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Selasa, 14 Juni 2011

Organic Light-Emitting Diode (OLED)

Organic Light-Emitting Diode (OLED) atau dioda cahaya organik adalah sebuah semikonduktor sebagai pemancar cahaya yang terbuat dari lapisan organik. OLED digunakan dalam teknologi elektroluminensi, seperti pada aplikasi tampilan layar atau sensor. Teknologi ini terkenal fleksibel dengan ketipisannya yang mencapai kurang dari 1 mm.















iPad 3 Menggunakan Layar OLED?



iPad 2 memang memiliki banyak pembaharuan dibagian dalam dibandingkan iPad generasi pertama, kecuali layarnya. iPad 2 masih menggunakan layar yang sama, dimana resolusinya lebih kecil dibandingkan dengan iPhone 4s yang sudah menerapkan teknologi retina display. Akankah ada perubahan pada layar iPad 3 nantinya?
Banyak rumor berkembang, bahwa Apple melalui staffnya Tim Cook telah mengunjungi Samsung di Korea Selatan untuk membicarakan penggunaan layar OLED untuk generasi tablet berikutnya. Tentu saja, penggunaan layar OLED sangat mahal apalagi untuk ukuran tablet 10 inci. Ini memungkinkan harga yang melonjak tinggi untuk iPad 3.


Selain itu PSP2 juga pake OLED lho???



Sony akan mengumumkan perangkat PlayStation Portable terbaru mereka yang disinyalir akan memiliki nama PSP2, menurut rumor yang keluar dari Jepang rencananya perangkat game konsol portabel ini akan hadir pada akhir bulan ini.
rencananya perangkat tersebut akan memiliki layar OLED dimana layar ini memiliki spesifikasi yang lebih baik dari pada perangkat PSP sebelumnya dan akan hadir juga fungsi koneksi Internet melalui 3G yang dibutuhkan untuk mengakses Internet, mengunduh game dan bergabung dengan game-game multiplayer secara online, namun sejauh ini akses Internet untuk penggunaan game online tersebut masih terbatas untuk jaringan DoCoMo yang ada di Jepang, jadi sudah dipastikan bahwa perangkat ini akan hadir pertama kali untuk pasar Jepang. Namun hingga tulisan ini dibuat, berita mengenai penggunhaan jaringan DoCoMo ini masih sebatas rumor.
Ini berarti bahwa perangkat PSP2 akan bersaing secara langsung dengan perangkat yang dibuat oleh perusahaan yang sama Sony Ericsson Xperia Play, namujn tentu kita semua tahu bahwa fungsi utama dari PSP2 adalah konsol game dan Xperia Play memiliki fungsi utama sebagai ponsel.
Pasar konsol game sepertinya sedang kembali bergeliat karena belakangan Nintendo juga tengah menyiapkan konsol game portable baru yang ebrtajuk Nintendo 3DS yang kabarnya akan mulai dirilis kepasaran pada kuartal pertama tahun 2011. Selain memiliki fitur layar 3D tanpa menggunakan kacamata Nintendo juga akan menjejali perangkat konsol game tersebut dengan kamera, pemutar musik dan browser Internet.

Sabtu, 11 Juni 2011

Cara Membuat Flag Counter di Blog

Caranya :

1. Buka halaman INI





2. Nah, setelah keluar halaman ini, silahkan edit pengaturannya.

>> Maximum Flags to Show = bendera yang dtampilkan

>> Columns of Flags = kolom

yang lainnya silahkan diedit sendiri




3. Lalu, klik “Get Your Flag Counter”




4. Apabila muncul halaman seperti ini, klik Skip aja






5. Lalu, pilih icon WordPress.





6. Lalu, isikan Username = yang biasanya dipake login ke wordpress.com

Password = password yang biasanya dipake buat login di wordpress.com

Blog : alamat blogmu

Lalu, klik Post






7. Kalau sudah selesai, akan ada tulisan “Item Posted. Thank You”


8. Nah, sekarang pergi ke Dasbor >> Tulisan >> All Post






9. Cari artikel yang berjudul “(tanpa judul)” lalu klik SUNTING





10. Pilih menu HTML





11. Setelah muncul kode-kode, copy kode itu dan pastekan di TEXT AREA (ada di Dasbor>>Tampilan>>Widget) seret text ke sidebar.






12. Pastekan kodenya di bawah judul, dan klik SAVE





13. Selesai. Sekarang widget ini sudah ada di blogmu :)
Selamat Mencoba

Kamis, 09 Juni 2011

Good Laboratory

Good Laboratory Practice
From Wikipedia, the free encyclopedia
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The examples and perspective in this article may not represent a worldwide view of the subject. Please improve this article and discuss the issue on the talk page. (October 2009)
In the experimental (non-clinical) research arena, the phrase good laboratory practice or GLP specifically refers to a quality system of management controls for research laboratories and organizations to try to ensure the uniformity, consistency, reliability, reproducibility, quality, and integrity of chemical (including pharmaceuticals) safety and efficacy tests.
GLP was instituted following cases of animal test fraud by pharmaceutical and industrial chemical (mainly pesticide) manufacturers. Industrial BioTest Labs (IBT) was the most notable case, where thousands of safety tests for chemical manufacturers were falsely claimed to have been performed or were so poor that police investigators could not piece together what work had been done...even though IBT superficially delivered the test results their contracts with the manufacturers specified. [1]
The original GLP regulatory mandate was promulgated in 1978 by US-FDA (though they may have got it from the New Zealand medicines agency) and published in the Federal Register 43 FR 59985-60020. It was followed a few years later by US-EPA, and (as outlined in the Organisation for Economic Co-operation and Development (OECD) Principles of GLP in 1992) the OECD has since help promulgate it to many countries, helping them place it into their national regulations.
GLP applies to nonclinical studies conducted for the assessment of the safety or efficacy of chemicals (including pharmaceuticals) to man, animals and the environment. An internationally recognized definition of GLP can be found on the website for the Medicines and Healthcare products Regulatory Agency-UK which defines GLP as:
Good Laboratory Practice (GLP) embodies a set of principles that provides a framework within which laboratory studies are planned, performed, monitored, recorded, reported and archived. These studies are undertaken to generate data by which the hazards and risks to users, consumers and third parties, including the environment, can be assessed for pharmaceuticals (only preclinical studies), agrochemicals, cosmetics, food additives, feed additives and contaminants, novel foods, biocides, detergents etc.... GLP helps assure regulatory authorities that the data submitted are a true reflection of the results obtained during the study and can therefore be relied upon when making risk/safety assessments.
GLP, a data quality system, should not be confused with standards for laboratory safety - appropriate gloves, glasses & clothing to handle lab materials safely.

Rabu, 08 Juni 2011

coruptor

Accord With Comptroller Will Help Attorney General Pursue Corruption Cases
By NICHOLAS CONFESSORE
Published: May 22, 2011
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Attorney General Eric T. Schneiderman and Thomas P. DiNapoli, the state comptroller, have entered into an agreement that will grant Mr. Schneiderman powers to criminally prosecute corruption involving taxpayer money, significantly expanding the attorney general’s authority to pursue public integrity cases.
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Katie Orlinsky for The New York Times
Comptroller Thomas P. DiNapoli, left, and Attorney General Eric T. Schneiderman are collaborating on public integrity.
Under the agreement, the comptroller and the attorney general will establish a joint task force on public integrity. Mr. Schneiderman’s prosecutors will work with Mr. DiNapoli’s investigators and auditors looking into legislative earmarks, state pensions and government contracts.
But in a twist, Mr. DiNapoli has also agreed to employ a little-known provision of state law to refer any findings from joint investigations to Mr. Schneiderman for criminal prosecution.
“We’ll coordinate our respective roles to uncover and prosecute government waste, fraud and abuse,” Mr. DiNapoli said in a statement. “This is a powerful message: New York’s two independently elected oversight officials are partnering together to ensure integrity and accountability to every level of government in New York State.
The arrangement could make it easier for Mr. Schneiderman to investigate and root out certain kinds of public corruption than past attorneys general. And it comes as Gov. Andrew M. Cuomo is seeking more aggressive and independent enforcement of state ethics laws and broader disclosure of lawmakers’ outside employment.
“It could be a very effective approach,” said Eric R. Dinallo, who headed the securities bureau in the attorney general’s office under Eliot Spitzer and was later superintendent of the State Insurance Department. “If you can’t get legislative relief around ethics issues in government and you’re trying to get jurisdiction, sometimes the law has all the jurisdiction you need — if you look at it in a creative way.”
The agreement between Mr. Schneiderman and Mr. DiNapoli has significant limits: The attorney general will still lack standing to investigate allegations of criminal violations of election law, or to investigate the Legislature for offenses unrelated to the expenditure of state money, like a lawmaker’s failure to disclose outside income. Mr. Cuomo is hoping to increase scrutiny in some of those areas through a comprehensive ethics deal with the Legislature; failing that, he could appoint an investigative commission under the state Moreland Act, though such a commission would be unable to bring criminal prosecutions.
But the new joint task force will give Mr. Schneiderman powerful legal tools to tackle a host of other problems that have sullied New York government in recent years: pension padding, no-show jobs, abuse of legislative earmarks, and fraud at the state’s secretive public authorities.
“Expanding the attorney general’s power to prosecute public corruption will be a major element of our comprehensive approach,” Mr. Schneiderman said in a statement.
Under the agreement, which was reached last week, Mr. Schneiderman subpoenaed a local development corporation in Monroe County and its prime contractor over a $224 million upgrade of the county’s emergency communications system. Some local Democratic officials have criticized the project, approved in 2009 by the Republican county executive and Republican-controlled County Legislature, alleging secrecy and potential conflicts of interest.
Mr. Schneiderman’s subpoenas were accompanied by a notice from Mr. DiNapoli’s office, informing officials of an impending audit.
Under state law, the attorney general cannot unilaterally investigate public officials for breaking campaign finance rules, violating ethics laws or even taking bribes. As a result, major investigations of New York officials in recent years have been conducted chiefly by district attorneys or federal prosecutors with jurisdiction over bribery, kickbacks, and other criminal forms of corruption.
Attorneys general have been able to pursue some corruption cases. Mr. Cuomo, for example, investigated the state pension fund and Pedro Espada Jr., the former state senator from the Bronx, using laws that give the attorney general jurisdiction over securities fraud and charities. Mr. Cuomo sought legislation to expand the attorney general’s criminal powers to investigate other forms of political corruption but was rebuffed by the Legislature.

KONSEP RETWEET DAN REPLY TWITTER

KONSEP RETWEET DAN REPLY
Twitter, sebagai salah satu microblog dan situs jejaring sosial baru, akhir-akhir ini menjadi cukup populer. Dari beberapa informasi yang berhasil saya kumpulkan, pengguna twitter di Indonesia menempati posisi lima besar teratas dari semua pengguna twitter di dunia. Sangat mengesankan bukan. Dari banyaknya pengguna twitter di indonesia ini, muncul sebuah komunikasi dua arah memanfaatkan twitter yang memungkinkan setiap pengguna twitter dapat merespons dan respons balik twitter pengguna yang lain.
Banyak pengguna twitter yang masih bingung bagaimana cara merespons tweet temannya dengan baik dan tidak menimbulkan kebingungan yang akhirnya menimbulkan kesalah pahaman. Memang pihak Developer twitter menyisipkan fitur Reply untuk membalas tweet dari user lain. Meski sudah ada fitur tersebut, masih banyak pengguna twitter yang masih bertanya-tanya dan bingung, hal ini dikarenakan fitur reply pada twitter tidak jelas untuk reply twit yang mana.
Bayak pengguna twitter yang salah kaprah menafsirkan fungsi Retweet ini. Fitur ReTweet yang ada di twitter sesungguhnya difungsikan untuk me-Tweet ulang tweet teman kita sehingga followers kita yang tidak follow teman kita tersebut dapat membaca tweet teman kita tersebut. Namun saking kreatif dan inovatifnya teman-teman pemakai twitter, akhirnya mereka memanfaatkan fungsi RT ini untuk membalas tweet pengguna twitter yang lain, hanya saja mereka perlu melakukan sedikit modifikasi atau edit ReTweet sebelum me-Tweet jawaban tersebut. Dan Edit ReTweet ini hanya bisa dilakukan di luar site utama twitter, entah itu Twitter For Web atau Mobile Twitter yaitu dengan memanfaatkan site pihak ke-3 yang menyediakan layanan Twitter Client seperti, dabr, tweete, ubertwitter, dll.


Memanfaatkan fitur ReTweet untuk membalas Tweet teman kita memang tidak salah dan merupakan hal yang sah-sah saja, tetapi alangkah baiknya jika kita melakukannya sesuai dengan fungsi yang ada. Dan terkadang ada beberapa Tweepes (pengguna twitter) yang risih dengan RT yang berulangkali dan bertumpuk-tumpuk (lihat gambar di atas), dan ada juga yang bilang aktifitas seperti ini penuh-penuhin Timeline. Nah lantas bagaiamana cara balas tweet yang bener dan tidak membuat pengguna twitter yang lain merasa risih?
Berdasarkan pengalaman dan apa yang saya liat dari teman-teman yang nge-Tweet, ada cukup banyak cara yang bisa digunakan untuk membalas tweet teman kita tanpa membuat teman kita risih. caranya adalah dengan melakukan reply langsung dan menambahkan re : twit mana yang di reply. Contoh variasinya adalah sebagai berikut :
1. Reply dengan nama tweet teman di depan disusul tweet mana yang kita reply. Syntaxnya : @namaTwitTemanJawaban atas twit teman kitare :tweet yang direply. Untuk tweet yang direply usahakan jangan di tulis semua, ambil fokusnya saja biar tidak terlalu menghabiskan character kita. Contohnya liat gambar di bawah ini.


2. Reply dengan jawaban di depan kemudian diikuti tweet mana yang kita reply. Syntaxnya : Jawaban tweetnya@namaTwittemanre :tweet yang direply. Hampir sama dengan yang pertama, usahakan tweet yang direply jangan di tulis semua, ambil fokusnya saja. Contohnya lihat gambar di bawah ini.

Untuk melakukan reply ini tidak ada fitur khusus atau otomatis, kita melakukan modifikasi dan edit manual. Dan saya rasa tidak ada kesulitan berarti untuk melakukan hal ini.
Nah mudah bukan?? Apa yang saya tulis di postingan kali ini bukanlah pakem atau standar yang harus dipatuhi untuk nge-Tweet, melainkan hanyalah sebuah tulisan berbagi ilmu bagaimana membuat reply tweet yang baik dan tidak membuat risih orang lain. Jika anda masih suka dengan cara RT dan RT yang bertumpuk-tumpuk ya silahkan itu hak anda. Kalo saya lebih suka reply dengan 2 cara di atas.
By: http://frenavit.com/konsep-retweet-dan-reply-di-twitter.html

my profil

https://lh4.googleusercontent.com/-eqjngFuEOLA/Te8iA_hdiUI/AAAAAAAAACI/2M7bmJAQ-BQ/s288/93.gif

Selasa, 07 Juni 2011

Skin Puncture

Skin Puncture Collection Of Plasma, Serum, & Whole Blood

Purpose:Procedure for the collection of blood by skin puncture technique
Materials:
The following equipment should be in order before proceeding with the skin puncture procedure:

1. Blood Drawing Site:
1. For Finger Stick Procedures: The drawing area should be wide enough for the patient's arm to rest comfortably. A chair with a wide, flat, clean surface on the arms will suffice or the patient may be lying in bed.

2. For inpatient Pediatric patients, the Pediatric treatment room should be used whenever possible.

2. Puncture Equipment: Spring-loaded lancets (Microtainer) are available in regular point (blue color) or medium point (yellow color). Blue lancets penetrate 2.4 mm and are used for finger sticks while yellow lancets penetrate 3.2 mm and are used for heel sticks. Also available are 3 sizes of Tenderfoot (used for finger sticks). These range in penetration depth from 0.85 mm (PINK/WHITE), 1.25 mm (BLUE/WHITE), to 1.75mm (RED/WHITE). There are also three sizes of Tenderfoot (heel sticks). These range in penetration depth from 0.85 mm (WHITE), 1.0 mm (BLUE/PINK), to 2.0 mm tissue damage than the spring-loaded lancets. See Pediatric "Special Considerations" for further explanation of these skin puncture devices.

3. Gauze: Non-sterile 2x2 inch gauze squares may be used for finger sticks or heel sticks.

4. Blood Collection Devices: Microtainers are available in 5 types:
1. Pick-top microtainers which contain no additives for blood bank procedures or for procedures not requiring the serum separator gel.

2. Red-top microtainers containing a small amount of serum separator gel for producing serum.

3. Purple-top microtainers containing EDTA anticoagulant for use in hematology procedures.

4. Green-top microtainer containing heparin and separator gel for use in chemistry procedures.

5. Gray-top microtainer containing Na fluoride/K oxalate for use in specific chemistry procedures.

6. Microhematocrit capillary tubes are used for collecting blood for the microhematocrit test. These are self-sealing. Natelson capillary tubes may be used for collecting blood directly from a heel stick. The tube can then be emptied into the appropriate microtubes, if required.


5. Gloves: Latex & non-Latex are available in various sizes and may be powdered or be powder free.

6. Antiseptics: Individually packaged 70% isopropyl alcohol wipes may be used to clean the puncture site for most specimens. Povidone-iodine swabs may also be used.

7. Large Test Tube: It may be impractical to label individual microtainers or capillary tubes. Instead, place the sealed or capped tubes in a single large test tube and label the test tube with the computer specimen label and the microtainers with the aliquot labels. If only adhesive labels available, label the specimen instead of the test tube.

8. Adhesive Labels: 1.0x2.5 inch adhesive labels and a permanent marking pet should be available for labeling the specimens. One may also use an addressograph label with name and medical record number.

9. Warm Washcloth: A clean, warm, wet washcloth may be used to warm the skin puncture site. It should be 42° C., or 108 degrees F., with additional warm water.

10. Chucks: A clean chucks should be available for heel sticks to protect the person holding the baby from dripping blood.

11. Sharps Disposal Container: An OSHA acceptable puncture-proof red container marked "Biohazardous" for disposing of lancet or partially filled capillary tubes.

12. Disinfectant: A plastic wash bottle with ASCEND germicidal solution should be available for cleaning up small blood spills.

Specimen Collection Procedure

Routine Skin Puncture Procedure

1. Assemble necessary equipment described in the Materials and Equipment section of this procedure.

2. Wash hands and put on gloves.

3. Identify patient.
1. Inpatient - the patient's name and Medical Record Number on their ID bracelet much match the requisition or the computer label.

2. Outpatient - we make initial ID by calling patient's name. This must be verified by asking or confirming with a parent or guardian the birth date of the patient.

4. Select the appropriate Microtainers for the specimens to be collected. Any Microtainers containing additives should be tapped to dislodge additives from the walls and stopper.

5. Position the patient.
1. For Finger Sticks: The patient should be seated with his or her non-dominant arm resting comfortably on the blood-drawing chair arm support or on the bed.

2. For Heel Sticks: The baby should be held by another adult if possible. Remove the baby's clothes and blanket so they will not interfere. A protective barrier should be placed under the baby. Protect the person holding the baby from possible blood contamination. If there is no one available to assist, position the baby either on their back or stomach in the center of the examination table.

NOTE: for infants up to the age of 6 months, the heel is usually the site of choice as the fingers of infants are too small for the trauma of a skin puncture.

6. Select the puncture site.
1. For Finger Sticks: For children and adults, use the 3rd or 4th finger of the non-dominant hand. The outer and upper region of the fingertip, halfway between the center of the fingerpad and the edge of the fingernail, is the site of choice. SEE DIAGRAM #3. One may refer to "Special Consideration" section on use of the Tenderlett

2. For Heel Sticks: Avoid previous heel stick sites. The site should be on the plantar surface of the heel, beyond the lateral and medial limits of the calcareous (heel bone). The heel bone is very close to the surface of the skin at the back of the heel, and could be damaged by a puncture in this area. The puncture should NEVER be performed on the central area of the infant's foot (area of the arch). SEE DIAGRAM #4. One may refer to "Special Considerations" section on use of the Tenderfoot.


7. Reassure the patient, if possible, by explaining the procedure.

8. Warm the puncture site, if necessary. Use a warm, wet washcloth or chucks to warm the puncture site for at least 3 minutes. Warming the site to 42 C can increase blood flow up to sevenfold.

9. Cleanse the puncture site. Use the alcohol or povidone-iodine prep to wipe the area vigorously. Allow the area to air dry or dry the skin with 2x2 gauze before the continuing. If the side is not dry, the blood will spread over the area making it difficult to collect and there is the possibility of contamination from the cleansing agent.

10. Open the puncture device packaging, being careful not to contaminate the side with the cutting device.

11. Perform the skin puncture.
For Finger Sticks:

1. Exert pressure on the finger tip by holding it with your index finger and thumb. Pressure should be directed upward.

2. Use the device to make a quick puncture into the site selected. Release it according to manufacturer's instructions.

3. Release the finger and wait for the first drip of blood to form.

4. Wipe away the first drop of blood. Avoid excessive squeezing or "milking" as tissue fluids will interfere with testing.

5. Collection of Lavender microtainer should be drawn first, with other types of microtainers following. Wipe puncture site between microtainer collection to prevent cross contamination and ensure further bleeding.
1. (Sartstdt) Lavender microtainers
1. Be sure vent on the collection top is facing upwards.

2. Place collection top at 45 degree angle to the drop of blood. Blood will flow by capillary action down the top and into the tube. Do not shake the tube as the capillary action may be lost. Fill the microtainer between the 250- and 500 ul mark. Remove collection top and replace cap. Mix gently 5-7 times.
2. "Scoop" type microtainers
1. Touch the top of the collector to the under surface of the drop and channel blood flow in groove of collector. Blood will flow freely through the collector and down the tube wall. When collection is complete, replace the collector with appropriate cap.

2. Always try to avoid "scooping" along the skin. This method will pick up micro clots that may interfere with testing.
6. Apply pressure to stop the bleeding.
For Heel Sticks:
1. Grasp the foot firmly and puncture the selected site.

2. Release the foot and allow the first drips of blood to form.

3. Wipe away the first drop of blood and avoid excessive squeezing.

4. Hold the foot firmly and collect the blood. The same steps can be following as in steps e and f of the finger stick procedure.

5. Release the foot and allow the baby to kick from time to time as this will increase the blood flow.

6. Wipe the site between specimen collections.

7. When specimen collection is complete, hold gauze on the puncture site and apply mile pressure. Hold it until the bleeding stops. Do not apply tape.


12. Dispose of the puncture device in the biohazardous sharps container.

13. Seal or cap the tubes.

14. Confirm that the patient is all right. Confirm the bleeding has stopped and the patient feels or looks normal.

Special Circumstances

Excessive Bleeding:

1. Apply direct pressure to the puncture site while bleeding continues.

2. If the bleeding persists more than 5 minutes, call the physician.

Handling Considerations

Universal Precautions apply to all specimens of blood, serum, plasma, blood products, vaginal secretions, semen, cerebrospinal fluid, synovial fluid, pleural fluid, peritoneal fluid, pericardial fluid, amniotic fluid, and concentrated HIV or HBV viruses. Any specimen of any type which contains visible traces of blood should be handled using Universal Precautions.

Capillary blood samples should be processed as soon as possible after being drawn. Follow the instructions outlined in the venipuncture procedure for preparing serum, plasma, or whole blood. The following general precautions for capillary specimens should be observed:

1. Keep Specimen tubes capped. This should be done for safety reasons as well as specimen preservation.

2. Avoid specimen agitation. Hemolysis (the breakdown of red blood cells) will occur when the specimen is agitated. A certain amount of hemolysis is unavoidable, but it would be minimal. Badly hemolyzed specimens are unacceptable for most chemistry and hematology procedures. Avoid shaking the specimen and always use gently inversion to mix specimens. Always handle specimens with care.

3. Adhere to specimen time constraints. Timing is critical in most chemistry and hematology procedures. Follow manufacturer's recommendations for minimum and maximum times which specimens may be left in the tube. The time constraints on capillary specimens are more stringent then those on venous samples obtained by venipuncture.

4. Refrigerate specimens not tested immediately. Anticoagulated capillary specimens should be stored at 2-8 degrees C. if they will be not bested within 4 hours. Heat may cause hemolysis.

PENETAPAN KADAR ASAM SALISILAT DALAM BEDAK TABUR SECARA ALKALIMETRI

Nama : Gani Septa Anggara
NIM : A101.14.019

PENETAPAN KADAR ASAM SALISILAT DALAM BEDAK TABUR SECARA ALKALIMETRI
Definisi
Alkalimetri (Alkali = Basa atau metri = pengukuran) diartikan sebagai titrasi untuk penetapan asam dengan larutan standar basa sebagai alat ukurnya. (Suharno, 1989)
Alkalimetri termasuk reaksi netralisasi yaitu antara ion hidrogen yang berasal dari asam dengan ion hidroksida yang berasal dari basa untuk menghasilkan air yang bersifat netral. Netralisasi dapat juga dikatakan sebagai reaksi antara donor proton (asam) dengan penerima proton (basa). Alkalimetri adalah penetapan adar senyawa-senyawa yang bersifat asam dengan menggunakan baku basa. (Mursyidi dan Rohman, 2006)

Prosedur Kerja Penetapan Kadar Asam Salisilat Secara Alkalimetri
Timbang seksama 3gram, larutkan dalam 15ml Etanol (95%)P hangat yang telah dinetralkan terhadap larutan merah fenol P tambahkan 20ml air. Titrasi dengan Natrium Hidroksida 0,5N menggunakan indikator larutan merah fenol P.

1ml Natrium Hidroksida 0,5N setara dengan 69,06mg C7H6O3
(Farmakope Ed.III, 1979)

Cara Kerja Sampel
Prosedur Standarisasi NaOH
Dipipet 10ml larutan H2C2O4.2H2O dimasukkan kedalam erlenmayer
Ditambahkan 2 tetes indikator PP1%
Dititrasi dengan larutan NaOH standar dari tidak berwarna menjadi warna merah muda
Cara Kerja Sampel
Uji Kualitatif
Reaksi Warna
Sejumlah zat dalam Etanol 95%, tambah dengan larutan besi (III) klorida dalam Etanol 90% akan memberikan warna violet
Reaksi Asam-Basa
Sejumlah larutan asam Salisilat, ditambah dengan beberapa tetes larutan merah metil, hingga terjadi reaksi asam dan membentuk warna merah.
Pembentukan Ester
Sejumlah asam salisilat ditambah beberapa tetes asam sulfat pekat dalam metanol kemudian panaskan akan tercium bau metil salisilat (bau gondopuro)
Uji Kuantitatif
Titrasi Asam Basa
Timbang seksama 10gram sampel, tambahkan 20ml Akohol netral 95% dalam gelas ukur dan ditetesi indikator PP1% ±15 tetes. Tambahkan aquadest 40ml dan 0,5ml indikator PP1%. Titrasi dengan larutan NaOH standar sampai terbentuk warna merah muda.

Reaksi Kimia
Reaksi antara Asam Salisilat dengan Natrium Hidroksida

COOH COONa

OH + NaOH OH + H2O

Reaksi antara Asam Oksalat dengan Natrium Hidroksida

H2C2O4 + 2NaOH Na2C2O4 + 2H2O

Perhitungan Kadar
Penentuan Kadar Asam Salisilat
1ml Natrium Hidroksida 0,1N setara dengan 13,812mg C7H6O3
Kadar Asam Salisilat =(N titran x Vtitran x 13,812)/(0,1 x berat sampel) x 100%







DAFTAR PUSTAKA

Suharno. 1989. Ilmu Kimia Analitik. Surabaya: Departemen Kesehatan Republik Indonesia
Mursyidi, A., dan Rohman, A. 2006. Pengantar Kimia Farmasi Analisis Volumetri dan Gravimetri. Yogyakarta: Yayasan Farmasi Indonesia bekerjasama Pustaka Pelajar (69-76)
Tim Penyusun Farmakope. 1979. Farmakope Indonesia Edisi III. Jakarta: Departemen Kesehatan Republik Indonesia (hal 57)
Purwaningrum, Ratna Chandra. 2008. KTI Penetapan Kadar Asam Salisilat Dalam Bedak Tabur Secara Alkalimetri. Surakarta: Akademi Farmasi Nasional Surakarta

PERADANGAN DAN SHOCK

PERADANGAN

A. Definisi
Radang (bahasa Inggris: inflammation) adalah respon dari suatu organisme terhadap patogen dan alterasi mekanis dalam jaringan, berupa rangkaian reaksi yang terjadi pada tempat jaringan yang mengalami cedera, seperti karena terbakar, atau terinfeksi. Radang atau inflamasi adalah satu dari respon utama sistem kekebalan terhadap infeksi dan iritasi. Inflamasi distimulasi oleh faktor kimia (histamin, bradikinin, serotonin, leukotrien, dan prostaglandin) yang dilepaskan oleh sel yang berperan sebagai mediator radang di dalam sistem kekebalan untuk melindungi jaringan sekitar dari penyebaran infeksi.
Radang mempunyai peran penting dalam perlawanan terhadap infeksi:
• memungkinkan penambahan molekul dan sel efektor ke lokasi infeksi untuk meningkatkan performa makrofaga,
• menyediakan rintangan untuk mencegah penyebaran infeksi,
• mencetuskan proses perbaikan untuk jaringan yang rusak.

B. Gejala Peradangan
Panas dalam bisa jadi gejala awal peradangan serius. Penyebabnya bisa bakteri ataupunvirus. Peradangan ialah cara paling dasar dan paling alami dilakukan tubuh manusia sebagai reaksi terhadap infeksi, iritasi dan luka-luka tubuh lain. Tampilan utama dari peradangan biasanya berupa bagian tubuh yang kemerahan, terasa peningkatan temperature pada beberapa bagian tubuh, pembengkakan dan munculnya rasa nyeri. Peradangan termasuk juga jenis respons kekebalan nonspesifik. Peradagangan merupakan proses saat sel darah putih bersama-sama dengan bahan-bahan kimiawi dalam tubuh melindungi tubuh dari infeksi dan substansi-substansi asing, seperti bakteri dan virus. Pada beberapa kasus, system kekebalan tubuh memancing respons berupa peradangan, padahal tidak ada substansi asing yang harus dilawan.Pada kasus seperti itu, sistem perlindungan tubuh justru bisa mengakibatkan kerusakan pada jaringannya sendiri. Saat peradangan terjadi, bahan-bahan kimiawi dilepaskan dari sel darah putih menuju jaringan darah atau jaringan tubuh yang dimasuki substansi asing. Pelepasan bahan kimiawi tersebut akan mengakibatkan peningkatan volume aliran darah menuju bagian yang dimasuki sustansi asing itu. Hal itu bisa menyebabkan kemerahan dan peningkatan temperatur di darah tersebut. Beberapa zat kimia bahkan bisa bocor hingga memenuhi jaringan yang dimasuki zat asing, kemudian membengkak. Proses peradangan juga dapat merangsang syaraf perasa sakit sehingga menimbulkan rasa nyeri.
Beberapa gejala peradangan biasanya ditandai timbulnya kemerahan pada bagian tubuh tertentu, peningkatan suhu, nyeri persendian atau rasa kaku pada sendi.Selain itu, peradangan meliputi beberapa gejala yang mirip flu biasa, seperti demam, kedinginan, rasa lelah, kekurangan tenaga, pusing-pusing, kehilangan selera makan dan otot kaku.

C. Tanda-Tanda Peradangan
Gambaran makroskopik peradangan sudah diuraikan 2000 tahun yang lampau. Tanda-tanda radang ini oleh Celsus, seorang sarjana Roma yang hidup pada abad pertama sesudah Masehi, sudah dikenal dan disebut tanda-tanda radang utama. Tanda-tanda radang ini masih digunakan hingga saat ini. Tanda-tanda radang mencakup:
• rubor (kemerahan)
• kalor (panas)
• dolor (rasa sakit)
• tumor (pembengkakan)
• functio laesa (perubahan fungsi)
(Abrams, 1995; Rukmono, 1973; Mitchell & Cotran, 2003).
Umumnya, rubor atau kemerahan merupakan hal pertama yang terlihat di daerah yang mengalami peradangan. Saat reaksi peradangan timbul, terjadi pelebaran arteriola yang mensuplai darah ke daerah peradangan. Sehingga lebih banyak darah mengalir ke mikrosirkulasi lokal dan kapiler meregang dengan cepat terisi penuh dengan darah. Keadaan ini disebut hiperemia atau kongesti, menyebabkan warna merah lokal karena peradangan akut (Abrams, 1995; Rukmono, 1973).
Kalor terjadi bersamaan dengan kemerahan dari reaksi peradangan akut. Kalor disebabkan pula oleh sirkulasi darah yang meningkat. Sebab darah yang memiliki suhu 37oC disalurkan ke permukaan tubuh yang mengalami radang lebih banyak daripada ke daerah normal (Abrams, 1995; Rukmono, 1973).
Perubahan pH lokal atau konsentrasi lokal ion-ion tertentu dapat merangsang ujung-ujung saraf. Pengeluaran zat seperti histamin atau zat bioaktif lainnya dapat merangsang saraf. Rasa sakit disebabkan pula oleh tekanan yang meninggi akibat pembengkakan jaringan yang meradang (Abrams, 1995; Rukmono, 1973).
Pembengkakan sebagian disebabkan hiperemi dan sebagian besar ditimbulkan oleh pengiriman cairan dan sel-sel dari sirkulasi darah ke jaringan-jaringan interstitial. Campuran dari cairan dan sel yang tertimbun di daerah peradangan disebut eksudat meradang (Abrams, 1995; Rukmono, 1973).
Berdasarkan asal katanya, functio laesa adalah fungsi yang hilang (Dorland, 2002). Functio laesa merupakan reaksi peradangan yang telah dikenal. Akan tetapi belum diketahui secara mendalam mekanisme terganggunya fungsi jaringan yang meradang (Abrams, 1995).

D. Mekanisme Radang
• Fase inflmasi atu fase lag
Berlangsung sampai hari ke lima,akibat luka terjadi pendarahan.ikut keluar trombosit dan sel radang. Trombosit mengeluarkan prostaglandin,tromboksanan bahan kimia tertentu dan asam amino ertentu yang mempengaruhi pembekuan darahmengetur tonus dinding pebuluh darah dan kemotaksis terhadap leukosit.
Tejadi faso konstriksi dan proses penghentian pendarahan.sel radan gkeluar dari pembulau darah secara diapedesisdan menuju daerah luka secarakemotaksis. Sel mast mengeluarkan serotonin dan histmin yang meninngikan permeabilitas sel,terjadi eksudasi cairan edema.
Pertauatan pada fase ini hanya oleh fibrin,belum ada kekuatan pertautan lukasehingga disebut fase tertinggal atau fase lag.

• Fase proliferasi atau fibroplasi
Berlangsung dari hari keenam sampai dengan tiga minggu. Terjadiproses prolifrasi da pembentukan fibrobalast yang berasal dari sel-sel mesenkim. Fibroblas menghasilkan mukopolisakaridadan serat kolagen yang erdiri dari asam-asam amino glisin,prolin,dan hidroksi prolin.mukopolisakarida mengatur deposisi serat-seratkolagen yang akan mempertaukan tepi luka. Pada fase ini luka diisi oleh sel-sel radang fibroblast dan serat-serat kolagen,kapiler-kapiler baru membentuk jaringan kemerahan dengan permukaan yang tidak rata disebut jaringan granulasi
.
• Fase remodeling atau fase reorpsi
Dapat berlangsung berbulan-bulandan berakhir bila tanda radang sudah hilang.parut dan sekitarnya berwarna pucat,tipis,lemas,tak ada rasa sakt maupun gatal.




SHOCK

A. Definisi
Shock ialah suatu keadaan yang disebabkan oleh defesiensi sirkulasi akibat disparitas (ketidak seimbangan) antara volume derah dengan ruang susunan vaskuler. Faktor-faktor yang menyebabkan timbulnya ketidakseimbangan ini ialah:
a) faktor yang meyebabkan bertambahnya kapasitas ruang susunan vaskuler
b) faktor yang nenyebabkan bcrkurangnya volume darah.
Shock sebenarnya suatu keadaan yang terdiri atas kupulan gcjala, jadi suatu sindrom, dan depat bersifat primer atau sekunder (true strock).
Shock Primer
Pada shock primer tcrjadi defisiensi sirkulasi akibat ruang vaskuler membesar karena vasodiletesi yang asalnya neurogen.
Ruang vaskulcr yang membesar mengakibatkan daerah seolah-olah diterik dari sirkulasi umum,dan segera masuk ke dadalam kapiler dan venule alat-alat dalam (viscera).
Peristiwa ini sering terjadi pada orang yang mengalami kecelakaan keras, rasa sangat nyeri atau rangsang yang berasal dari jaringan yang rusak. Juga dapat disebabkan rasa nyeri yang sangat keras pada beberapa penyakit tertentu seperti radang akut pankreas, hernia incarcalita , atau oleh reaksi-reaksi emosi seperti keadaan takut yang mendadak, kesusahan yang sangat, karena melihat keadaan yang mengerikan seperti pada orang yang tidak biasa melihat daerah banyak akibat luka bcsar. Penderita menjadi sangat pucat, pingsan, sangat lemah. denyut nadi kesil dan cepat, disertai tekanan dareh yang rendah. Biasanya shock hanya sebentar saja, kecuali apabila terdapat trauma yang keras, perdarahan; dalam hal ini akan terjad shock sekunder.
Shock Sekunder
Pada shock sekundcr terjadi gangguan cairan yang menyebabkan defisiensi sirkulasi perifer disertai jumlah volue darah yang mcnurun, aliran darah yang bcrkurang, hemokonsentrasi dan fungsi ginjal yang terganggu. Sirkulasi yang bcrkurang tidak tcrjajidi segera setelah terkena kerusakan, tetapi baru beberapa waktu sesudahnya; olch karcna itu disebut shock sckunder atau delayed shock.

B. Gejala Shock
Gejala-gejalanya terjadinya shock ialah:
• rasa lesu dan lemas kulit yang basah
• kolaps vena terutama vena-vena superficial
• pernapasan dangkal
• nadi cepat dan lemah
• tekanan darah rendah
• oliguria dan kadang-kadang disertai muntah-muntah yang berwarna seperti air kopi akibat perdarahan dalam lambung (hematemesis).
Apabila keadaan terus progresif, maka penderita menjadi apatik, kemudian stupor, koma dan akhirnya dapat meninggal.
C. Mekanisme Shock
Mekanisme terjadinya shock, terjadi dalam 3 tahap:
1. Tahap nonprogresif
Mekanisme neurohormonal membantu mempertahankan curah jantung dan tekanan darah. Meliputi refleks baroreseptor, pelepasan katekolamin, aktivasi poros rennin-angiotensin, pelepasan hormonan antidiuretik dan perangsangan simpatis umum. Efek akhirnya adalah takikardi, vasokontriksi perifer dan pemeliharaan cairan ginjal. Pembuluh darah jantung dan otak kurang sensitive terhadap respon simpatis tersebut sehingga akan mempertahankan diameter pembuluh darah, aliran darah dan pengiriman oksigen yang relative normal ke setiap organ vitalnya.
2. Tahap progresif
Jika penyebab shock yang mendasar tidak diperbaiki, shock secara tidak terduga akan berlanjut ke tahap progresif. Pada keadaan kekurangan oksigen yang menetap, respirasi aerobic intrasel digantikan oleh glikolisis anaerobik disertai dengan produksi asam laktat yang berlebihan. Asidosis laktat metabolic yang diakibatkannnya menurunkan pH jaringan dan menumpulkan respon vasomotor, arteriol berdilatasi dan darah mulai mengumpul dalam mikrosirulasi. Pegumpulan perifer tersebut tidak hanya akan memperburuk curah jantung, tetapi sel endotel juga berisiko mengalami cedera anoksia yang selanjutnya disertai DIC. Dengan hipoksia jaringan yang meluas, organ vital akan terserang dan mulai mengalami kegagalan. Secara klinis penderita mengalami kebingungan dan pengeluaran urine menurun.
3. Tahap irreversible
Jika tidak dilakukan intervensi, proses tersebut akhirnya memasuki tahap irreversible. Jejas sel yang meluas tercermin oleh adanya kebocoran enzim lisososm, yang semakin memperberat keadaan syok. Fungsi kontraksi miokard akan memburuk yang sebagiannya disebabkan oleh sintesis nitrit oksida. Pada tahap ini, klien mempunyai ginjal yang sama sekali tidak berfungsi akibat nekrosis tubular akut dan meskipun dilakukan upaya yang hebat, kemunduran klinis yang terus terjadi hamper secara pasti menimbulkan kematian


D. Macam-Macam Shock
• Shock hipovolemik (disebabkan kurangnya volume darah intravaskular)
Selama shock hipovolemik mengakibatkan aliran balik vena ke jantung menurun sehingga pengisian ventrikel menurun dan mengakibatkan stroke
• Shock kardiogenik (disebabkan kegagalan jantung untuk memompakan darah)
Kegagalan jantung mengakibatkan ketidakmampuan memepertahankan CO dan perfusi ke jaringan
• Shock sepsis (disebabkan produksi toksin menjadi infeksi)
Shock sepsis disebabkan efek toksin yang diproduksi agen infeksius
• Shock neurogenik (disebabkan perubahan perubahan tegangan vaskuler)
ketidakseimbangan stimulasi saraf simpatis dan saraf parasimpatis pada otot pembuluh darah
• Shock anaphylactic (disebabkan reaksi imunologik)
Shock anaphylactic terjadi karena reaksi hypersensitif; perubahan fisiologi terjadi akibat seseorang kontak dengan allergen







DAFTAR PUSTAKA

http://id.wikipedia.org/wiki/Radang diunduh tanggal 03 Juni 2011
http://w4h48.multiply.com/reviews/item/6 diunduh tanggal 03 Juni 2011
http://satkes-alfah.blogspot.com/2010/06/mekanisme-terjadinya-shock.html diunduh tanggal 03 Juni 2011

Sabtu, 21 Mei 2011

endocrine hormone

SISTEM ENDOKRIN

Nama : Gani Septa Anggara Mata Kuliah : Fisiologi Manusia
NIM : A101.14.019 Dosen : dr. Suwarni
Kelas : 1A1

NO. HIPOTALAMUS HIPOFISE KELENJAR HORMON FUNGSI KETERANGAN
1. TRH (Thyrotropin Releasing Hormon) • TSH (Thyroid Stimulating Hormon)




• Prolaktin Tiroid







Kelenjar susu • Yodium • Perkembangan fetus
• Konsumsi oksigen dan produksi panas
• Kardiovaskuler, simpatetik dan pulmo

Merangsang awal produksi susu Pelepasan tiroid dirangsang oleh TSH. Tiroid membutuhkan yodium untuk menghasilkan T3 dan T4.
Sehingga sekresi TRH dipengaruhi oleh kadar T3 dan T4. Sedangkan produksi sekresi utamanya adalah T4.
• T3 mempunyai iktan besar dengan Albumine.
• T4 mempunyai ikatan besar dengan Globuline
Jika Yodium berkurang maka terjadi pembesaran tiroid (gondok) untuk mengejar kekurangan hormon yang dihasilkan.
2. GnRH (Gonandotropin Releasing Hormon) • FSH (Folikel Stimulating Hormon)
• LH (Luteinizing Hormon)
Gonade • Estrogen

















• Progesteron





















• Testosteron • Pertumbuhan alat-alat kelamin
• Perkembangan payudara
• Menyebabkan lendir servic menjadi lebih tipis ehingga sperma mudah menembus
• Meningkatkan osteoblastik
• Menyebabkan retensi Na, Cl dan H2O sehingga menyebabkan ekskresi urin berkurang

• Nidasi dipersiapkan oleh endometrium dan pada wanita hamil mengurangi kepekaan terhadap oxytosin

• Menyebabkan secret leher rahim kental, keruh dan sedikit sehingga menyulitkan sperma menembus

• Menyebabkan peningkatan ekskresi Na

• Untuk kontrasepsi hormonal

• Perkembangan kelamin sekunder

• Tingkah laku pola pria

• Metabolisme anabolik

• Pengaturan gen

• Spermatogenesis

• Diferensiasi seksual

Saat premenstruasi kadar urin menajadi sedikit. Sedangkan saat menopause akan terjadi osteoporosis pada wanita akibat menghilangnya estrogen.













Progesteron menimbulkan umpan balik negatif terhadap hipotalamus.




















Testosteron dihasilkan oleh testis pada pria. Sel leidyg mensekresi protein pengikat androgen atau ABP yang akan mengikat testosteron sebagai jawaban terhadap rangsangan FSH.

FSH mengalami feedback mechanisme oleh hormon Estrogen sedangkan LH mengalami feedback mechanisme oleh hormon progesteron dan hormon testosteron.


Hipofungsi kelenjar gonad dimana adanya gangguan pada awal proses maturasi juga adanya regresi dari ciri-ciri seks yang sebelumnya berkembang normal
3. CRH (Corticotropin Releasing Hormon) ACTH (Adenocorticotropin Hormon) Korteks Kelenjar Adrenal/Suprarenal Kortikosteroid (glukokortikoid, mineralokortikoid dan hormon androgen adrenal Metabolisme bahan makanan (fungsi korteks kelj.adrenal) Pelepasan hormon kortikosteroid dipacu oleh ACTH. Sedangkan pengeluaran ACTH diatur oleh kadar hormon glukokorticoid bebas yang beredar.
Hormon androgen adrenal diubah menjadi testosteron oleh liver, biasanya pada wanita.
• Pada pria 17 ketosteroid berasal dari androgen testis
• Pada wanita 17 ketosteroid berasal dari adrenal
Hipofungsi kortikosteroid menyebabkan penyakit Addison
Hiperfungsi kortikosteroid menyebabkan Cushing Syndrome dan menyebabkan hipersekresi ACTH

Mineralokortikoid utama yaitu Aldosteron
Sekresi mineralokortikoid dipacu oleh Angiotensin
Hiperaldosteronisme menyebabkan Sindroma Conn

4. GHRIH (Growth Hormon Releasing Inhibiing Hormon) GH (Growth Hormon) Kartilago epifisealis tulang panjang • Metabolisme lemak
• Metabolisme protein
• Metabolisme karbohidrat
• Metabolisme mineral Produksi GH berlebihan terjadi pada orang dewasa karena adanya tumor sel asidofil/tumor sel kromofob. Gejala berupa akromegali, hipertrofi otot jantung dan otot rangka serta pembengkaan tulang rawan.
Kadar pada orang dewasa 400 µg/dl
Pada remaja 700 µg/dl
Pada pagi hari sekitar 5 µg/dl

Produksi GH berkurang terjadi pada anak dengan tubuh kecil dan proporsi bagian tubuh normal.
Sekresi GH dipacu oleh:
• Kadar glukosa darah yang rendah
• Dopamin
• Latihan
• Stress
GHRIH menghambat hipofise dalam mensekresi GH sehingga GH yg dikeluarkan menjadi lebih sedikit.
5. PRIH (Prolacting Releasing Inhibiting Hormon) PRL (Prolaktin) Kelenjar susu Untuk perangsangan awal produksi air susu Prolaktin disekresikan oleh sel asidopil pada hipofise.
Kadar prolaktin yang berlebih dapat memacu perkembangan payudara.
Prolatkin meningkat pada kadar dopamin rendah dan adanya kerusakan hipotalamus/tumor.
PRIH menghambat dalam mensekresi prolaktin. Prolaktin tersebut hanya dapat merangsang produksi susu saja. Sehingga air susu tidak dikeluarkan dan apabila kadar dari prolaktin tersebut berlebihan maka akan memacu perkembangan payudara.
6. Beta Endorphin Hipofise Beta Endorphin akan disekresikan saat seseorang mendapatkan suatu kenikmatan seperti saat laki-laki mengalami ejakulasi, perempuan mengalami masturbasi ataupun saat seseorang mengalami kenikmatan dalam merokok. Beta Endorphin tersebut merupakan lobus anterior dari hipofise.
7. ADH (Antidiuretik Hormon) atau Vasopresin Untuk mempengaruhi jumlah air yang disekresikan melalui ginjal di tubulus kontortus distal dan duktus kolektifus. Kadar rata-rata orang dewasa: 2,3 – 3,1 µg/ml.
Sekresi ADH dipacu oleh:
• Berkurangnya volume darah sampai 10%
• Obat-obat morfin, barbiturat, kolinergik dan histamin.
Gangguan sekresi ADH yaitu Diabetes Insipidus dan SIADHS
8. Oksitosin Merangsang kontraksi sel mioepitel yang mengelilingi alveoli mammae sehingga memacu aliran susu kedalam sistem duktus alveolaris dan menyebabkan ejeksi air susu. Sekresi akan meningkat saat awal laktasi.
Apabila oksitosin berlebih maka ejeksi air susu akan berlebih dan susah dikontrol sedangkan kekurangan oksitosin maka ejeksi air susu akan sedikit bahkan tidak keluar.

Penyebab Infertil pada Wanita

penyebab infertilitas pada wanita;
1. Faktor Vagina :
Vaginismus (kejang otot vagina), Vaginitis (radang/infeksi vagina), dll
2. Faktor Uterus (rahim) :
Myoma (tumor otot rahim), Endometritis (radang sel. lendir rahim), Endometriosis (tumbuh sel. ender rahim bukan pada tempatnya), Uterus bicornis, arcuatus, asherman’s syndrome, retrofleksi (kelainan bentuk dan posisi rahim), Prolap (pemburutan, penyembulan rahim ke bawah).
3. Faktor Cervix (Mulut Rahim) :
Polip (tumor jinak), Stenosis (kekakuan mulut rahim), Non Hostile Mucus (kualitas lendir mulut rahim jelek), Anti Sperm Antibody (antibody terhadap sperma), dll.
4. Faktor Tuba Fallopi (Saluran Telur) :
Pembuntuan, penyempitan, perlengketan saluran telur (bias karena infeksi atau kelainan bawaan).
5. Faktor Ovarium (Indung Telur) :
Tumor, Cyste, Gangguan menstruasi (Amenorhoe, Oligomenorhoe dengan/tanpa ovulasi). Organ ini berinteraksi dengan pusat pengendali hormone di otak (Hypothalamus dan Hipofisis) dalam mengatur siklus menstruasi.
6. Faktor Lain :
Prolactinoma (tumor pada Hipofisis), Hiper/hypotroid (kelebihan/ kekurangan hormone tiroid), dll.
Infertilitas adalah keadaan seorang wanita tidak dapat hamil secara alami dalam satu tahun setelah secara teratur melakukan aktifitas seksual tanpa alat kontrasepsi.

Faktor penyebab infertilitas bisa pada pihak wanita (istri) maupun pria ( suami).

Adapun penyebab infertilitas pada wanita adalah :
- faktor vagina : vaginismus, vaginistis
- faktor serviks : polip, stenosis, non hostile mukus, antibodi terhadap sperma
- faktor uterus : mioma, endometritis, endometriosis, uterus bicornis, arcuatus
- faktor tuba fallopi : tuba buntu, penyempitan, perlengketan
- faktor ovarium : tumor, kista, gangguan menstruasi dengan / tanpa ovulasi
- faktor hormon : gangguan hormon pada poros hipothalamus-hipofisis-ovarium
- faktor lain : obesitas, hiper/hipotiroid, penyakit sistemik lainnya.

Sindroma infertilitas pada wanita:

sindroma defisiensi ginjal
kelainan bawaan, kelainan haid dengan siklus haid memanjang, darah haid sedikit, libido seksual menurun, tubuh kurus.

sindroma hati tertekan
siklus haid tidak teratur, gejala premenstrual sindrom seperti bengkak di payudara, emosi labil, mudah tersinggung.

sindroma defisiensi darah / xue
fisik yang lemah, anemi, penyakit kronis, sakit berat, mengakibatkan tubuh kekurangan darah sehingga tidak terjadi haid.

sindroma reak lembab
Timbunan reak lembab atau lendir, kegemukan, siklus haid memanjang, banyak keputihan.

Sindroma stagnasi darah
siklus haid memanjang, jumlah darah haid sedikit, berwarna gelap disertai gumpalan, dismenore

Sumber: http://id.shvoong.com/medicine-and-health/gynecology/1968246-infertilitas-pada-wanita/#ixzz1LlIRDFuP


Pengertian Infertilitas : Keadaan dimana pasangan suami isteri selama satu tahun belum memiliki anak walaupun keduanya melakukan hubungan intim secara rutin dan tidak menggunakan kontrasepsi .
Ada 2 macam, infertilitas primer yaitu keadaan dimana seorang isteri belum pernah memiliki/melahirkan anak dalam keadaan hidup . Infertilitas sekunder yaitu jika seorang isteri pernah melahirkan anak dan namun tidak mampu melahirkan lagi sementara masih dalam masa produktif/belum menopause .
Perawatan medis
Pengobatan infertilitas umumnya melibatkan penggunaan obat kesuburan, perangkat medis, operasi, atau kombinasi dari berikut. Jika sperma yang berkualitas baik, dan mekanisme struktur reproduksi wanita yang baik (saluran tuba paten, tidak ada adhesi atau bekas luka) dokter mungkin mulai dengan resep kursus obat merangsang ovarium.
Dokter mungkin juga menyarankan menggunakan topi konsepsi penutup serviks mana pasien menggunakan di rumah dengan menempatkan sperma di dalam topi dan meletakkan perangkat konsepsi pada leher rahim, inseminasi intrauterin (IUI), di mana dokter memperkenalkan sperma ke dalam rahim selama ovulasi , melalui kateter. Dalam metode ini, pembuahan terjadi di dalam tubuh.
Jika perawatan medis konservatif gagal untuk mencapai kehamilan istilah penuh, dokter mungkin menyarankan pasien menjalani fertilisasi in vitro (IVF). IVF dan teknik terkait (ICSI, ZIFT, GIFT) disebut teknologi reproduksi yang dibantu (ART) teknik.
teknik ART umumnya dimulai dengan merangsang ovarium untuk meningkatkan produksi telur. Setelah stimulasi, dokter pembedahan ekstrak satu atau lebih telur dari indung telur, dan menyatukan mereka dengan sperma di laboratorium, dengan tujuan untuk memproduksi satu atau lebih embrio. Pemupukan terjadi di luar tubuh, dan telur dibuahi ini dimasukkan kembali ke dalam saluran reproduksi wanita tersebut, dalam sebuah prosedur yang disebut transfer embrio.
teknik pengobatan lainnya adalah misalnya tuboplasty, dibantu menetas, dan diagnosis praimplantasi genetik.
Komplementer dan pengobatan alternatif
Tiga pelengkap atau alternatif perawatan kesuburan perempuan telah teruji secara ilmiah, dengan hasil yang dipublikasikan dalam jurnal medis peer-review.
1. Kelompok intervensi psikologis: Sebuah 2000 Harvard Medical School studi meneliti efek dari kelompok intervensi psikologis pada wanita subur (berusaha untuk hamil durasi satu sampai dua tahun). Kelompok intervensi dua kelompok pendukung dan kelompok perilaku kognitif-telah signifikan secara statistik tingkat kehamilan lebih tinggi dari kelompok kontrol.
2. Akupunktur: Akupunktur dilakukan 25 menit sebelum dan setelah transfer embrio IVF IVF peningkatan angka kehamilan dalam sebuah penelitian di Jerman yang diterbitkan pada tahun 2002. Dalam sebuah studi tahun 2006 yang sama yang dilakukan oleh University of South Australia, peluang kelompok akupunktur (meskipun tidak signifikan secara statistik) adalah lebih tinggi 1,5 daripada kelompok kontrol. Walaupun hasil definitif efek akupunktur pada transfer embrio tetap menjadi topik diskusi, studi penulis menyatakan bahwa tampaknya menjadi tambahan yang aman untuk IVF.
3. Manual terapi fisik: Teknik Wurn, fisik terapi pengobatan manipulatif manual, ditunjukkan dalam publikasi peer review untuk meningkatkan kehamilan IVF tarif dan alami pada wanita subur dalam sebuah studi tahun 2004, dan untuk membuka dan mengembalikan fungsi tuba falopi diblokir dalam sebuah penelitian di tahun 2008 . Terapi ini dirancang untuk mengatasi adhesi membatasi fungsi dan mobilitas dari organ reproduksi. Ini mungkin dianggap sebagai bentuk pariwisata medis. Alasan utama bagi pariwisata kesuburan adalah peraturan hukum dari prosedur dicari di negara asal, atau harga yang lebih rendah. In-vitro fertilisasi dan inseminasi donor prosedur utama yang terlibat.
http://www.news-medical.net/health/Infertility-Treatments-%28Indonesian%29.aspx

Sabtu, 14 Mei 2011

Systemic lupus erythematosus
From Wikipedia, the free encyclopedia
Jump to: navigation, search
For other uses, see lupus (disambiguation).
Systemic lupus erythematosus
Classification and external resources
ICD-10 L93., M32.
ICD-9 710.0
OMIM 152700
DiseasesDB 12782
MedlinePlus 000435
eMedicine med/2228 emerg/564
MeSH D008180

Systemic lupus erythematosus (pronounced /sɪˈstɛmɪk ˈlupəs ˌɛrɪˌθiməˈtʰoʊsəs/ ( listen)), often abbreviated to SLE or lupus, is a systemic autoimmune disease (or autoimmune connective tissue disease) that can affect any part of the body. As occurs in other autoimmune diseases, the immune system attacks the body's cells and tissue, resulting in inflammation and tissue damage.[1] It is a Type III hypersensitivity reaction caused by antibody-immune complex formation.

SLE most often harms the heart, joints, skin, lungs, blood vessels, liver, kidneys, and nervous system. The course of the disease is unpredictable, with periods of illness (called flares) alternating with remissions. The disease occurs nine times more often in women than in men, especially in women in child-bearing years ages 15 to 35, and is also more common in those of non-European descent.[2][3][4]

SLE is treatable through addressing its symptoms, mainly with cyclophosphamide, corticosteroids and immunosuppressants; there is currently no cure. SLE can be fatal, although with recent medical advances, fatalities are becoming increasingly rare. Survival for people with SLE in the United States, Canada, and Europe is approximately 95% at five years, 90% at 10 years, and 78% at 20 years.[4]
Signs and symptoms
Common symptoms of SLE.[5]

SLE is one of several diseases known as "the great imitators" because it often mimics or is mistaken for other illnesses.[6] SLE is a classical item in differential diagnosis,[2] because SLE symptoms vary widely and come and go unpredictably. Diagnosis can thus be elusive, with some people suffering unexplained symptoms of untreated SLE for years.

Common initial and chronic complaints include fever, malaise, joint pains, myalgias, fatigue, and temporary loss of cognitive abilities. Because they are so often seen with other diseases, these signs and symptoms are not part of the diagnostic criteria for SLE. When occurring in conjunction with other signs and symptoms (see below), however, they are considered suggestive.[7]

Dermatological manifestations

As many as 30% of sufferers have some dermatological symptoms (and 65% suffer such symptoms at some point), with 30% to 50% suffering from the classic malar rash (or butterfly rash) associated with the disease. Some may exhibit thick, red scaly patches on the skin (referred to as discoid lupus). Alopecia; mouth, nasal, and vaginal ulcers; and lesions on the skin are also possible manifestations.

Musculoskeletal

The most commonly sought medical attention is for joint pain, with the small joints of the hand and wrist usually affected, although all joints are at risk. The Lupus Foundation of America estimates more than 90 percent of those affected will experience joint and/or muscle pain at some time during the course of their illness.[8] Unlike rheumatoid arthritis, lupus arthritis is less disabling and usually does not cause severe destruction of the joints. Fewer than ten percent of people with lupus arthritis will develop deformities of the hands and feet.[8] SLE patients are at particular risk of developing osteoarticular tuberculosis.[9]

A possible association between rheumatoid arthritis and SLE has been suggested,[10] and SLE may be associated with an increased risk of bone fractures in relatively young women.[11]

Hematological

Anemia may develop in up to 50% of cases. Low platelet and white blood cell counts may be due to the disease or a side effect of pharmacological treatment. People with SLE may have an association with antiphospholipid antibody syndrome[12] (a thrombotic disorder), wherein autoantibodies to phospholipids are present in their serum. Abnormalities associated with antiphospholipid antibody syndrome include a paradoxical prolonged partial thromboplastin time (which usually occurs in hemorrhagic disorders) and a positive test for antiphospholipid antibodies; the combination of such findings have earned the term "lupus anticoagulant-positive". Another autoantibody finding in SLE is the anticardiolipin antibody, which can cause a false positive test for syphilis.

Cardiac

A person with SLE may have inflammation of various parts of the heart, such as pericarditis, myocarditis, and endocarditis. The endocarditis of SLE is characteristically noninfective (Libman-Sacks endocarditis), and involves either the mitral valve or the tricuspid valve. Atherosclerosis also tends to occur more often and advances more rapidly than in the general population.[13][14][15]

Pulmonary

Lung and pleura inflammation can cause pleuritis, pleural effusion, lupus pneumonitis, chronic diffuse interstitial lung disease, pulmonary hypertension, pulmonary emboli, pulmonary hemorrhage, and shrinking lung syndrome.

Renal

Painless hematuria or proteinuria may often be the only presenting renal symptom. Acute or chronic renal impairment may develop with lupus nephritis, leading to acute or end-stage renal failure. Because of early recognition and management of SLE, end-stage renal failure occurs in less than 5% of cases.

A histological hallmark of SLE is membranous glomerulonephritis with "wire loop" abnormalities.[16] This finding is due to immune complex deposition along the glomerular basement membrane, leading to a typical granular appearance in immunofluorescence testing.

Neuropsychiatric

Neuropsychiatric syndromes can result when SLE affects the central or peripheral nervous systems. The American College of Rheumatology defines 19 neuropsychiatric syndromes in systemic lupus erythematosus.[17] The diagnosis of neuropsychiatric syndromes concurrent with SLE is one of the most difficult challenges in medicine, because it can involve so many different patterns of symptoms, some of which may be mistaken for signs of infectious disease or stroke.[18]

The most common neuropsychiatric disorder people with SLE have is headache,[19] although the existence of a specific lupus headache and the optimal approach to headache in SLE cases remains controversial.[20] Other common neuropsychiatric manifestation of SLE include cognitive dysfunction, mood disorder, cerebrovascular disease,[19] seizures, polyneuropathy,[19] anxiety disorder, and psychosis. It can rarely present with intracranial hypertension syndrome, characterized by an elevated intracranial pressure, papilledema, and headache with occasional abducens nerve paresis, absence of a space-occupying lesion or ventricular enlargement, and normal cerebrospinal fluid chemical and hematological constituents.[21]

More rare manifestations are acute confusional state, Guillain-Barré syndrome, aseptic meningitis, autonomic disorder, demyelinating syndrome, mononeuropathy (which might manifest as mononeuritis multiplex), movement disorder (more specifically, chorea), myasthenia gravis, myelopathy, cranial neuropathy and plexopathy.

Neurological

Neural symptoms contribute to a significant percentage of morbidity and mortality in patients with lupus.[22] As a result, the neural side of lupus is being studied in hopes of reducing morbidity and mortality rates.[23] The neural manifestation of lupus is known as neuropsychiatric systematic lupus erythematosus (NPSLE). One aspect of this disease is severe damage to the epithelial cells of the blood-brain barrier.

Lupus has a wide range of symptoms which span the body. The neurological symptoms include headaches,[19] depression, seizures, cognitive dysfunction, mood disorder, cerebrovascular disease,[19] polyneuropathy,[19] anxiety disorder, psychosis, and in some extreme cases, personality disorders.[24] In certain regions, depression reportedly affects up to 60% of women suffering from SLE.[25]

Reproductive

Further information: Systemic lupus erythematosus and pregnancy

SLE causes an increased rate of fetal death in utero and spontaneous abortion (miscarriage). The overall live-birth rate in SLE patient has been estimated to be 72%.[26] Pregnancy outcome appears to be worse in SLE patients whose disease flares up during pregnancy.[27]

Neonatal lupus is the occurrence of SLE symptoms in an infant born from a mother with SLE, most commonly presenting with a rash resembling discoid lupus erythematosus, and sometimes with systemic abnormalities such as heart block or hepatosplenomegaly.[28] Neonatal lupus is usually benign and self-limited.[28]

Systemic

Fatigue in SLE is probably multifactorial and has been related to not only disease activity or complications such as anemia or hypothyroidism, but also to pain, depression, poor sleep quality, poor physical fitness and perceived lack of social support.[29][30]
[edit] Causes

There is no one specific cause of SLE. There are, however, a number of environmental triggers and a number of genetic susceptibilities.[31][32]
[edit] Genetics

The first mechanism may arise genetically. Research indicates SLE may have a genetic link. SLE does run in families, but no single causal gene has been identified. Instead, multiple genes appear to influence a person's chance of developing lupus when triggered by environmental factors. The most important genes are located in the HLA region on chromosome 6, where mutations may occur randomly (de novo) or may be inherited. HLA class I, class II, and class III are associated with SLE, but only classes I and II contribute independently to increased risk of SLE.[33] Other genes which contain risk variants for SLE are IRF5, PTPN22, STAT4,[34] CDKN1A,[35] ITGAM, BLK,[34] TNFSF4 and BANK1.[36] some of the susceptibility genes may be population specific.[34]
[edit] Environmental triggers

The second mechanism may be due to environmental factors. These factors may not only exacerbate existing SLE conditions, but also trigger the initial onset.

Researchers have sought to find a connection between certain infectious agents (viruses and bacteria), but no pathogen can be consistently linked to the disease. Some researchers have found that women with silicone gel-filled breast implants have produced antibodies to their own collagen, but it is not known how often these antibodies occur in the general population, and there are no data that show these antibodies cause connective tissue diseases such as SLE. There is also a small but growing body of evidence linking SLE to lipstick usage.[37][38][39]
[edit] Drug reactions

Drug-induced lupus erythematosus is a (generally) reversible condition that usually occurs in people being treated for a long-term illness. Drug-induced lupus mimics SLE. However, symptoms of drug-induced lupus generally disappear once the medication that triggered the episode is stopped. There are about 400 medications that can cause this condition, the most common of which are procainamide, hydralazine, quinidine, and phenytoin.[2]
[edit] Non-SLE forms of lupus

Discoid (cutaneous) lupus is limited to skin symptoms and is diagnosed by biopsy of rash on the face, neck, scalp or arms.
[edit] Pathophysiology

One manifestation of SLE is abnormalities in apoptosis, a type of programmed cell death in which aging or damaged cells are neatly disposed of as a part of normal growth or functioning.
[edit] Transmission

In SLE, the body's immune system produces antibodies against itself, particularly against proteins in the cell nucleus. SLE is triggered by environmental factors that are unknown.

"All the key components of the immune system are involved in the underlying mechanisms [of SLE]" according to Rahman, and SLE is the prototypical autoimmune disease. The immune system must have a balance (homeostasis) between being sensitive enough to protect against infection, and being too sensitive and attacking the body's own proteins (autoimmunity). From an evolutionary perspective, according to Crow, the population must have enough genetic diversity to protect itself against a wide range of possible infection; some genetic combinations result in autoimmunity. The likely environmental triggers include ultraviolet light, drugs, and viruses. These stimuli cause the destruction of cells and expose their DNA, histones, and other proteins, particularly parts of the cell nucleus. Because of genetic variations in different components of the immune system, in some people the immune system attacks these nuclear-related proteins and produces antibodies against them. In the end, these antibody complexes damage blood vessels in critical areas of the body, such as the glomeruli of the kidney; these antibody attacks are the cause of SLE. Researchers are now identifying the individual genes, the proteins they produce, and their role in the immune system. Each protein is a link on the autoimmune chain, and researchers are trying to find drugs to break each of those links.[2][40][41]

SLE is a chronic inflammatory disease believed to be a type III hypersensitivity response with potential type II involvement.[42] Reticulate and stellate acral pigmentation should be considered a possible manifestation of SLE and high titers of anticardiolipin antibodies, or a consequence of therapy.[43]
[edit] Abnormalities in apoptosis

* Apoptosis is increased in monocytes and keratinocytes
* Expression of Fas by B cells and T cells is increased
* There are correlations between the apoptotic rates of lymphocytes and disease activity.

Tingible body macrophages (TBMs) – large phagocytic cells in the germinal centers of secondary lymph nodes – express CD68 protein. These cells normally engulf B cells that have undergone apoptosis after somatic hypermutation. In some people with SLE, significantly fewer TBMs can be found, and these cells rarely contain material from apoptotic B cells. Also, uningested apoptotic nuclei can be found outside of TBMs. This material may present a threat to the tolerization of B cells and T cells. Dendritic cells in the germinal center may endocytose such antigenic material and present it to T cells, activating them. Also, apoptotic chromatin and nuclei may attach to the surfaces of follicular dendritic cells and make this material available for activating other B cells that may have randomly acquired self-specificity through somatic hypermutation.[44]
[edit] Clearance deficiency
Clearance deficiency

The exact mechanisms for the development of SLE are still unclear, since the pathogenesis is a multifactorial event. Beside discussed causations, impaired clearance of dying cells is a potential pathway for the development of this systemic autoimmune disease. This includes deficient phagocytic activity and scant serum components in addition to increased apoptosis.

Monocytes isolated from whole blood of SLE sufferers show reduced expression of CD44 surface molecules involved in the uptake of apoptotic cells. Most of the monocytes and tingible body macrophages (TBMs), which are found in the germinal centres of lymph nodes, even show a definitely different morphology; they are smaller or scarce and die earlier. Serum components like complement factors, CRP, and some glycoproteins are, furthermore, decisively important for an efficiently operating phagocytosis. With SLE, these components are often missing, diminished, or inefficient.

Recent research has found an association between certain lupus patients (especially those with lupus nephritis) and an impairment in degrading neutrophil extracellular traps (NETs). These were due to DNAse1 inhibiting factors, or NET protecting factors in patient serum, rather than abnormalities in the DNAse1 itself.[45] DNAse1 mutations in lupus have so far only been found in some Japanese cohorts.[46]

The clearance of early apoptotic cells is an important function in multicellular organisms. It leads to a progression of the apoptosis process and finally to secondary necrosis of the cells if this ability is disturbed. Necrotic cells release nuclear fragments as potential autoantigens, as well as internal danger signals, inducing maturation of dendritic cells (DCs), since they have lost their membranes' integrity. Increased appearance of apoptotic cells also simulates inefficient clearance. That leads to maturation of DCs and also to the presentation of intracellular antigens of late apoptotic or secondary necrotic cells, via MHC molecules. Autoimmunity possibly results by the extended exposure to nuclear and intracellular autoantigens derived from late apoptotic and secondary necrotic cells. B and T cell tolerance for apoptotic cells is abrogated, and the lymphocytes get activated by these autoantigens; inflammation and the production of autoantibodies by plasma cells is initiated. A clearance deficiency in the skin for apoptotic cells has also been observed in people with cutaneous lupus erythematosus (CLE).[47]
Germinal centres
[edit] Accumulation in germinal centres (GC)

In healthy conditions, apoptotic lymphocytes are removed in germinal centres by specialized phagocytes, the tingible body macrophages (TBM), which is why no free apoptotic and potential autoantigenic material can be seen. In some people with SLE, accumulation of apoptotic debris can be observed in GC because of an ineffective clearance of apoptotic cells. In close proximity to TBM, follicular dendritic cells (FDC) are localised in GC, which attach antigen material to their surface and, in contrast to bone marrow-derived DC, neither take it up nor present it via MHC molecules.

Autoreactive B cells can accidentally emerge during somatic hypermutation and migrate into the GC light zone. Autoreactive B cells, maturated coincidentally, normally do not receive survival signals by antigen planted on follicular dendritic cells, and perish by apoptosis. In the case of clearance deficiency, apoptotic nuclear debris accumulates in the light zone of GC and gets attached to FDC. This serves as a germinal centre survival signal for autoreactive B-cells. After migration into the mantle zone, autoreactive B cells require further survival signals from autoreactive helper T cells, which promote the maturation of autoantibody-producing plasma cells and B memory cells. In the presence of autoreactive T cells, a chronic autoimmune disease may be the consequence.
[edit] Anti-nRNP autoimmunity

Autoantibodies to nRNP A and nRNP C initially targeted restricted, proline-rich motifs. Antibody binding subsequently spread to other epitopes. The similarity and cross-reactivity between the initial targets of nRNP and Sm autoantibodies identifies a likely commonality in cause and a focal point for intermolecular epitope spreading.[48]
[edit] Others

Elevated expression of HMGB1 was found in the sera of patients and mice with systemic lupus erythematosus, high mobility group box 1 (HMGB1) is a nuclear protein participating in chromatin architecture and transcriptional regulation. Recently, there is increasing evidence HMGB1 contributes to the pathogenesis of chronic inflammatory and autoimmune diseases due to its proinflammatory and immunostimulatory properties.[49]
[edit] Diagnosis
Microphotograph of a histological section of human skin prepared for direct immunofluorescence using an anti-IgG antibody. The skin is from a person with systemic lupus erythematosus and shows IgG deposits at two different places: The first is a bandlike deposit along the epidermal basement membrane ("lupus band test" is positive); the second is within the nuclei of the epidermal cells (antinuclear antibodies are present).
Sodium pertechnate scan showing diffusely increased uptake in lupus cerebritis
[edit] Laboratory tests

Antinuclear antibody (ANA) testing and anti-extractable nuclear antigen (anti-ENA) form the mainstay of serologic testing for SLE. Several techniques are used to detect ANAs. Clinically the most widely used method is indirect immunofluorescence. The pattern of fluorescence suggests the type of antibody present in the patient's serum.

ANA screening yields positive results in many connective tissue disorders and other autoimmune diseases, and may occur in normal individuals. Subtypes of antinuclear antibodies include anti-Smith and anti-double stranded DNA (dsDNA) antibodies (which are linked to SLE) and anti-histone antibodies (which are linked to drug-induced lupus). Anti-dsDNA antibodies are highly specific for SLE; they are present in 70% of cases, whereas they appear in only 0.5% of people without SLE.[2] The anti-dsDNA antibody titers also tend to reflect disease activity, although not in all cases.[2] Other ANA that may occur in SLE sufferers are anti-U1 RNP (which also appears in systemic sclerosis), SS-A (or anti-Ro) and SS-B (or anti-La; both of which are more common in Sjögren's syndrome). SS-A and SS-B confer a specific risk for heart conduction block in neonatal lupus.[50]

Other tests routinely performed in suspected SLE are complement system levels (low levels suggest consumption by the immune system), electrolytes and renal function (disturbed if the kidney is involved), liver enzymes, and complete blood count.

The lupus erythematosus (LE) cell test was commonly used for diagnosis, but it is no longer used because the LE cells are only found in 50–75% of SLE cases, and they are also found in some people with rheumatoid arthritis, scleroderma, and drug sensitivities. Because of this, the LE cell test is now performed only rarely and is mostly of historical significance.[51]
[edit] Diagnostic criteria

Some physicians make a diagnosis on the basis of the American College of Rheumatology (ACR) classification criteria. The criteria, however, were established mainly for use in scientific research including use in randomized controlled trials which require higher confidence levels, so some people with SLE may not pass the full criteria.
[edit] Criteria

The American College of Rheumatology established eleven criteria in 1982,[52] which were revised in 1997[53] as a classificatory instrument to operationalise the definition of SLE in clinical trials. They were not intended to be used to diagnose individuals and do not do well in that capacity. For the purpose of identifying patients for clinical studies, a person has SLE if any 4 out of 11 symptoms are present simultaneously or serially on two separate occasions.

1. Malar rash (rash on cheeks); sensitivity = 57%; specificity = 96%.[54]
2. Discoid rash (red, scaly patches on skin that cause scarring); sensitivity = 18%; specificity = 99%.[54]
3. Serositis: Pleurisy (inflammation of the membrane around the lungs) or pericarditis (inflammation of the membrane around the heart); sensitivity = 56%; specificity = 86% (pleural is more sensitive; cardiac is more specific).[54]
4. Oral ulcers (includes oral or nasopharyngeal ulcers); sensitivity = 27%; specificity = 96%.[54]
5. Arthritis: nonerosive arthritis of two or more peripheral joints, with tenderness, swelling, or effusion; sensitivity = 86%; specificity = 37%.[54]
6. Photosensitivity (exposure to ultraviolet light causes rash, or other symptoms of SLE flareups); sensitivity = 43%; specificity = 96%.[54]
7. Blood—hematologic disorder—hemolytic anemia (low red blood cell count) or leukopenia (white blood cell count<4000/µl), lymphopenia (<1500/µl) or thrombocytopenia (<100000/µl) in the absence of offending drug; sensitivity = 59%; specificity = 89%.[54] Hypocomplementemia is also seen, due to either consumption of C3 and C4 by immune complex-induced inflammation or to congenitally complement deficiency, which may predispose to SLE.
8. Renal disorder: More than 0.5 g per day protein in urine or cellular casts seen in urine under a microscope; sensitivity = 51%; specificity = 94%.[54]
9. Antinuclear antibody test positive; sensitivity = 99%; specificity = 49%.[54]
10. Immunologic disorder: Positive anti-Smith, anti-ds DNA, antiphospholipid antibody, and/or false positive serological test for syphilis; sensitivity = 85%; specificity = 93%.[54] Presence of anti-ss DNA in 70% of cases (though also positive with rheumatic disease and healthy persons).[55]
11. Neurologic disorder: Seizures or psychosis; sensitivity = 20%; specificity = 98%.[54]

The mnemonic to remember the 11 symptoms is 'MD SOAP BRAIN' or 'DOPAMIN(E) RASH'.[56]
[edit] Criteria for individual diagnosis

Some people, especially those with antiphospholipid syndrome, may have SLE without four of the above criteria, and also SLE may present with features other than those listed in the criteria.[57][58][59]

Recursive partitioning has been used to identify more parsimonious criteria.[54] This analysis presented two diagnostic classification trees:

1. Simplest classification tree: SLE is diagnosed if a person has an immunologic disorder (anti-DNA antibody, anti-Smith antibody, false positive syphilis test, or LE cells) or malar rash. It has sensitivity = 92% and specificity = 92%.
2. Full classification tree: Uses 6 criteria. It has sensitivity = 97% and specificity = 95%.

Other alternative criteria have been suggested, e.g. the St. Thomas' Hospital "alternative" criteria in 1998.[60]
[edit] Prevention

SLE is not understood well enough to be prevented, but, when the disease develops, quality of life can be improved through flare prevention. The warning signs of an impending flare include increased fatigue, pain, rash, fever, abdominal discomfort, headache, and dizziness. Early recognition of warning signs and good communication with a doctor can help individuals remain active, experience less pain, and reduce medical visits.[61]

As longevity of people with SLE increases, the likelihood of complications also increases in four areas: cardiovascular disease, infections, osteoporosis, and cancer. Standard preventive measures, screening for related diseases may be necessary to deal with the increased risks due to the side effects of medications. Extra vigilance is considered warranted in particular for cancers affecting the immune system.[62]
[edit] Treatment

The treatment of SLE involves preventing flares and reducing their severity and duration when they occur.

Treatment can include corticosteroids and anti-malarial drugs. Certain types of lupus nephritis such as diffuse proliferative glomerulonephritis require bouts of cytotoxic drugs. These drugs include cyclophosphamide and mycophenolate.

Hydroxychloroquine (HCQ) was the last medication approved by the FDA for lupus in 1955.[63] Some drugs approved for other diseases are used for SLE 'off-label'. In November 2010, an FDA advisory panel recommended approving Benlysta (belimumab) as a treatment for the pain and flare-ups common in lupus. The drug was approved by the FDA in March 2011. [64]
[edit] Medications

Due to the variety of symptoms and organ system involvement with SLE, its severity in an individual must be assessed in order to successfully treat SLE. Mild or remittant disease can sometimes be safely left untreated. If required, nonsteroidal anti-inflammatory drugs and antimalarials may be used. Medications such as Prednisone, Cellcept and Prograf has been used in the past. A number of potential treatments are in clinical trials.[65]
[edit] Disease-modifying antirheumatic drugs

Disease-modifying antirheumatic drugs (DMARDs) are used preventively to reduce the incidence of flares, the process of the disease, and lower the need for steroid use; when flares occur, they are treated with corticosteroids. DMARDs commonly in use are antimalarials such as plaquenil and immunosuppressants (e.g. methotrexate and azathioprine). Hydroxychloroquine is an FDA-approved antimalarial used for constitutional, cutaneous, and articular manifestations. Hydroxychloroquine has relatively few side effects, and there is evidence that it improves survival among people who have SLE.[63] Cyclophosphamide is used for severe glomerulonephritis or other organ-damaging complications. Mycophenolic acid is also used for treatment of lupus nephritis, but it is not FDA-approved for this indication, and FDA is investigating reports that it may be associated with birth defects when used by pregnant women.[66]
[edit] Immunosuppressive drugs

In more severe cases, medications that modulate the immune system (primarily corticosteroids and immunosuppressants) are used to control the disease and prevent recurrence of symptoms (known as flares). Depending on the dosage, people who require steroids may develop Cushing's syndrome, side-effects of which may include obesity, puffy round face, diabetes mellitus, large appetite, difficulty sleeping and osteoporosis. Those side-effects can subside if and when the large initial dosage is reduced, but long-term use of even low doses can cause elevated blood pressure and cataracts.

Numerous new immunosuppressive drugs are being actively tested for SLE. Rather than suppressing the immune system nonspecifically, as corticosteroids do, they target the responses of individual [types of] immune cells. Some of these drugs are already FDA-approved for treatment of rheumatoid arthritis.[63] See also Belimumab and Atacicept. Lupuzor has given encouraging results in a phase IIb trial[67]
[edit] Analgesia

Since a large percentage of people with SLE suffer from varying amounts of chronic pain, stronger prescription analgesics (pain killers) may be used if over-the-counter drugs (mainly nonsteroidal anti-inflammatory drugs) do not provide effective relief. Potent NSAIDs such as indomethacin and diclofenac are relatively contraindicated for patients with SLE because they increase the risk of kidney failure and heart failure.[63]

Moderate pain is typically treated with mild prescription opiates such as dextropropoxyphene and co-codamol. Moderate to severe chronic pain is treated with stronger opioids, such as hydrocodone or longer-acting continuous-release opioids, such as oxycodone, MS Contin, or methadone. The fentanyl duragesic transdermal patch is also a widely-used treatment option for the chronic pain caused by complications because of its long-acting timed release and ease of use. When opioids are used for prolonged periods, drug tolerance, chemical dependency, and addiction may occur. Opiate addiction is not typically a concern, since the condition is not likely to ever completely disappear. Thus, lifelong treatment with opioids is fairly common for chronic pain symptoms, accompanied by periodic titration that is typical of any long-term opioid regimen.
[edit] Intravenous Immunoglobulins (IVIGs)

Intravenous immunoglobulins may be used to control SLE with organ involvement, or vasculitis. It is believed that they reduce antibody production or promote the clearance of immune complexes from the body, even though their mechanism of action is not well-understood.[68] Unlike immunosuppressives and corticosteroids, IVIGs do not suppress the immune system, so there is less risk of serious infections with these drugs.[69]
[edit] Lifestyle changes

Avoiding sunlight is the primary change to the lifestyle of SLE sufferers, as sunlight is known to exacerbate the disease, as is the debilitating effect of intense fatigue. These two problems can lead to patients becoming housebound for long periods of time. Drugs unrelated to SLE should be prescribed only when known not to exacerbate the disease. Occupational exposure to silica, pesticides and mercury can also make the disease worsen.[31]
[edit] Renal transplantation

Renal transplants are the treatment of choice for end-stage renal disease, which is one of the complications of lupus nephritis, but the recurrence of the full disease is common in up to 30% of patients.[70]
[edit] Hughes syndrome

Hughes syndrome, also known as the antiphospholipid syndrome or sticky blood syndrome, is also related to the onset of neural lupus symptoms in the brain. In this form of the disease the cause is very different from lupus: thromboses (blood clots or "sticky blood") form in blood vessels, which prove to be fatal if they move within the blood stream.[71] If the thromboses migrate to the brain, they can potentially cause a stroke by blocking the blood supply to the brain.

If this disorder is suspected in patients, brain scans are usually required for early detection. These scans can show localized areas of the brain where blood supply has not been adequate. The treatment plan for these patients requires thinning of the blood. Often, aspirin is prescribed for this purpose, although in more severe cases anticoagulants such as warfarin are used.[72]
[edit] Management of pregnancy
Further information: Systemic lupus erythematosus and pregnancy

While most infants born to mothers who have SLE are healthy, pregnant mothers with SLE should remain under medical care until delivery. Neonatal lupus is rare, but identification of mothers at highest risk for complications allows for prompt treatment before or after birth. In addition, SLE can flare up during pregnancy, and proper treatment can maintain the health of the mother longer. Women pregnant and known to have anti-Ro (SSA) or anti-La antibodies (SSB) often have echocardiograms during the 16th and 30th weeks of pregnancy to monitor the health of the heart and surrounding vasculature.[61]

Contraception and other reliable forms of pregnancy prevention is routinely advised for women with SLE, since getting pregnant during active disease was found to be harmful. Lupus nephritis was the most common manifestation.
[edit] Prognosis

SLE is considered incurable, but highly treatable.

In the 1950s, most people diagnosed with SLE lived fewer than five years. Advances in diagnosis and treatment have improved survival to the point where over 90% now survive for more than ten years, and many can live relatively asymptomatically. (It is important to note that "ten years" in this statistic does not indicate an average survival rate, but is merely the length of the referenced study. According to the Lupus Foundation of America, "the majority of people with lupus today can expect to live a normal lifespan."[73])

Prognosis is normally worse for men and children than for women; however, if symptoms are present after age 60, the disease tends to run a more benign course. Early mortality, within 5 years, is due to organ failure or overwhelming infections, both of which can be modified by early diagnosis and treatment. The mortality risk is fivefold when compared to the normal population in the late stages, which can be attributed to cardiovascular diseases acquired from corticosteroid therapy, the leading cause of death for people with SLE.[63]

To reduce potential for cardiovascular issues, high blood pressure and high cholesterol should be prevented or treated aggressively. Steroids should be used at the lowest dose for the shortest possible period, and other drugs that can reduce symptoms should be used whenever possible.[63] High serum creatinine, hypertension, nephrotic syndrome, anemia and hypoalbuminemia are poor prognostic factors.[74]

The ANA is the most sensitive screening test for evaluation, whereas anti-Sm (anti-Smith) is the most specific. The dsDNA (double-stranded DNA) antibody is also fairly specific and often fluctuates with disease activity; as such, the dsDNA titre is sometimes useful to monitor disease flares or response to treatment.[75]
[edit] Epidemiology

The rate of SLE varies considerably between countries, ethnicity, gender, and changes over time.[76] In the United States the prevalence of SLE is estimated to be about 53 per 100,000, translating to about 159,000 out of 300 million people in the US being affected.[76][77] In Northern Europe the rate is about 40 per 100,000 people.[78] SLE occurs more frequently and with greater severity among those of non-European descent.[77] That rate has been found to be as high as 159 per 100,000 among those of Afro-Caribbean descent.[76]

SLE, like many autoimmune diseases, affects females more frequently than males, at a rate of almost 9 to 1.[76]

The incidence of SLE in the United States increased from 1.0 in 1955 to 7.6 in 1974. Whether the increase is due to better diagnosis or to increasing frequency of the disease is unknown.[76]
[edit] History and culture
[edit] Etymology

There are several explanations ventured for the term lupus erythematosus. Lupus is Latin for wolf,[79] and "erythro" is derived from ερυθρός, Greek for "red." All explanations originate with the reddish, butterfly-shaped malar rash that the disease classically exhibits across the nose and cheeks.

1. In various accounts, some doctors thought the rash resembled the pattern of fur on a wolf's face.
2. In other accounts, doctors thought that the rash, which was often more severe in earlier centuries, created lesions that resembled wolf bites or scratches.
3. Another account claims that the term "lupus" did not come from Latin directly, but from the term for a French style of mask that women reportedly wore to conceal the rash on their faces. The mask is called a "loup," French for "wolf."

[edit] History

The history of SLE can be divided into three periods: classical, neoclassical, and modern. The classical period began when the disease was first recognized in the Middle Ages and saw the description of the dermatological manifestation of the disorder. The term lupus is attributed to 12th-century physician Rogerius, who used it to describe the classic malar rash. The neoclassical period was heralded by Móric Kaposi's recognition in 1872 of the systemic manifestations of the disease. The modern period began in 1948 with the discovery of the LE cell (the lupus erythematosus cell—a misnomer, as it occurs with other diseases as well) and is characterised by advances in our knowledge of the pathophysiology and clinical-laboratory features of the disease, as well as advances in treatment.[80]

Medical historians have theorized that people with porphyria (a disease that shares many symptoms with SLE) generated folklore stories of vampires and werewolves, due to the photosensitivity, scarring, hair growth, and porphyrin brownish-red stained teeth in severe recessive forms of porphyria (or combinations of the disorder, known as dual, homozygous, or compound heterozygous porphyrias).[80]

Useful medication for the disease was first found in 1894, when quinine was first reported as an effective therapy. Four years later, the use of salicylates in conjunction with quinine was noted to be of still greater benefit. This was the best available treatment until the middle of the twentieth century, when Hench discovered the efficacy of corticosteroids in the treatment of SLE.[80]
[edit] Notable cases

* Michael Jackson suffered from both SLE and vitiligo.[81] Diagnosed in 1986, and confirmed by his dermatologist, Dr. Arnold Klein, who presented legal documents during court depositions.
* Lady Gaga has been tested borderline positive for SLE, however she claims not to be affected by the symptoms yet. The revelations caused considerable dismay amongst her fans, leading to Gaga herself addressing the matter in an interview with Larry King,[82] saying she hopes to avoid symptoms by maintaining a healthy lifestyle.[83]
* Louisa May Alcott, American author best known for her novel Little Women, has been suggested to have had SLE.[84]
* Inday Ba (also known as N'Deaye Ba), a Swedish-born actress who died from SLE complications at age 32.[85]
* Donald Byrne, American chess player who died from SLE complications in 1976.[86]
* Caroline Dorough-Cochran, sister of Howie D. of the Backstreet Boys, died of SLE complications. He founded the Dorough Lupus Foundation in her memory.
* J Dilla (also known as Jay Dee), a hip-hop producer and beat maker who died of SLE complications in 2006.[87]
* Lauren Shuler Donner, American movie producer.[88]
* Hugh Gaitskell, British politician who died of SLE complications in 1963 aged 56.[89]
* Seal, British musician (discoid lupus)
* Sophie Howard, British glamour model[90]
* Teddi King, American singer, died of SLE complications in 1977.[91]
* Charles Kuralt, former anchor of CBS Sunday Morning, died of SLE complications in 1997.[92]
* Ferdinand Marcos, former Philippine president, died of SLE complications in 1989.[93]
* Mary Elizabeth McDonough, American actress; blames her SLE on leaky silicone breast implants.[94]
* Flannery O'Connor, American fiction writer who died of SLE complications in 1964.[95]
* Elaine Paige, British actress and singer[96]
* Tim Raines, former major league baseball player[97]
* Mercedes Scelba-Shorte, America's Next Top Model Season Two runner-up and model.[98]
* Ray Walston, character actor who died of SLE complications in 2001 after a six-year battle with the disease.[99]
* Michael Wayne, Hollywood director, and producer, part owner of Batjac Productions, son of legendary actor John Wayne, died of heart failure resulting from SLE complications in 2003.[100]
* Kéllé Bryan, member of 90s British pop group Eternal, became ill with lupus in 1999.[101]
* Toni Braxton, American R&B singer, songwriter and actress.[102]


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