3-30%), hemopneumothorax, hemorrhage, hypotension (low blood pressure due to a vasovagal response) and reexpansion pulmonary edema.
Minor complications include a dry tap (no fluid return), subcutaneous hematoma or seroma, anxiety, dyspnea and cough (after removing large volume of fluid).
The use of ultrasound for needle guidance can minimize the complication rate.
Interpretation of pleural fluid analysis
Several diagnostic tools are available to determine the etiology of pleural fluid.
Transudate versus exudate
First the fluid is either transudate or exudate.
A transudate is defined as pleural fluid to serum total protein ratio of less than 0.5, pleural fluid to serum LDH ratio < 0.6, and absolute pleural fluid LDH < 200 IU or < 2/3 of the normal serum.
An exudate is any fluid that filters from the circulatory system into lesions or areas of inflammation. It can apply to plants as well as animals. Its composition varies but generally includes water and the dissolved solutes of the main circulatory fluid such as sap or blood. In the case of blood: it will contain some or all plasma proteins, white blood cells, platelets and (in the case of local vascular damage) red blood cells.
Exudate
• hemorrhage
• Infection
• Inflammation
• Malignancy
• Iatrogenic
• Connective tissue disease
• Endocrine disorders
• Lymphatic disorders vs Constrictive pericarditis
Transudate
• Congestive heart failure
• Nephrotic syndrome
• Hypoalbuminemia
• Cirrhosis
• Atelectasis
• trapped lung
• Peritoneal dialysis
• Superior vena cava obstruction
Amylase
A high amylase level (twice the serum level or the absolute value is greater than 160 Somogy units) in the pleural fluid is indicative of either acute or chronic pancreatitis, pancreatic pseudocyst that has dissected or ruptured into the pleural space, cancer or esophageal rupture.
Glucose
This is considered low if pleural fluid value is less than 50% of normal serum value. The differential diagnosis for this is:
• rheumatoid effusion.The levels are characteristically low (<15 mg/dL).
• lupus effusion
• bacterial empyema
• malignancy
• tuberculosis
• esophageal rupture (Boerhaave syndrome)
pH
Normal pleural fluid pH is approximately 7.60. A pleural fluid pH below 7.30 with normal arterial blood pH has the same differential diagnosis as low pleural fluid glucose.
Triglyceride and cholesterol
Chylothorax (fluid from lymph vessels leaking into the pleural cavity) may be identified by determining triglyceride and cholesterol levels, which are relatively high in lymph. A triglyceride level over 110 mg/dl and the presence of chylomicrons indicate a chylous effusion. The appearance is generally milky but can be serous.
The main cause for chylothorax is rupture of the thoracic duct, most frequently as a result of trauma or malignancy (such as lymphoma).
Cell count and differential
The number of white blood cells can give an indication of infection. The specific subtypes can also give clues as to the type on infection. The amount of red blood cells are an obvious sign of bleeding.
Cultures and stains
If the effusion is caused by infection, microbiological culture may yield the infectious organism responsible for the infection, sometimes before other cultures (e.g. blood cultures and sputum cultures) become positive. A Gram stain may give a rough indication of the causative organism. A Ziehl-Neelsen stain may identify tuberculosis or other mycobacterial diseases.
Cytology
Cytology is an important tool in identifying effusions due to malignancy. The most common causes for pleural fluid are lung cancer, metastasis from elsewhere and mesothelioma. The latter often presents with an effusion. Normal cytology results do not reliably rule out malignancy, but make the diagnosis more unlikely.

Abdominal tap
Alternative Names: Peritoneal tap; Paracentesis
An abdominal tap is a procedure used to remove fluid from the abdomen.
How the Test is Performed
This test may be done in an office setting, treatment room, or hospital.
The puncture site will be cleaned and shaved, if necessary. You then receive a local numbing medicine. The tap needle is inserted 1 - 2 inches into the abdomen. Sometimes a small cut is made to help insert the needle. The fluid is pulled out into a syringe.
The needle is removed. A dressing is placed on the puncture site. If a cut was made, one or two stitches may be used to close it.
There are two kinds of abdominal taps:
• Diagnostic tap -- a small amount of fluid is taken and sent to the laboratory for testing
• Large volume tap -- several liters may be removed to relieve abdominal pain and fluid buildup
How to Prepare for the Test
Let your health care provider know if you:
• Have any allergies to medications or numbing medicine
• Are taking any medications (including herbal remedies)
• Have any bleeding problems
• Might be pregnant
Infants and children:
The preparation you can provide for this test depends on your child's age, previous experience, and level of trust. For general information regarding how you can prepare your child, see the following topics:
• Infant test/procedure preparation (birth - 1 year)
• Toddler test/procedure preparation (1 - 3 years)
• Preschooler test/procedure preparation (3 - 6 years)
• School age test/procedure preparation (6 - 12 years)
• Adolescent test/procedure preparation (12 - 18 years)
How the Test Will Feel
You may feel a stinging sensation from the numbing medicine, or pressure as the needle is inserted.
If a large amount of fluid is taken out, you may feel dizzy or light-headed. Tell the health care provider if you feel dizzy.
Why the Test is Performed
Normally, the abdomen contains only a small amount of fluid. In certain conditions, large amounts of fluid can build up in the abdomen.
An abdominal tap may be done to diagnose the cause of fluid buildup. It may also be done to diagnose infected abdominal fluid, or to remove a large amount of fluid to reduce abdominal pain.
Normal Results
Normally, there should be little or no fluid in the abdomen.
What Abnormal Results Mean
An examination of abdominal fluid may show:
• Appendicitis
• Cirrhosis of the liver
• Damaged bowel
• Heart disease
• Infection
• Kidney disease
• Pancreatic disease
• Tumor (cancerous or noncancerous)
Risks
There is a slight chance of the needle puncturing the bowel, bladder, or a blood vessel in the abdomen. If a large quantity of fluid is removed, there is a slight risk of lowered blood pressure and kidney failure. There is also a slight chance of infection.
______________________________________________________________________________

Bone marrow examination
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A Wright's stained bone marrow aspirate smear from a patient with leukemia.

Bone marrow examination refers to the pathologic analysis of samples of bone marrow obtained by bone marrow biopsy (often called a trephine biopsy) and bone marrow aspiration. Bone marrow examination is used in the diagnosis of a number of conditions, including leukemia, multiple myeloma, anemia, and pancytopenia. The bone marrow produces the cellular elements of the blood, including platelets, red blood cells and white blood cells. While much information can be gleaned by testing the blood itself (drawn from a vein by phlebotomy), it is sometimes necessary to examine the source of the blood cells in the bone marrow to obtain more information on hematopoiesis; this is the role of bone marrow aspiration and biopsy.
Components of the procedure

A bone marrow harvest.

A volunteer donating bone marrow for scientific research.
Bone marrow samples can be obtained by aspiration and trephine biopsy. Sometimes, a bone marrow examination will include both an aspirate and a biopsy. The aspirate yields semi-liquid bone marrow, which can be examined by a pathologist under a light microscope as well as analyzed by flow cytometry, chromosome analysis, or polymerase chain reaction (PCR). Frequently, a trephine biopsy is also obtained, which yields a narrow, cylindrically shaped solid piece of bone marrow, 2mm wide and 2 cm long (60 μL), which is examined microscopically (sometimes with the aid of immunohistochemistry) for cellularity and infiltrative processes. An aspiration, using a 20 mL syringe, yields approximately 300 μL of bone marrow.[1] A volume greater than 300 μL is not recommended, since it may dilute the sample with peripheral blood.[1]
Comparison
Aspiration Biopsy
Advantages • Fast
• Gives relative quantity of different cell types
• Gives material to further study, e.g. molecular genetics and flow cytometry
• Gives cell and stroma constitution
• Represents all cells
• Explains cause of "dry tap" (aspiration gives no blood cells)
Drawbacks Doesn't represent all cells Slow processing
Aspiration doesn't always represent all cells since, as some such as lymphoma stick to the trabecula, and would thus be missed by a simple aspiration.
Site of procedure
Bone marrow aspiration and trephine biopsy are usually performed on the back of the hipbone, or posterior iliac crest. However, an aspirate can also be obtained from the sternum (breastbone). A trephine biopsy should never be performed on the sternum, due to the risk of injury to blood vessels, lungs or the heart.
How the test is performed

A needle used for bone marrow aspiration, with removable stylet.
A bone marrow biopsy may be done in a health care provider's office or in a hospital. Informed consent for the procedure is typically required. The patient is asked to lie on his or her abdomen (prone position) or on his/her side (lateral decubitus position). The skin is cleansed, and a local anesthetic such as lidocaine is injected to numb the area. Patients may also be pretreated with analgesics and/or anti-anxiety medications, although this is not a routine practice.
Typically, the aspirate is performed first. An aspirate needle is inserted through the skin until it abuts the bone. Then, with a twisting motion, the needle is advanced through the bony cortex (the hard outer layer of the bone) and into the marrow cavity. Once the needle is in the marrow cavity, a syringe is attached and used to aspirate ("suck out") liquid bone marrow. A twisting motion is performed during the aspiration to avoid excess content of blood in the sample, which might be the case if an excessively large sample from one single point is taken.
Subsequently, the biopsy is performed if indicated. A different, larger trephine needle is inserted and anchored in the bony cortex. The needle is then advanced with a twisting motion and rotated to obtain a solid piece of bone marrow. This piece is then removed along with the needle. The entire procedure, once preparation is complete, typically takes 10–15 minutes.
If several samples are taken, the needle is removed between the samples to avoid blood coagulation.
After the procedure
After the procedure is complete, the patient is typically asked to lie flat for 5–10 minutes to provide pressure over the procedure site. After that, assuming no bleeding is observed, the patient can get up and go about their normal activities. Paracetamol (acetaminophen) or other simple analgesics can be used to ease soreness, which is common for 2–3 days after the procedure. Any worsening pain, redness, fever, bleeding or swelling may suggest a complication. Patients are also advised to avoid washing the procedure site for at least 24 hours after the procedure is completed.
Contraindications
There are few contraindications to bone marrow examination. The only absolute reason to avoid performing a bone marrow examination is the presence of a severe bleeding disorder which may lead to serious bleeding after the procedure. If there is a skin or soft tissue infection over the hip, a different site should be chosen for bone marrow examination. Bone marrow aspiration and biopsy can be safely performed even in the setting of extreme thrombocytopenia (low platelet count).
Complications
While mild soreness lasting 12–24 hours is common after a bone marrow examination, serious complications are extremely rare. In a large review, an estimated 55,000 bone marrow examinations were performed, with 26 serious adverse events (0.05%), including one fatality. The same author collected data on over 19,000 bone marrow examinations performed in the United Kingdom in 2003, and found 16 adverse events (0.08% of total procedures), the most common of which was bleeding. In this report, complications, while rare, were serious in individual cases.

Tracheotomy

Completed tracheotomy:
1 - Vocal cords
2 - Thyroid cartilage
3 - Cricoid cartilage
4 - Tracheal cartilages
5 - Balloon cuff

Tracheotomy and tracheostomy are surgical procedures on the neck to open a direct airway through an incision in the trachea (the windpipe). They are performed by emergency physicians, and surgeons. Both surgical and percutaneous techniques are now widely used.
While tracheostomy may have possibly been portrayed on ancient Egyptian tablets,[1] the first correct description of the tracheotomy operation for patients who are suffocating was described by Ibn Zuhr in the 12th century,[2] and the currently used surgical tracheostomy technique was described in 1909 by Dr. Chevalier Jackson of Pittsburgh, Pennsylvania.
Terminology
Tracheotomy, from the Greek root tom- meaning "to cut," refers to the procedure of cutting into the trachea and is an emergency procedure.[3]
A tracheostomy, from the root stom- meaning "mouth," refers to the making of a semi-permanent or permanent opening, and to the opening itself.
Some sources offer different definitions of the above terms. Part of the ambiguity is due to the uncertainty of the intended permanence of the stoma at the time it is created.[4]
Uses of tracheotomy
The conditions in which a tracheotomy may be used are:
• Acute setting - maxillofacial injuries, large tumors of the head and neck, congenital tumors, e.g. branchial cyst, acute inflammation of head and neck, and
• Chronic / elective setting - when there is need for long term mechanical ventilation and tracheal toilet, e.g. comatose patients, surgery to the head and neck.
In emergency settings, in the context of failed endotracheal intubation or where intubation is contraindicated, cricothyroidotomy or mini-tracheostomy may be performed in preference to a tracheostomy.
Tracheotomy procedure
1. Curvilinear skin incision along relaxed skin tension lines (RSTL) between sternal notch and cricoid cartilage.
2. Midline vertical incision dividing strap muscles.
3. Division of thyroid isthmus between ligatures.
4. Elevation of cricoid with cricoid hook.
5. Placement of tracheal incision. An inferior based flap, or Björk flap, (through second and third tracheal rings) is commonly used. The flap is then sutured to the inferior skin margin. Alternatives include a vertical tracheal incision (pediatric) or excision of an ellipse of anterior tracheal wall.
6. Insert tracheostomy tube (with concomitant withdrawal of endotracheal tube), inflate cuff, secure with tape around neck or stay sutures.
7. Connect ventilator tubing.
It is also possible to make a simple vertical incision between tracheal rings (typically 2nd and 3rd) for the incision. Rear end flaps may produce more intratracheal granulation tissue at the site of the incisions, making it less favorable to some surgeons.
Percutaneous tracheotomy procedure
1. Curvilinear skin incision along relaxed skin tension lines between sternal notch and cricoid cartilage.
2. Midline blunt dissection down to the trachea (optional depending on technique).
3. Insertion of 14-gauge plastic cannula and needle with fluid filled syringe attached into trachea. Aspiration of air confirms correct placement of the tip in the trachea.
4. Removal of needle leaving cannula in place.
5. Insertion of soft tipped guide wire into trachea through cannula.
6. Removal of cannula leaving guide wire in place.
7. Tracheal dilatation is now undertaken - different techniques do this in different ways.
1. Ciaglia - the sequential insertion and removal of a series (usually 4-5) of increasing larger dilators over the wire into the trachea.
2. Griggs - insertion of a specially designed pair of guide-wire forceps along the wire into the trachea and then are opened to complete the dilation in one step.
3. Rhino - insertion of a single large tapered dilator over a plastic guidewire reinforcement.
4. Frova Percutwist - insertion of a specially designed screw of increasing diameter which rotates to create the dilatation.
8. Insert tracheostomy tube (with concomitant withdrawal of endotracheal tube), inflate cuff, secure with tape around neck or stay sutures.
9. Connect ventilator tubing.
Risks
During the procedure, there is a risk of damaging the recurrent laryngeal nerves. These nerves control the vocal cords. If one of the nerves is damaged a patient will probably have a problem with his/her voice; if both of the nerves are damaged, the patient will lose his/her speech. This risk of nerve damage is the reason emergency tracheotomies are performed higher up, in the larynx and why tracheotomies have to be done in hospital under anesthetic. Professor Stephen Hawking lost his speech due to a tracheotomy after contracting pneumonia.
Moreover, if the recurrent laryngeal nerve is damaged, the patient will have trouble controlling the flow of air through the rima glottidis, thus ultimately leading to inhibited breathing or suffocation.

LATTITUDE AND LONGITUDE OF VAIKOM

2010-06-08T09:37:00.000-07:00

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2010-06-03T08:40:00.001-07:00

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NATURAL TREATMENT FOR CANCER

2008-09-07T19:31:00.000-07:00

For seven years a major U.S. pharmaceutical company knew of an astounding cancer killer--but decided to tell nobody about it...ever!!

My Dear Friend,

There isn't a scarier moment in anyone's life than when a biopsy comes back positive. It's cancer...It's the beginning of a battle in which no holds are barred. Anyone with any sense will do almost anything at all to try and destroy the killer disease...

Imagine one pharmaceutical company had the answer...had it, as it was, for SEVEN FULL YEARS...yet, not only didn't tell anyone about it--but decided not to tell anyone about it ever!?

Why? Because the substance they researched is completely natural so they couldn't take out a patent on it.

For seven long years they tried to artificially mimic the compound's effect in the lab but couldn't. Mother Nature is the only thing that worked. They had no way to make money on the stuff--so they shelved all of their research.

Can you imagine how many Americans may have died in vain during that time?

Read on to learn the full story of the astounding tree from the Amazon Rainforest they kept from you--but that's just the beginning.

Within the next 10 years almost 50% of all Americans will discover, to their horror, that the "tight feeling" is, indeed, a heart attack...

And almost one out of every three of them will die...

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Needlessly , because, right now, as you read these words, brilliant medical researchers are successfully treating cancer...heart disease...high-blood pressure...diabetes...osteoporosis...prostate problems...back pain...chronic fatigue...allergies...asthma and arthritis--without resorting to dangerous drugs or surgery.

Yet, while these therapies are available today--almost none of them will get to the people who need them so desperately for at least 10 years!

Can you, or someone you love dearly, afford to wait?

You need these breakthroughs now because you or someone you love may be in pain now...or taking toxic drugs...or facing surgery.

You may actually be in danger of losing your life. You need to know about all your options. And, unfortunately, your doctor doesn't have all the answers. Chances are he doesn't know about these cures himself! Hard to believe?

Over 10 years ago, a brilliant group of researchers set out to evaluate the cancer-blocking properties of the common mineral selenium. They found it reduced lung cancer risk by a whopping 46%, colon cancer risk by 58%, and prostate cancer by 62%!! Their findings were published in the Journal of The American Medical Association...finally!

Through no fault of his own, it could take your doctor an additional 10 long years to hear about a natural cancer treatment that's revolutionary and could help make cancer more manageable. But is there a reason why you should wait that long to know? Absolutely not! I'll tell you all about it--keep reading...

It will take most Americans another 10 years to be told the vitamin E they've been taking is NOT aiding them in their fight against heart disease. Chances are, even your doctor doesn't know that a safe, more effective, form of vitamin E is just a single miracle-pill away! You, however, won't have to wait that long. You'll find details if you keep reading.

And, similarly, your doctor knows there's little that can be done against the ravages of aging. He may know that human growth hormone (HGH) can turn back your biological clock by as much as 20 years. But he also knows that HGH treatment is not only very expensive, but is also dangerous and fraught with severe side effects.

What your doctor probably doesn't know, and isn't likely to learn about for another 10 years, is that RIGHT NOW there's an HGH treatment available that DOES NOT involve the administration of any hormone. This treatment is as effective as HGH hormone therapy, but is completely safe and costs about as much as a cup of coffee a day!

Imagine regaining lost muscle mass and tone...more hair...flexibility... sharper vision...thicker, smoother, and more supple skin...it's available today and I'll tell you all about it.

But, believe it or not, not knowing
about these cures isn't the worst of it!

Some of the latest breakthroughs your doctor DOES know about and use are actually worse than the health problems he's trying to solve!

Do you--or anyone you know--suffer from arthritis? Millions of Americans do. In some cases, the illness turns their lives into a living hell of disability and pain.

If you're one of those people, just walk into any doctor's office and I'll bet you'll walk out with an NSAID (Non-steroidal anti-inflammatory drug).

You're probably nodding your head and saying: "been there...done that"...and I bet you're still in pain! Do you know why? Because NSAIDs are ultimately ineffective in beating arthritis!

Yes, they mask the pain for a little while--but they don't ever get to the root of the problem. What temporary relief you do find can come at a great cost. For starters, they can damage your liver and kidneys and induce gastrointestinal bleeding. Plus, they can actually make your arthritis worse by damaging your cartilage!

And all that suffering is needless!

I'll tell you about an amazing compound that goes well beyond reducing arthritis pain. It can actually repair and rebuild damaged joints, and, in effect, help to reverse arthritis-- without side effects!

So the question returns, more emphatic than ever:

If these cures are so wonderful, what keeps them away from the American people? Why is it happening?

Alas, your health is BIG business!

The main reason why natural, cutting-edge cures are doomed to remain the privilege of the very lucky few is because the mainstream medical establishment and the big drug manufacturers make sure of that.

No, it's not a conspiracy. It's just that hundreds of billions of dollars are at stake. Like it or not, your health happens to be a huge business and the "big boys" of the establishment play hard ball, and they play for keeps.

Think about it for a moment: The most powerful drug makers in the world have invested hundreds of millions to create a number of anti- cholesterol drugs. These drugs are only partially effective and are laden with serious side effects.

So, you tell me: Why would those drug makers let anyone tell you that you can lower your cholesterol--without any side effects--by eating about 4 cents worth of...simple onion a day?

You have the right to know about all these breakthroughs today and make your own decisions. After all, it's your life!

And this is why Health Sciences Institute, or HSI, was created.

Some of the most brilliant medical minds
on earth got together, because you have
the right to know NOW!

The obstacles that stand in the way of pioneering natural medical research scientists are immense. Dedicated researchers who wish to bring you breakthrough, life-saving, natural cures find their ways all but completely blocked.

...they face the scorn of the establishment and interest groups

...they face the financial pressure of drug makers (who, by the way, monitor almost all pharmacies and know almost to a "t" exactly how many prescriptions each doctor writes for their products. They actually call "underperforming" doctors to task!)

...they're made to face suffocating, endless red tape

...they're blocked at every step by out-of-control regulators

Traditionally, most of them just gave up...until now.

Now, for the first time ever, instead of throwing their hands up in frustration, a world-wide group of brilliant doctors and scientists did the unthinkable. They got together.

Pioneers of revolutionary medicine--from aging and allergies to cancer and heart disease--realized that with a combined voice they could get their discoveries to light--and bring them to you.

This is why they joined Health Sciences Institute--a unique members-only organization that's dedicated to doing one thing: breaking the barriers big-money medicine has placed before revolutionary natural cures--and bringing breakthrough information on those cures to you RIGHT NOW!! No more waiting.

As a result, the Health Sciences Institute has become one of the world's most important and revolutionary sources for cutting-edge medical information. Unlike anything before it, HSI doesn't represent the opinion of a single, self-appointed "guru," but contains the unmatched combined wisdom of the world's most formidable medical minds.

And, as you'll find ahead, Health Sciences Institute doesn't just tell you about a new therapy--it also tells you where to get it, recommended dosages, what results you may reasonably expect, and how quickly.

HSI does all this through a monthly publication called the Health Sciences Institute Members Alert.

Almost overnight, the clear and easy-to-read HSI Members Alert , has become a legend in the alternative medical industry as the quintessential source for cutting-edge medical discoveries. Many physicians all over the world use the HSI Members Alert to bring their own patients medical solutions and treatments available nowhere else.

The reason I'm writing you this letter today is to invite you to become a member of the Health Sciences Institute--to become one of the privileged few who can learn ways to eradicate pain and illness from their lives today, while the rest of America, unfortunately, has to wait.

To help you make up your mind, we've gathered some of the recent natural healing breakthroughs discovered by Health Sciences Institute doctors and researchers in this report. The therapies detailed here are taken from the pages of the HSI Members Alert and are only a small sampling of the life-saving breakthroughs that can be yours.

Should you choose to become a member, the complete story of these exciting therapies is waiting for you in your FREE Urgent Health Alert Library . But I'll tell you more about it later.

So, go ahead and read. When you've finished and are ready to make your decision, just ask yourself a simple question:

Can you and your loved ones afford NOT to know about any of this?

Sincerely yours,
Jenny Thompson
Director, Health Sciences Institute

Chapter 1

How many people died in vain while this billion-dollar
drug maker concealed the secret of the miraculous Graviola tree?

If there ever was a single example that makes it dramatically clear why the existence of Health Sciences Institute is so vital to Americans like you, it's the incredible story behind the Graviola tree.

The truth is stunningly simple: Deep within the Amazon Rainforest grows a tree that could literally revolutionize what you, your doctor, and the rest of the world thinks about cancer treatment and chances of survival. The future has never looked more promising.

Research shows that with extracts from this miraculous tree it now may be possible to...

* Attack cancer safely and effectively with an all-natural therapy that does not cause extreme nausea, weight loss and hair loss
* Protect your immune system and avoid deadly infections
* Feel stronger and healthier throughout the course of the treatment
* Boost your energy and improve your outlook on life

The source of this information is just as stunning: It comes from one of America's largest drug manufacturers, the fruit of over 20 laboratory tests conducted since the 1970's! What those tests revealed was nothing short of mind numbing... Extracts from the tree were shown to:

* Effectively target and kill malignant cells in 12 types of cancer, including colon, breast, prostate, lung and pancreatic cancer.
* The tree compounds proved to be up to 10,000 times stronger in slowing the growth of cancer cells than Adriamycin, a commonly used chemotherapeutic drug!
* What's more, unlike chemotherapy, the compound extracted from the Graviola tree selectively hunts down and kills only cancer cells. It does not harm healthy cells!

The amazing anti-cancer properties of the Graviola tree have been extensively researched--so why haven't you heard anything about it? If Graviola extract is as half as promising as it appears to be--why doesn't every single oncologist at every major hospital insist on using it on all his or her patients?

The spine-chilling answer illustrates just how easily our health--and for many, our very lives(!)--are controlled by money and power.

Graviola--the plant that worked too well

One of America's biggest billion-dollar drug makers began a search for a cancer cure and their research centered on Graviola, a legendary healing tree from the Amazon Rainforest.

Various parts of the Graviola tree--including the bark, leaves, roots, fruit and fruit-seeds--have been used for centuries by medicine men and native Indians in South America to treat heart disease, asthma, liver problems and arthritis. Going on very little documented scientific evidence, the company poured money and resources into testing the tree's anti-cancerous properties--and were shocked by the results. Graviola proved itself to be a cancer-killing dynamo.

But that's where the Graviola story nearly ended.

The company had one huge problem with the Graviola tree--it's completely natural, and so, under federal law, not patentable. There's no way to make serious profits from it.

It turns out the drug company invested nearly seven years trying to synthesize two of the Graviola tree's most powerful anti-cancer ingredients. If they could isolate and produce man-made clones of what makes the Graviola so potent, they'd be able to patent it and make their money back. Alas, they hit a brick wall. The original simply could not be replicated. There was no way the company could protect its profits--or even make back the millions it poured into research.

As the dream of huge profits evaporated, their testing on Graviola came to a screeching halt. Even worse, the company shelved the entire project and chose not to publish the findings of its research!

Luckily, however, there was one scientist from the Graviola research team whose conscience wouldn't let him see such atrocity committed. Risking his career, he contacted a company that's dedicated to harvesting medical plants from the Amazon Rainforest and blew the whistle.

Miracle unleashed

When researchers at the Health Sciences Institute were alerted to the news of Graviola, they began tracking the research done on the cancer-killing tree. Evidence of the astounding effectiveness of Graviola--and its shocking cover-up--came in fast and furious...

...The National Cancer Institute performed the first scientific research in 1976. The results showed that Graviola's "leaves and stems were found effective in attacking and destroying malignant cells." Inexplicably, the results were published in an internal report and never released to the public...

...Since 1976, Graviola has proven to be an immensely potent cancer killer in 20 independent laboratory tests, yet no double-blind clinical trials--the typical benchmark mainstream doctors and journals use to judge a treatment's value--were ever initiated...

...A study published in the Journal of Natural Products, following a recent study conducted at Catholic University of South Korea stated that one chemical in Graviola was found to selectively kill colon cancer cells at "10,000 times the potency of (the commonly used chemotherapy drug) Adriamycin..."

...The most significant part of the Catholic University of South Korea report is that Graviola was shown to selectively target the cancer cells, leaving healthy cells untouched. Unlike chemotherapy, which indiscriminately targets all actively reproducing cells (such as stomach and hair cells), causing the often devastating side effects of nausea and hair loss in cancer patients.

...A study at Purdue University recently found that leaves from the Graviola tree killed cancer cells among six human cell lines and were especially effective against prostate, pancreatic and lung cancers...

Seven years of silence broken--it's finally here!

A limited supply of Graviola extract, grown and harvested by indigenous people in Brazil, is finally available in America. The full Graviola story--including where you can get it and how to use it--is included in Beyond Chemotherapy: New Cancer Killers, Safe as Mother's Milk, a Health Sciences Institute FREE special bonus report on natural substances that will effectively revolutionize the fight against cancer.

This crucial report (along with five more FREE reports) is yours ABSOLUTELY FREE with a new membership to the Health Sciences Institute. It's just one example of how absolutely vital each report from the Institute can be to your life and those of your loved ones.

From breakthrough cancer and heart research and revolutionary Amazon Rainforest herbology to world-leading anti-aging research and nutritional medicine, every monthly Health Sciences Institute Member's Alert puts in your hands today cures the rest of America--including your own doctor(!)--is likely to find out only ten years from now.

You need the Health Sciences Institute in your life because you and your loved ones deserve to know--and you deserve to know it NOW!!

MEDICAL TERMINOLOGIES

2008-08-28T05:28:00.000-07:00

MEDICAL TERMINOLOGIES
WOCKHARDT INSTITUTE OF NURSING
BANGALORE-78.
CREATED BY SHYAM MOHAN

>>>>GIT<<<<

Antacids - Antacids are medicines that neutralize stomach acid.

Antiemitics - Antiemetic drugs are used to prevent vomiting (emesis) in chemotherapy patients and postoperative patients. Antiemetic drugs are drugs used to combat nausea and vomiting.

H2-receptor antagonist - The H2 antagonists are competitive inhibitors of histamine at the parietal cell H2 receptor. They suppress the normal secretion of acid by parietal cells and the meal-stimulated secretion of acid.

Proton pump inhibitor - They are a group of drugs whose main action is pronounced and long-lasting reduction of gastric acid production. They are the most potent inhibitors of acid secretion available today.

Laxatives - Laxatives are products that promote bowel movements.

Antidiarrhoeal -Drug used to treat diarrhoea by absorbing water from the intestine, altering intestinal motility, or adsorbing toxins.

>>>>BLOOD AND BLOOD FORMING ORGANS<<<<

Anticoagulant - Compounds that prevent or slow the process of blood clotting or coagulation, either in samples of blood taken for analysis or in the body.
There are two main types of anticoagulants: heparin and vitamin K antagonists (e.g., warfarin).

Antihypertensives - They are a class of drugs that are used in medicine and pharmacology to treat hypertension (high blood pressure).

Diuretics - Diuretics are medicines that help reduce the amount of water in the body.
Diuretics are used to treat the buildup of excess fluid in the body that occurs with some medical conditions such as congestive heart failure, liver disease, and kidney disease. Some diuretics are also prescribed to treat high blood pressure & help the kidneys eliminate excess salt and water from the body's tissues and blood.

Vasodilators - Vasodilators are medicines that act directly on muscles in blood vessel walls to make blood vessels widen (dilate).
Examples of vasodilators are hydralazine (Apreso-line) and minoxidil (Loniten).

Antianginal - An antianginal is any drug used in the treatment of angina pectoris, a symptom of ischaemic heart disease.

Thrombolytic drug - substance, such as streptokinase or tissue plasminogen activator (tPA), that causes the breakdown of blood clots that obstruct the flow of blood through the vessels. Its uses include injection during or shortly after a heart attack or stroke to prevent clots from blocking blood flow to the heart muscle or brain.

Antiarrhythmic agent - Antiarrhythmic agents are a group of pharmaceuticals that are used to suppress fast rhythms of the heart (cardiac arrhythmias), such as atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation.

Angiotensin - Converting Enzyme Inhibitors- Angiotensin-converting enzyme inhibitors (also called ACE inhibitors) are medicines that block the conversion of the chemical angiotensin I to a substance that increases salt and water retention in the body.

ACE inhibitor - Any of a class of drugs that cause vasodilation and are used to treat hypertension and heart failure.

Hypolipidemic agent - are a diverse group of pharmaceuticals that are used in the treatment of hyperlipidemias. They are called lipid-lowering drugs (LLD) or agents.

Beta Blockers - Beta blockers are medicines that affect the body's response to certain nerve impulses. This, in turn, decreases the force and rate of the heart's contractions, which lowers blood pressure and reduces the heart's demand for oxygen.

>>>>SKIN<<<<

Antipruritic - Antipruritics, also known as anti-itch drugs, are medications that inhibit the itching (Latin: pruritus) that is often associated with sunburns, allergic reactions, eczema, psoriasis, chickenpox, fungal infections, insect bites and stings like those from mosquitoes, fleas, and mites, and contact dermatitis and urticaria caused by plants such as poison ivy (urushiol-induced contact dermatitis) or stinging nettle.
Eg : Antihistamines such as diphenhydramine (Benedryl), Corticosteroids such as hydrocortisone topical cream, Local anesthetics such as benzocaine topical cream (Lanacaine), Counterirritants such as mint oil, menthol, or camphor

>>>>REPRODUCTIVE SYSTEM <<<<

Hormonal contraception - Hormonal contraception refers to birth control methods that act on the hormonal system.

Fertility drug - Any of a variety of substances used to increase the possibility of conception and successful pregnancy.

Selective estrogen receptor modulator- Selective estrogen receptor modulators (SERMs) are a class of medication that acts on the estrogen receptor.[1] A characteristic that distinguishes these substances from pure receptor agonists and antagonists is that their action is different in various tissues, thereby granting the possibility to selectively inhibit or stimulate estrogen-like action in various tissues.

Sex hormone - Any of various hormones, such as estrogen and androgen, affecting the growth or function of the reproductive organs, the development of secondary sex characteristics, and the behavioral patterns of animals.

>>>>ENDOCRINE SYSTEM<<<<

Antidiabetic drugs - are medicines that help control blood sugar levels in people with diabetes mellitus (sugar diabetes).

Corticosteroids - Corticosteriods are a group of natural and synthetic analogues of the hormones secreted by the hypothalamic-anterior pituitary-adrenocortical (HPA) axis, more commonly referred to as the pituitary gland. These include glucocorticoids, which are anti-inflammatory agents with a large number of other functions; mineralocorticoids, which control salt and water balance primarily through action on the kidneys; and corticotropins, which control secretion of hormones by the pituitary gland.

Thyroid Hormones - Thyroid hormones are artificially made hormones that make up for a lack of natural hormones produced by the thyroid gland.eg-levothyroxine (Synthroid, Levoxyl, Levothroid).

>>>>INFECTION & INFESTATIONS<<<<

Antibiotics - Antibiotics may be informally defined as the sub-group of anti-infectives that are derived from bacterial sources and are used to treat bacterial infections.
Eg -Sulfonamides,Declomycin

Antiviral Drugs - Antiviral drugs are medicines that cure or control virus infections.
Eg - there are currently only 11 antiviral drugs available, covering four types of virus.
Acyclovir (Zovirax), famciclovir (Famvir), and valacyclovir (Valtrex) are effective against herpesvirus, including herpes zoster and herpes genitalis.
Amantadine (Symmetrel), oseltamivir (Tamiflu), rimantidine (Flumadine), and zanamivir (Relenza) are useful in treatment of influenza virus.
Amantadine, rimantadine, and oseltamivir may be administered throughout the flu season as preventatives for patients who cannot take influenza virus vaccine.
Cidofovir (Vistide), foscarnet (Foscavir), and ganciclovir (Cytovene) have been beneficial in treatment of cytomegalovirus in immunosupressed patients, primarily HIV-positive patients and transplant recipients.

Vaccine - Agent prepared to produce active immunity that usually kills microbes, attenuated live microbes, or variant strains of microbes and can induce antibody production without producing disease.
A preparation of a weakened or killed pathogen, such as a bacterium or virus, or of a portion of the pathogen's structure that upon administration stimulates antibody production or cellular immunity against the pathogen but is incapable of causing severe infection.

Antifungal drug - An antifungal drug is medication used to treat fungal infections such as athlete's foot, ringworm, candidiasis (thrush), serious systemic infections such as cryptococcal meningitis, and others.

Antiprotozoal agent - is a class of pharmaceuticals used in treatment of protozoal infections.
Examples : Eflornithine,Furazolidone,Melarsoprol,Metronidazole,Ornidazole,Paromomycin sulfate,Pentamidine,Pyrimethamine,Tinidazole.

Anthelmintic - Anthelmintics are drugs that expel parasitic worms (helminths) from the body, by either killing or stunning them. A traditional remedy of this type is often called a vermifuge or vermicide.

>>>>MALIGNANT & IMMUNE DISEASE<<<<

Chemotherapy - Chemotherapy is treatment of cancer with anticancer drugs.

Immunosuppressive drug - any of a variety of substances used to prevent production of antibodies. They are commonly used to prevent rejection by a recipient's body of an organ transplanted from a donor

>>>>MUSCLES, BONES & JOINTS<<<<

Anabolic steroid - A group of synthetic hormones that promote the storage of protein and the growth of tissue, sometimes used by athletes to increase muscle size and strength.

Anti-inflammatory - Preventing or reducing inflammation.

Disease-modifying antirheumatic drug - is a category of drugs used in many autoimmune disorders to slow down disease progression. Their use was first propagated in rheumatoid arthritis (hence their name) but has come to include many other diseases, such as Crohn's disease, lupus erythematosus (SLE), idiopathic thrombocytopenic purpura (ITP), myasthenia gravis and various others.

Muscle relaxant - An agent that specifically aids in reducing muscle tone. Most such agents inhibit the transmission of nerve impulses at the somatic neuromuscular junctions. They include tubocurarine, gallamine, pancuronium, succinylcholine and decamethonium bromide.

>>>>BRAIN & NERVOUS SYSTEM<<<<

Anesthesia - A drug, administered for medical or surgical purposes, that induces partial or total loss of sensation and may be topical, local, regional, or general, depending on the method of administration and area of the body affected.

Analgesic - is any member of the diverse group of drugs used to relieve pain (achieve analgesia).

Anticonvulsants - Anticonvulsants are a class of drugs indicated for the treatment of various types of seizures associated with seizure disorders such as epilepsy, a neurological dysfunction in which excessive surges of electrical energy are emitted in the brain, and other disorders.

Mood stabilizer - A mood stabilizer is a psychiatric medication used to treat mood disorders characterized by rapid and unstable mood shifts. The most common is bipolar disorder, where mood stabilizers suppress swings between mania and depression, and these drugs are also used in borderline personality disorder. Most mood stabilizers are anticonvulsants, with the important exception of lithium, which is the oldest and best known mood stabilizing drug.

Anxiolytic drugs - Preventing or reducing anxiety.Anxiolytic drugs are drugs having anti-anxiety effects. They are sometimes referred to as minor tranquilizers.

Antipsychotic drugs - Antipsychotic drugs are a class of medicines used to treat psychosis and other mental and emotional conditions

Antidepressant Drugs - Antidepressant drugs are medicines that relieve symptoms of depressive disorders.

Stimulant - Something that causes and encourages a given response. A food or drink, especially an alcoholic drink, believed to have a stimulating effect.

>>>>RESPIRATORY SYSTEM<<<<

Bronchodilators - Bronchodilators are medicines that help open the bronchial tubes (airways) of the lungs, allowing more air to flow through them.

Decongestants - Decongestants are medicines used to relieve nasal congestion (stuffy nose).

Antihistamines - Antihistamines are drugs that block the action of histamine (a compound released in allergic inflammatory reactions) at the H1 receptor sites, responsible for immediate hypersensitivity reactions such as sneezing and itching. Members of this class of drugs may also be used for their side effects, including sedation and antiemesis (prevention of nausea and vomiting).

Antipyretic - A drug that reduces fever primarily through action on the hypothalamus, thereby resulting in increased heat dissipation through augmented peripheral blood flow and sweating.
drugs that lower your body temperature from a raised state.

MOBILE PHONE WEBS

2008-08-28T05:23:00.000-07:00

ZEDGE, MOBILE9,GET-JAR,MOSH.NOKIA,CRAZY4MOBILZ,FUNMAZA,NOKIASOFTWARE.NL,s60v3,DOTNEXT....

SOFTWARE DOWNLOADS

2008-08-28T05:19:00.000-07:00

http://www.trinityfiles.com/

http://www.ddlspot.com/

http://www.games-for-gamers.com/

http://www.freecovers.net/

An Overview of IELTS

2008-08-28T05:16:00.000-07:00

An Overview of IELTS Academic Reading
Module format
IELTS Academic Reading has 3 passages and 40 items (questions). The number of items for any one passage may vary. Each item is worth one mark.
The texts and items appear in Question Booklets.
Answer format
Candidates record their responses on Answer Sheets.
Timing
IELTS Academic Reading takes 60 minutes to complete. Candidates are not given extra time to transfer their answers onto the Answer Sheet. They should do this as they work through the test.
Marks
One mark is awarded for each correct answer.
Texts
The passages used in the test are based on authentic texts, and are taken from sources such as magazines, journals, books and newspapers. They are designed to present the candidate with materials similar to those which they might need to read on a university course. Passages may also contain non-verbal material such as diagrams, graphs, illustrations etc. The passages may be written in a variety of styles, for example narrative, descriptive or discursive/argumentative. They deal with issues which are interesting, recognisably appropriate, and accessible to candidates entering postgraduate or undergraduate courses or seeking professional registration. At least one of the passages will contain detailed argument.
Length
The total word count for the three passages is between 2000 and 2750 words.
Task Types
There are 10 basic task types, some with possible variations. They are:
Task Type 1 Multiple Choice
Task Type 2 Short-answer Questions
Task Type 3 Sentence Completion
Task Type 4 Notes, Summary or Table/Flow-chart Completion
Task Type 5 Labelling a Diagram
Task Type 6 Choosing Headings for Paragraphs or Sections of a Text
Task Type 7 Locating Information
Task Type 8 Identification of Writer’s Views/Claims or of Information in a Text
Task Type 9 Classification
Task Type 10 Matching

An Overview of IELTS Academic Writing
Module format
IELTS Academic Writing lasts a total of 60 minutes. It consists of 2 tasks (Writing Task 1 and Writing Task 2) and candidates must answer BOTH tasks.
Answer format
Candidates write their answers in pen or pencil on Answer Sheets provided.
Timing
Students are advised to spend 20 minutes on Task 1 and 40 minutes on Task 2. They must complete both tasks in one hour.
Task 1
For Writing Task 1 candidates are given some visual information which may be presented in the form of one or more related diagrams, charts, graphs or tables. Candidates are asked to describe the information or data. They must write at least 150 words on this task.
Writing Task 1 assessment is based on the following criteria:
1) Task Achievement
2) Coherence and Cohesion
3) Lexical Resource
4) Grammatical Range and Accuracy
Task 2
For Writing Task 2, candidates are presented with an opinion, problem or issue which they must discuss. They may be asked to present the solution to a problem, present and justify an opinion, compare and contrast evidence or opinions, or evaluate and challenge an argument or idea. Candidates must write at least 250 words and are advised to spend 40 minutes on this task.

Writing Task 2 assessment is based on the following criteria:
1) Task Response
2) Coherence and Cohesion
3) Lexical Resource
4) Grammatical Range and Accuracy
Each of the tasks is assessed separately by a trained and qualified examiner and given a score. Writing Task 2 is worth more marks than Writing Task 1 so candidates should be sure to leave plenty of time to complete Writing Task 2. Academic Writing band scores are reported in whole bands or half bands.
An Overview of IELTS General Training Reading
Module format
IELTS General Training Reading has three sections of increasing difficulty and 40 items (questions). Section 1 has 14 items and sections 2 and 3 have 13 items each.
Section 1 may contain 2 or 3 short texts or several shorter texts such as advertisements, Section 2 usually comprises 2 texts and in Section 3 there is 1 long text. The texts vary in topic and text type and are graded with the most difficult appearing in Section 3.
The texts and items appear in Question Booklets.
Answer format
Candidates record their responses on Answer Sheets.
Timing
IELTS General Training Reading takes 60 minutes to complete. Candidates are not given extra time to transfer their answers onto the Answer Sheet.
Marks
One mark is awarded for each correct answert.
Texts
Texts for the first Section are taken from notices, advertisements, timetables, publicity material and similar sources. Texts for the second Section are taken from college prospectuses, course summaries, guides to libraries, rules and regulations and similar sources. Texts for the third Section are taken from newspapers, magazines or journal articles, fictional or non-fictional book extracts and similar sources.
Length
The texts have a total word count of approximately 2,400 words.
Task Types
There are 11 basic task types, some with possible variations. They are
Task Type 1 Multiple Choice
Task Type 2 Multiple Matching
Task Type 3 Short-answer Questions
Task Type 4 Sentence Completion
Task Type 5 Notes/Table/Diagram/Flow-chart Completion
Task Type 6 Summary Completion
Task Type 7 Choosing Headings for Paragraphs or Sections of a Text
Task Type 8 Locating Information
Task Type 9 Identification of Writer’s Views, Claims or Information in the Text
Task Type 10 Classification
Task Type 11 Matching

An Overview of IELTS General Training Writing
Module format
IELTS General Training Writing lasts a total of 60 minutes. The paper consists of 2 tasks (Writing Task 1 and Writing Task 2) and candidates must answer BOTH tasks.
Answer format
Candidates write their answers in pen or pencil on Answer Sheets provided.
Timing
Students are advised to spend 20 minutes on Task 1 and 40 minutes on Task 2. They must complete both tasks in one hour.
Task 1
Candidates are asked to write a personal informal, semi-formal or formal letter, responding to a given problem or situation. Input to Task 1 includes a brief description of the problem or situation followed by 3 bullet points which tell the candidate what information is required in the letter. Candidates must write at least 150 words for this task.

Writing Task 1 assessment is based on the following criteria:
1) Task Achievement
2) Coherence and Cohesion
3) Lexical Resource
4) Grammatical Range and Accuracy
Task 2
The input to Task 2 consists of a statement of a point of view, argument or problem about a specific topic. This is followed by instructions asking candidates to discuss the topic by providing general factual information, outlining and/or presenting a solution, justifying an opinion, or evaluating ideas and evidence. Candidates are expected to produce a discursive piece of writing. Candidates must write at least 250 words for this task.
Writing Task 2 assessment is based on the following criteria:
1) Task Response
2) Coherence and Cohesion
3) Lexical Resource
4) Grammatical Range and Accuracy
Each of the tasks is assessed separately by a trained and qualified examiner and given a score. Writing Task 2 is worth more marks than Writing Task 1 so candidates should be sure to leave plenty of time to complete Writing Task 2. From July 1 2007 General Training Writing band scores will be reported in whole bands or half bands.

An Overview of IELTS Listening
Module format
IELTS Listening has four sections, each with 10 items (or questions). Each item is worth one mark. The items are designed so that the answers appear in order in the listening passage. During the test, time is given for candidates to read the questions and write down and check their answers. Answers are written on the Question Paper as candidates listen. When the tape ends, ten minutes are allowed for candidates to transfer their answers onto an Answer Sheet.
The table below provides a summary of IELTS Listening.
SECTION Topic Area Input Main Skill Focus Number of Questions
1 Social needs Conversation with a transactional purpose e.g. finding out about travel services Listening for and noting specific factual information 10
2 Social needs Monologue or prompted monologue with a transactional purpose e.g. giving information about a public event Listening for and noting specific factual information 10
3 Education and training Discussion between 2 – 4 people in an academic context, e.g. tutorial or seminar Following a conversation which involves negotiation of meaning. Listening for specific information, attitudes, and speakers' opinions 10
4 Education and training Monologue in an academic context e.g. lecture Following an academic argument. Listening for main ideas, specific information, attitude and speaker's opinion 10
Answer format
Candidates write their answers on an answer sheet.
Timing
Approximately 30 minutes plus 10 minutes transfer time.
Marks
Each question carries one mark, giving a total of 40 marks.
Listening texts
The first two sections are concerned with social needs. There is a dialogue between two speakers, for example a conversation about travel arrangements, and then a monologue, for example a recording about museum opening times.
The final two sections are concerned with situations related more closely to educational or training contexts. There is a conversation between up to four people, for example a conversation between a tutor and a student about an assignment, and then a further monologue, for example a lecture of general academic interest.
Task types
A variety of task types is used. The principal task types are:
Task Type 1 Forms/Notes/Table/Flow-chart/Summary Completion
Task Type 2 Multiple Choice
Task Type 3 Short-answer Questions
Task Type 4 Sentence Completion
Task Type 5 Labeling a Diagram/Plan/Map
Task Type 6 Classification
Task Type 7 Matching
Recordings
Each section is played ONCE only. The recordings include a range of accents, including British, Australian, New Zealand and American.
An Overview of IELTS Speaking
Module format
IELTS Speaking is a one-to-one interaction between the candidate and an examiner. The three parts give the candidate the opportunity to use a range of different speaking skills.
IELTS Speaking is recorded.
Timing
11 – 14 minutes
Marks
Candidates are assessed on their performance throughout the test.
PART Nature of Interaction Timing
1 Introduction and interview
After introductions and identity check, the examiner asks the candidate questions about familiar topics. 4 – 5 minutes
2 Long turn
The candidate receives a task card with a topic. S/He then has 1 minute to prepare and make notes before speaking about the topic for 1 to 2 minutes. 3 – 4 minutes
3 Discussion
The examiner discusses with the candidate more abstract aspects of the topic in Part 2. 4 – 5 minutes

An Overview of IELTS Speaking
Module format
IELTS Speaking is a one-to-one interaction between the candidate and an examiner. The three parts give the candidate the opportunity to use a range of different speaking skills.
IELTS Speaking is recorded.
Timing
11 – 14 minutes
Marks
Candidates are assessed on their performance throughout the test.
PART Nature of Interaction Timing
1 Introduction and interview
After introductions and identity check, the examiner asks the candidate questions about familiar topics. 4 – 5 minutes
2 Long turn
The candidate receives a task card with a topic. S/He then has 1 minute to prepare and make notes before speaking about the topic for 1 to 2 minutes. 3 – 4 minutes
3 Discussion
The examiner discusses with the candidate more abstract aspects of the topic in Part 2. 4 – 5 minutes

shyamstyles

2007-07-22T22:33:00.000-07:00

hai this is shyam. i am from vaikom (kottayam dist),kerela.now i m studying in bangalore 4 bsc nursing.