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Multiple Myeloma

2009-01-18T10:50:00.000-08:00

What is Multiple Myeloma

Multiple myeloma is a cancer of plasma cells in the bone marrow.

Normally, plasma cells form part of the immune system. They produce immunoglobulins (antibodies) which help fight infection. In multiple myeloma, abnormal plasma cells in the bone marrow multiply too fast. They take up too much space in the bone marrow and prevent the normal production of other blood cells, such as red and white blood cells. The plasma cells of multiple myeloma also produce large quantities of abnormal immunoglobulins, which cannot fight infection and which can cause damage to the kidneys.

The type of abnormal protein (called paraprotein) produced may be of any of the immunoglobulin types. (Immunoglobulins are specifically shaped antibodies made of protein.) The commonest are IgG (50%) and IgA (20%) with 20% also being of the "light chain" (part of the antibody) type. The rest are made up of a mixture of IgM, IgD and IgE myeloma while only 1 in 10 000 are non-secretory (i.e. has malignant cells in the bone marrow which do not produce any protein).

Who gets Multiple Myeloma?

Worldwide, the incidence of multiple myeloma is approximately 4 cases per every 100,000 people. In Australia, approximately 1200 new patients are diagnosed with multiple myeloma every year.

Multiple myeloma affects men more commonly than women. It is generally a disease of the elderly, with most patients being diagnosed at around 60 years of age. Multiple myeloma is rare before the age of 40.

Multiple myeloma is found more commonly in black African populations, and only rarely in Asian populations.

Predisposing Factors

There are a number of associations with multiple myeloma. Most of these are observed, rather than explained.

Occupations which may be associated with a higher risk of multiple myeloma include:

* Farming
* Woodworking
* Leather working
* Any occupation involving exposure to petroleum products.

In addition, exposure to high levels of ionising radiation may predispose to the development of multiple myeloma.

One factor which has been associated with a definite increase in risk of multiple myeloma is the presence of monoclonal gammopathy of undetermined significance (MGUS) in the blood. This is a condition which is seen in approximately 3-5% of people over 80 years of age. It is normally benign (not cancerous), but the presence of MGUS carries an annual 1-1.5% risk of developing active myeloma.

Progression

There are three major features of multiple myeloma:

* Bone destruction: the expansion of the abnormal plasma cells in the bone marrow causes destruction of normal bone. This causes bone pain, and may lead to fractures where the bone has been weakened.
* Bone marrow infiltration: the bone marrow is infiltrated by plasma cells. This means that normal blood cells cannot be produced, leading to low levels of red blood cells (anaemia), white blood cells (neutropaenia) and platelets (thrombocytopenia). Patients with multiple myeloma are at increased risk of developing infections, partly due to their impaired white cell production.
* Kidney impairment: the kidneys may be damaged in multiple myeloma in a number of ways. Bone destruction by plasma cells leads to increased levels of calcium in the blood (hypercalcemia), which is harmful to the kidneys. In addition, the abnormal immunoglobulins produced by the plasma cells can be deposited in the kidney tubules and cause damage. Overall, kidney failure occurs in approximately one quarter of multiple myeloma patients.

Tumour spread in multiple myeloma is usually confined to the bones and bone marrow only. Rarely, the tumour may spread to the spleen, lymph nodes, or other organs.

Probable Outcomes

There are a number of features which have been identified as being associated with a poor prognosis in multiple myeloma:

* Older age at diagnosis
* Poor performance status.
* Anaemia or low platelet count at presentation.
* Renal failure.
* Raised B2-microglobulin.

Overall, approximately 15% of patients will die within 3 months of diagnosis, with a subsequent death rate of 15% per year. Causes of death include progression of myeloma, renal failure, or sepsis (overwhelming infection). With treatment, the average survival is approximately 5 years. One in ten patients will have a very slow (indolent) course, with only gradual progression of disease.

How Will Multiple Myeloma Affect Me?

Common symptoms of multiple myeloma include:

* Bone pain
* Symptoms of anaemia, such as fatigue or dizziness
* Recurrent infections
* Symptoms of hypercalcemia (excess calcium in the blood), such as nausea, vomiting, constipation or confusion
* Symptoms of renal failure, such as fatigue, weakness, breathlessness or ankle swelling.

Some patients have no symptoms, and are diagnosed incidentally on routine blood tests.

How is Multiple Myeloma Diagnosed?

For the diagnosis of multiple myeloma to be made, 2 out of the following 3 criteria have to be met:

1. Monoclonal immunoglobulin in the blood and/or urine. (An abnormal single protein produced by abnormal plasma cells. The protein is of the type which in normal circumstances would be an antibody).
2. Infiltration of bone marrow by malignant plasma cells.
3. Osteolytic bone lesion (holes eroded in bone by the malignant cells).

Blood tests:

* Full blood picture: haemoglobin, white cell count and platelet counts are normal to low.
* ESR / CRP: raised.
* Urea and electrolytes: may show evidence of kidney impairment.
* Calcium: normal or raised.
* Uric acid: normal or raised.
* Serum B2 microglobulin, serum LDH: these may be useful when predicting the course of disease (prognosis).
* Total protein: normal or raised. Serum albumin will be normal or low.
* Serum protein electrophoresis: a monoclonal band is usually seen.

Imaging investigations:

* A skeletal survey is required for baseline evaluation. Additional x-ray imaging of specific areas of concern, such as ribs, may be helpful.
* CT: to investigate areas of concern, particularly if radiotherapy or surgery is being considered.
* MRI: this may be used to assess disease bulk, or if spinal cord compression is suspected.

A bone marrow biopsy may also be necessary.

How is Multiple Myeloma treated?

Treatment depends upon the stage and form of myeloma, but most people require both systemic chemotherapy and supportive symptomatic care.

Chemotherapy

The standard treatment chemotherapeutic regime for multiple myeloma includes an alkylating agent (melphalan, cyclophosphamide or chlorambucil) and prednisone administered for 4 to 7 days every 4 to 6 weeks. This is continued for one to two years.

While around 50% of patients respond well to this treatment, relapse of disease usually occurs within a year of stopping treatment.

In patients under 65 years who are otherwise healthy, autologous bone marrow transplant is a standard treatment option. This involves 3-6 months of 'induction' chemotherapy, designed to reduce the number of myeloma cells in the body, and remove myeloma cells from the blood. Healthy bone marrow stem cells are then 'harvested' from the patient's blood, before intensive high-dose chemotherapy is given to kill any remaining cancer cells. The patient's own harvested stem cells are then returned to the patient to 'rescue' the depleted bone marrow.

Newly developed drugs offer alternative treatment options, particularly for patients with relapsed refractory disease. Bortezomib is a new type of drug which is able to kill myeloma cells which are resistant to dexamethasone, alkylating agents, and anthracycline. When used alone in the treatment of refractory disease, bortezomib has a response rate of approximately 30%; when combined with dexamethasone, the response rate is 60-70%.

Thalidomide is an older drug which has found a new role in the treatment of multiple myeloma. When combined with dexamethasone in treating refractory myeloma, thalidomide has a response rate of 26-48%. With chemotherapy, the response rate is higher, at 44-86%.

Supportive care

Supportive care includes treatment of anaemia, pathological bone fractures, bone pain (eg. by radiation therapy), strengthening the skeleton (vitamin D, calcium and fluorides), treatment of electrolyte disturbances and antibiotics to prevent infections. Information on other types of leukaemia:

* Chronic Myeloid Leukaemia
* Promyelocytic leukaemia
* Myelodysplastic syndrome
* Chronic lymphocytic leukaemia
* Acute lymphoblastic leukaemia
* Acute myeloid leukaemia

Multiple Myeloma References

1. Braunwald, Fauci, Kasper, Hauser, Longo, Jameson. Harrison's Principles of Internal Medicine. 16th Edition. McGraw-Hill. 2001
2. Cotran RS, Kumar V, Collins T. Robbins Pathological Basis of Disease Sixth Ed. WB Saunders Company 1999.
3. Durie BGM et al. Myeloma management guidelines: a consensus report from the Scientific Advisors of the International Myeloma Foundation. Hematology Journal 2003; 4(6): 379-98.
4. Joshua DE. Multiple myeloma: the present and the future. MJA 2005; 183(7): 344.
5. Kumar P, Clark M. Clinical Medicine. WB Saunders 2002.
6. Sirohi B, Poles R. Multiple myeloma. Lancet. 2004. 363: 875-87.

Regimens Used in the Treatment of This Disease:

* Carmustine
* Interferon
* Melphalan + Prednisolone

Symptoms of This Disease:

* Hypercalcaemia

Treatments Used in This Disease:

* Bone Marrow Transplant
* Blood Transfusion

Drugs/Products Used in the Treatment of This Disease:

* Vincristine sulfate injection
(Vincristine sulfate)

* Vincristine Sulfate Injection (DBL)
(Vincristine sulfate)

* Alkeran
(Melphalan)

* Alkeran Injection
(Melphalan)

* Aredia
(Disodium pamidronate)

* Bonefos
(Sodium clodronate)

* Cycloblastin
(Cyclophosphamide)

* Endoxan
(Cyclophosphamide)

* Pamisol
(Disodium pamidronate)

* Thalidomide Pharmion
(Thalidomide)

* Velcade
(Bortezomib)

* Zometa
(Zoledronic acid)

Chronic Myeloid Leukaemia

2009-01-18T09:51:00.000-08:00

What is Chronic Myeloid Leukaemia

Chronic Myeloid Leukaemia usually arises from the precursors of myeloid cells which would subsequently, in normal circumstances, evolve into normal white cells.

Bone marrow is found inside most of the bones in the body. By adulthood, a large proportion of bone marrow has become relatively inactive. Generally speaking, it is the marrow inside the vertebra, ribs and pelvis, which is responsible for producing the blood cells in adults. In times of crisis or when these areas of bone marrow are damaged, marrow activity may switch on in the other bones.

The bone marrow is a collection of cells inside a connective tissue and fatty stroma. It is necessary to understand the different types of cell found within the bone marrow.

Stem cells are the ultimate origin of the other cells. Stem cells differentiate to form 3 main types of 'progenitor' cells. Each of these cells is then responsible to produce red cells, white cells and megakaryocytes (which produce platelets).

There are a number of proteins, which stimulate production of blood cells. These include erythropoietin, (EPO) granulocyte-macrophage colony stimulating factor (GM-CSF), granulocyte-CSF (G-CSF), Interleukin 3, 5 and 6 (IL-3, IL-5, IL-6). Generally speaking, these proteins interact with receptors on the surface of the primitive bone marrow cells and stimulate them to produce the adult cells.

Who gets Chronic Myeloid Leukaemia?

It is relatively uncommon and occurs in approximately 1 in 100,000 people, rarely affecting those below the age of 20 and usually occurring in the 40-50 year age group, with sex incidence being slightly more common in males.

Geographically, the tumour is found worldwide.

Predisposing Factors

The characteristic feature of CML is the presence of certain genetic translocation in affected stem cells in the bone marrow - the translocation between chromosomes 9 and 22 (9;22)(q34;q11) - the so called Philadelphia chromosome. This translocation is believed to be the cause of the unchecked proliferation of the stem cells, with further chromosomal transformations important for further progression of the disease.

The only real predisposing factor for this type of leukaemia is exposure to high doses of radiation such as that caused by nuclear accidents. Most cases occur with no obvious cause. Cigarette smoking has been shown to accelerate the progression to blast crisis.

Progression

This type of tumour spreads by expansion within the marrow space and the marrow of the bones in the body.

Probable Outcomes

Chronic myeloid leukaemia can be quite variable in terms of its natural history. The relatively stable chronic phase of this leukaemia averages approximately 4 years. Having said that, some patients have had prolonged chronic phases of more than 15 years, although this is much less common.

Following the chronic phase, an accelerated phase, sometimes called transformation can occur, with the development of a rapidly increasing number of blasts in the peripheral circulation. Once this occurs, survival is normally between 2 and 6 months.

How is Chronic Myeloid Leukaemia Diagnosed?

General investigations may show anaemia or low platelet count. The peripheral white blood cell count can vary between 50-200 x 10/9 per litre. The peripheral blast count is less than 10% in the chronic phase.

How is Chronic Myeloid Leukaemia treated?

The exact treatment given can depend upon the initial white cell count. Initial treatment may be with single agent chemotherapy such as Hydroxyurea or Busulphan.

Younger patients with the disease may be suitable for bone marrow transplantation.

There are a number of newer targeted biological therapies which are showing promise for the treatment of chronic myeloid leukaemia. Interferon can be used and has a reasonable response rate. Specific tyrosine kinase inhibitors can also have an excellent result .

Improvement in symptoms is an important measurement. Specific monitoring may be by measurement of the peripheral white blood cell count. If transformation is thought to have taken place, the peripheral blast count will rise to greater than 15% of the circulating white cell count and bone marrow examination can confirm the presence of a large number of blasts.

The symptoms that may require attention are infection, bleeding and anaemia.

Anaemia may be treated with blood transfusion. Patients may require platelet transfusions. Bacterial infections due to low neutrophil counts usually require urgent treatment with intravenous antibiotics. Care should also be taken to treat more unusual infections such as candida (thrush) in the mouth.

Particularly during chemotherapy, the destruction of the leukaemic cells can produce large amounts of uric acid and prophylactic treatment with Allopurinol is mandatory.

Pain from massive enlargement of the spleen can cause visceral pain and if infarction of the spleen occurs and the peritoneum becomes irritated, somatic pain can also ensue.
Information on other types of leukaemia:

* Promyelocytic leukaemia
* Multiple myeloma
* Myelodysplastic syndrome
* Chronic cymphocytic leukaemia
* Acute lymphoblastic leukaemia
* Acute myeloid leukaemia

Regimens Used in the Treatment of This Disease:

* Interferon
* Mitozantrone

Treatments Used in This Disease:

* Bone Marrow Transplant
* Blood Transfusion

Drugs/Products Used in the Treatment of This Disease:

* Euhypnos
(Temazepam)

* Glivec
(Imatinib mesylate)

* Navelbine
(Vinorelbine tartrate)

* Quadramet
(Samarium-153 Ethylenediaminetetramethylene Phosphate (EDTMP))

* Sprycel
(Dasatinib)

Take a Pregnancy Test to Find Out if You're Pregnant!

2008-08-31T06:54:00.000-07:00

If you miss a period and want to quickly check if you are pregnant, before you visit your doctor, try the home pregnancy test. This is is especially convenient for women who are trying to get pregnant. After all, you do not want to go rushing to a doctor each time you experience some telltale sign of pregnancy but are not sure you are pregnant.

When should I take a pregnancy test?
Most women take a home pregnancy test (HPT) when they have a pregnancy symptom or two. For many women the first pregnancy symptom is usually a missed period. You may have other pregnancy symptoms as well. Pregnancy tests are usually good at the minimum on the first day that you miss your period. There are a few tests that are extra sensitive that can be used sooner, but may not be as reliable as if you were to wait.

How do home pregnancy tests work?:
Home pregnancy tests work by measuring the quantity of a hormone called human chorionic gonadotropin (hCG) in your urine. Once you have conceived, it will take about 10-14 days for hCG to show up in your urine.

Where can I get a home pregnancy test?
You can buy home pregnancy tests at nearly any store, including most grocery stores and major chain retailers like Target® or Wal-Mart®. Many women will also buy bulk pregnancy tests online. These tests contain less packaging, but work just as well for much less money.
How is the test performed?

Try to perform the test first thing in the morning for optimal results, though this is not mandatory.

* Pregnancy tests are usually stored in the refrigerator. So, make sure you bring the test kit to room temperature before you use it.
* Collect urine in a clean, dry glass or plastic container. Ensure that there is no detergent residue in the container.
* Take out the pregcolor card (see image below) and place it on a flat surface.
* Draw out a little urine with a dropper (provided with the kit) and put just two drops in the circular test well that is usually marked 'S'. Do not spill urine on the reading strip.
* Wait for three to five minutes (depending on manufacturer's instructions) and then read the test results. Trying to read the results before the stipulated time or waiting too long, can both lead to inaccurate readings.
Some newly launched pregnancy test kits (for example, Clearview) can be held directly in the urine stream and do not require you to collect urine in a container. These kits are usually more expensive (around Rs 150), Simple Pregnancy Tester will come in 50 Rs .

How do I interpret the results?

1. Look at the regions marked 'C' and 'T' on the test card. 'C' indicates a control. This band must always appear because this is the comparison band. 'T' indicates the test sample.

2. If only one pink/purple band appear, in the region marked 'C', it means that the test is negative for pregnancy.

3. If two pink/purple bands appear, one in the region marked 'C' and the other in the region marked 'T', it means that the test is positive for pregnancy

4. In case no bands appear, then the test is invalid. Repeat the test with a new pack of pregcolor cards after 72 hours.

5. If the line formed in region 'T' is faint, this could be due to low levels of hCG hormone. In case of a faint band, repeat the test with a new pack of pregcolor cards after 72 hours.

Will the test work if I have just missed my period?

In most cases, the test is sensitive enough to detect pregnancy even on the day of the missed period. In some women though, the levels of hCG are not detectable so early in the pregnancy. If the test is negative, you might want to try and repeat it after 72 hours.
It is, in fact, advisable to wait a couple of days to a week after missing your period, before you perform the test. This will help avoid a falsely negative test.

Can the test be falsely positive?

Though very rare, this could happen. Certain drugs, especially drugs used for treatment of infertility, including hCG shots might cause the test to be falsely positive. So could an ectopic pregnancy (when the foetus is implanted in an area other than the uterus like the Fallopian tubes or the cervix), though technically it is a pregnancy.

Pain medication, oral contraceptives, antibiotics, etc, usually do not affect the test results.

What if the test is negative?

If the test is negative the first time you perform it, wait for 72 hours and repeat the test. The first negative result might be because the test was taken too early and the hormone levels had not risen enough to be detected. On the other hand, it could be because of faulty technique. Follow the instructions carefully when you repeat the test.

"If you are experiencing other symptoms of pregnancy and yet your test turns out negative twice, see your obstetrician immediately. "

What kinds of home pregnancy tests are available in the market and where do I buy them?

In addition to Clearview, the other kits available are Pregcolor Card, Pregtest Card and Veklocit. The average cost per kit is around Rs 50.

Home pregnancy tests are usually available at most chemist/medical shops.

What should I do if the test is positive?

If the test is positive do a test at your nearest lab and then visit your obstetrician to confirm the pregnancy and get further medical advice.

If you r in Trouble I can ... Help you ,you can Post the comments without hesitation ....for getting Solutions

Non - Specific Urethritis (NSU) STDs

2008-08-31T06:00:00.000-07:00

Urethritis is inflammation of the urethra (the passage in the penis that urine and semen pass through). It can be specific or non-specific caused by gonorrhoea or chlamydia respectively. NSU one of the most common STDs can be acquired through vaginal sex or, less commonly, through anal or oral sex with men or women. It can also be contracted with out sexual contact. NSU can be caused by a number of different micro-organisms, one of them is Chlamydia trachomatis which is responsible for around 50% of the infections. It is commonly found in the rectum, urethra, conjunctiva of the eye, vagina, cervix and mouth.

Symptoms
Symptoms usually appear 7-28 days after infection.

* White, clear or yellowish discharge from the penis
* Stinging or burning sensation during urination
* Itching, tingling, burning or irritation inside the penis.
* Pain or swelling in the testicles in advanced infections.

Adverse effects
If nonspecific urethritis is left untreated, it can cause complications. It can spread to the bladder which will cause pain during urinating and perhaps some bleeding. It may also spread to the testicles and cause infection or inflammation which will result in pain, swelling and tenderness of the testicles and/or rectum. If NSU spreads to the prostate there will be pain in the groin. Less commonly there may be conjunctivitis or pain and inflammation in the joints. In extreme cases it can cause pelvic inflammatory disease in women and infertility in both men and women.

Tests
A sample of the discharge is taken to detect the micro-organism present. The sample is then examined in the laboratory for signs of infection. Samples should be taken 3 or 4 hours after you last passed urine. Although NSU does not cause symptoms in women, female partners of men with NSU may need to be examined.

Treatment
The infection is treated with tetracycline or alternative antibiotics if allergies are a concern until the infection is clear. It is completely curable but symptoms can reoccur and may require further treatment.
It is better not to have sex until all results of your tests are back and you have finished taking all the tablets. Antibiotics treatment should be given to sexual partners, even if they do not show symptoms and barrier methods of contraception should be used to prevent re-infection.

Syphilis STDs

2008-08-31T05:47:00.001-07:00

Syphilis is a complex sexually transmitted disease (STD) caused by the bacterium Treponema pallidum. It is highly infectious and shows symptoms in three stages. Bacteria which enters the body through mucous membranes during sexual intercourse may be found on the penis, vagina, vulva and in the mouth or anus depending up on the site of infection. Bacteria can also be transmitted from an infected mother to her child during child birth. This infection can be effectively treated and later stages can be avoided if diagnosed early and treatment is given promptly and routinely.

Symptoms
In the first stage, an infection causes an ulcer at the site of infection; with in a short time the Lymph nodes around the infection and then all over the body enlarges and harden. The ulcer can appear within 10 days to three months after exposure, but it generally appears within two to six week and these symptoms persists for several weeks. If adequate treatment is not administered, the infection progresses to the secondary stage.
Secondary symptoms appear about two months after initial infection and may overlap with the first stage; these include fever, pains, enlarged lymph nodes and a rash usually found on the chest, on the palms of the hands and on the bottoms of the feet. The rash often appears as rough, red or reddish brown spots. In addition symptoms may include sore throat, patchy hair loss, headaches, weight loss, muscle aches, and tiredness. An infected person who has not been treated can easily infect sexual partners during the first two stages, which usually last one to two years. In the second stage infection can also spread through the broken skin of an infected sore by any physical contact either sexual or non-sexual.

The third and final stage may not appear until many months or years after infection, in untreated people. It comprises the infection of numerous tumour-like masses throughout the body in skin, muscle, bone, brain, spinal cord and the other organ such as the liver, stomach etc.

In infected infants, symptoms may include skin sores, rashes, fever, weakened or hoarse crying sounds, swollen liver and spleen, yellowish skin (jaundice), anemia, and various deformities.

Adverse effects
Syphilis increases the risk of transmitting and acquiring the human immunodeficiency virus (HIV) that causes AIDS. The third stage can cause serious damage to the heart, brain or spinal cord resulting in blindness, paralysis, numbness, mental disability and even lead to death.
In addition, a pregnant woman with syphilis can pass the bacterium to her unborn child, who may be born with serious mental and physical problems as a result of this infection. Sometimes symptoms in infants go undetected and as they grow older they may develop the symptoms of late-stage syphilis including damage to their bones, teeth, eyes, ears, and brain. In pregnancy if the infection is left untreated, it can even cause still birth or neonatal death.

Test
Diagnosis is confirmed by taking a swab from the infectious sores and by examining using dark field microscopy in a lab. If syphilis bacteria are present in the sore, they will show up with a characteristic appearance. A blood test is another way of testing for syphilis. Shortly after infection, the body produces syphilis antibodies that can be detected by the blood test. As blood tests may show false results, repeated tests are sometimes necessary to confirm the diagnosis. A low level of antibodies will stay in the blood for months or years even after the disease has been successfully treated. Follow up tests are carried out to ensure success of the treatment. In the late stage of syphilis, a lumbar puncture (spinal tap) is done to check for infection of the nervous system.

Treatment
Treatment is through administration of penicillin, usually by injection, which is normally very successful. Single dose of penicillin can cure persons who has had syphilis for less than a year but larger doses may be needed for others. The treatment is successful in stopping further damage, but it will not repair any damage already done.
Persons who receive syphilis treatment must abstain from sexual contact with new partners until the syphilis sores are completely healed. Because untreated syphilis in a pregnant woman can infect and possibly kill her developing baby, every pregnant woman should have a blood test for syphilis.

Genital Herpes STDs

2008-08-31T04:56:00.000-07:00

Herpes can be caused by two types of virus. Herpes Simplex Virus I (type I) causes labial or oral which exist around the face and mouth. Symptoms may include cold sores (fever blisters) on the face and mouth or herpes sores on the eye.
Genital herpes is a very common, highly contagious and painful STD caused by the Herpes Simplex II Virus (HSV2). This infection is serious since the virus once acquired cannot be eliminated from the body. It can be spread to partners through sexual or other close contact. It is more common in women as warm, moist conditions in the genital region favour infection. Wet or damp cloth or towels could carry the virus.

Symptoms
Symptoms can be mild or severe for different people and may last for several weeks. The symptoms may occur in the upper thighs, buttocks and anus. In men they may arise in the external genitalia such as the penis, scrotum, or testicles and internally on the mucus membranes including in and around the anus. In women in genital areas such vagina, vulva etc. Symptoms include:

* Painful blisters or rashes, bumps, cuts or sores in the genital area.
* Itching, burning, or tingling in the genital area.
* Aches or pains in the genital area.
* Burning sensation or pain while urinating.
* Flu-like symptoms such as headache, fever, and swollen glands in the lymph nodes near the groin.
* Numbness of the vulva.

Genital herpes usually begins with mild irritation in the genital region followed by the irruption of blisters filled with clear liquid. The blisters appear 3-20 days after infection. Gradually the blisters turn yellow, burst and discharge the liquid before crusting over and healing. The attack keeps on re-occurring every two or three months but the frequency and severity lessens with advancing age. During its dormant period the herpes virus lies inactive in the bundle of nerves at the base of the spine.

Adverse effects
Genital herpes increases the risk of cervical cancer and an infected mother can pass on the virus to the baby possibly causing brain damage and /or blindness. It will considerably affect the normal sexual life between partners.

Tests
Consult a doctor at the first signs of any kind of rash or discomfort. The tests for herpes may not give 100% accurate results.

1. The most common method of testing is a herpes culture, which is taken from a scrapping from an open sore. This scrapping is them sent to a laboratory for analysis. This method sometimes show a 'false negative' result. Even if there is actually a real herpes infection, the test fails to identify it. This can be misleading, but when a similar outbreak occurs in the exact same location at a later time you can be more assured that there is a herpes virus causing this infection.

2. Another test is an expensive blood test which include Herpes Simplex Virus (HSV) IgG ( immunoglobin) and IgM (immunoglobin) serology( blood) tests. These test check for certain levels of antibodies in the blood. The specific tests involve checking titer (amounts) levels of each immunoglobin, with each being representative of either an old infection or a relatively new infection. This test may also give false results

Treatment
There is no cure available for herpes and the disease goes through cycles of activity and dormancy. Therefore treatment is directed at relieving discomfort and preventing bacterial infection. Anti-viral drugs such Zovirax or Acyclovir may also be useful in treating herpes.
Always keep your genital areas clean to prevent infection. The virus is destroyed by heat so hot tubs are good. Prepare a hot bath 2-3 times daily with some salt added to the water. Avoid touching the sores and then rubbing your eyes or other parts of the body which are susceptible to infection. Ensure that you wash your hands immediately after touching the sores. It is best to refrain from sex when you or your partner is having an outbreak of the disease. Condoms must be used at the other times to reduce the possibility of transmitting the virus. As there is a risk of cervical cancer in women, regular cervical smear or pap smear test should be done. If an infection is diagnosed during pregnancy it is advised to avoid vaginal delivery as the virus can be passed to the baby.

Gonorrhea STDs

2008-08-31T04:41:00.000-07:00

Gonorrhea, is a common STD caused by the bacteria Neisseria gonorrhoeae. It is found in the mucous membranes of the vagina, urethra, throat, mouth and anus. The bacteria grows and multiples in the warm moist areas of the body. Gonorrhea is primarily spread through sexual contact (vaginal, oral, or anal). Ejaculation does not have to occur for gonorrhea to be transmitted or acquired. Gonorrhea can also spread through contact with infected discharge on clothing, towels, sheets etc. and from mother to child during birth. This infection is treatable and curable if detected early.

Symptoms
The early symptoms of gonorrhea are often mild, and many women who are infected have no symptoms of infection. Symptoms develop about 1-2 weeks after infection and they are:-

In Men

* A pain or burning sensation when urinating.
* A yellowish white discharge or pus from the penis.
* Painful or swollen testicles.
* Painful sore throat.
* Pus containing discharge from the anus with pain and inflammation of the rectum.

In Women

* Vaginal discharge green or yellow green in colour.
* Pain or burning sensation when urinating
* Inflammation of the rectum causing discharge, anal itching, painful bowel movements and bleeding.
* Sore throat in case of oral sex

Adverse effects
Untreated gonorrhea can cause serious and permanent problems in both women and men.
Women with no or mild gonorrhea symptoms are still at risk of developing serious complications from the infection. Untreated gonorrhea in women can develop into pelvic inflammatory disease (PID) in which the fallopian tube may be damaged leading to infertility and increase the risk of future ectopic (tubal) pregnancy. Oral sex can result in infection and inflammation of the throat and anal sex in the infection or inflammation of rectal tissues. Gonorrhea can spread to near by organs and glands especially the prostate and testes in men affecting fertility. Further complications in untreated gonorrhea are inflammation of the joints, heart valves, eyes (conjunctivitis) and septicaemia (blood poisoning). In pregnancy, gonorrhea can cause miscarriage or tubal infection in the early months. From an infected mother, an infant can get gonorrhea causing blindness at birth.

Tests
Several laboratory tests are available to diagnose gonorrhea. A sample of fluid from the infected mucus membrane (cervix, urethra, rectum, or throat) is taken and send to the laboratory for analysis. Pelvic examination may be carried out to ascertain if there is other damages. Gonorrhea that is present in the male or female genital tract can be diagnosed in a laboratory by using a urine specimen from an infected person. A quick laboratory test for gonorrhea that can be done in the clinic or doctor’s office is a Gram stain. The Gram stain allows the doctor to see the gonorrhea bacteria under a microscope. This test works better for men than for women. Persons with gonorrhea should also be screened for other STDs like syphilis.

Treatments
Treatment with antibiotics is effective against gonorrhea. One very large dose of Penicillin or tetracycline are commonly used, however some strains of gonorrhea have developed resistance to these treatments and other drugs such as ceftriaxone or spectinomycin may also be used. Often Chlamydia and gonorrhea occur simultaneously and are treated together.

It is important to take the complete course of medication prescribed to cure gonorrhea, even if the symptoms or signs stop, before all the medication is over. Although medication will stop the infection, it will not repair any permanent damage done by the disease.
Individuals who have had gonorrhea and received treatment may get infected again if they have sexual contact with persons infected with gonorrhea. Follow up tests are carried out weekly for a month to ensure that the disease has been eradicated and all sexual contacts should be avoided until this is confirmed.

Genital Warts STDs

2008-08-23T01:55:00.000-07:00

Genital warts is a common STD caused by Human Papilloma Virus. They occur as small pinkish-red irregular lumps either singly or in clusters. Both men and women mostly in the age group of 15 to 40 are equally susceptible for infection. The vulva and the perineum (area between the vaginal opening and the anus) are the areas most affected in women. They also appear on the vagina, cervix and anus. In men, the warts most often appear on the glans, foreskin and urethral opening. They may also appear on the shaft of the penis, scrotum and anus. Genital warts are extremely contagious. The disease is spread by intimate sexual contact: vaginal, oral, and anal sex. The virus is also easily transmitted when the skin or mucous membrane is already injured. People with weak immune systems will have more widespread infections.

Symptoms
The warts appear between one and six months after infection. Symptoms may be slow to appear and are usually painless and if internal they may cause very few symptoms other than slight itching and mild irritation. Symptoms may include discomfort and pain, to bleeding and difficulty in urination (if they occur in the urethra, penis or vagina) and difficulty in swallowing (if they appear in the mouth or throat). HPV can easily be spread unknowingly by infected people.

Adverse effects
Untreated genital warts can eventually spread, grow, and multiply into large clusters. These may cause a variety of health complications depending on where they are located. Genital warts are also closely associated with cancer of the cervix, anus, penis, scrotum, and vagina. Infected pregnant women can pass them on to their newborns, causing many potentially serious health problems for the infant.

Tests
External warts are usually diagnosed visually. Internally, particularly in women, the urologist or gynecologist will apply a solution of acetic acid (vinegar) to areas where he or she suspects an infection, causing the warts to whiten and making identification easier. A magnifying instrument called a colposcope may be used to diagnose warts in the vagina or on the cervix. A tissue biopsy or Pap smear may be taken to determine if the warts are cancerous. Both infected women and their sex partners should be tested for warts. Female sexual partner of a man with genital warts requires an annual cervical smear test.

Treatment
Often these warts will disappear without any treatment. There are a wide variety of treatments available for genital wars such as trichloroecetic acid or podophyllin solution which kills the virus. These treatments are applied directly to the infected region and are washed off several hours later. There is a topical cream Aldara for application or interferon which can be directly injected, which is used as a treatment for warts. The warts themselves may require surgical removal by laser, cauterisation, cryotherapy (freezing off external warts with liquid nitrogen) or conventional surgery. These treatments are effective in eliminating the warts but the virus remains. Consequently warts may appear after treatment.

Crabs (Pediculosis Pubis)

2008-08-23T01:39:00.000-07:00

Peduculosis Pubis or crabs are insect parasites seen in pubic and other hairy parts of the body. Crab lice are small, light brown, flat insects that can be transmitted by infected clothing, bedding, toilet seats or by sexual contact. They feed on blood and lay numerous eggs throughout their 30 day lifespan. The most common symptom is severe itching in the genital region. These 'crabs' bite their host which results in the appearance of bluish spots in the genital area.
The usual means of diagnosis is a report of infestation by the victim or clinical observation of the symptoms. Doctors or other healthcare practitioners may perform a microscopic examination of the lice and/or nits for diagnosis confirmation.

Treatment
Pediculicide, a mild insecticidal shampoo or insecticidal cream such as Malathion are the most common treatment for pubic lice. Generally this treatment is quite effective. Eyelash infestations are treated with white petroleum jelly ointment for 10 days. Nits and parasites in the lashes of children can also be tweezed out carefully by a doctor. Pregnant women should not be treated with lindane, but with Rid, a liquid pediculicide, which kills both lice and eggs.

Clothes and bedding should be laundered thoroughly in boiling water or dry cleaned. Items that are inconvenient to clean, such as large quilts or blankets, can be stored away from other clothing and bedding for a month; without blood, the lice and any nits that hatch will die during this time.

Anyone who has had sexual contact with an infected person should be treated. Other household members may require treatment if symptoms emerge. Patients are advised to abstain from sexual contact for 48 hours after treatment. A follow-up examination is recommended after one week to determine if any live nits remain.

Chlamydia ( STDs)

2008-08-23T01:34:00.000-07:00

Chlamydia is a very common STD, caused by the bacteria 'chlamydia trachomatis'. The bacteria lives in the mouth, eyes, liver, lungs, throat and urinary tract etc. and primarily affects the urethra in men and the cervix or neck of the womb in women. The disease is particularly common among young people between 15 and 25 years and is highly infectious and easily transferred from person to person.

Chlamydia is primarily transmitted through sexual intercourse. Using contraceptives such as condoms or diaphragms help to prevent infection. It effects both hetero sexual and Homosexual men. Women with multiple sexual partners those taking oral contraceptive pill may be at increased risk of infection. Mothers with chlamydia can infect their children during delivery.

Symptoms :
Chlamydia is a particularly dangerous disease because there are many infected individuals who experience no symptoms. Symptoms may include:

In men

1. Painful urination, due to inflammation of the urethra. This can be quite a mild symptom and may only last for a few days so can be easily missed.
2. Watery or milky discharge from the urethra.
3. Pain or tenderness in the testicles.

In women
1. Frequent and painful urination.
2. Unusual vaginal discharge.
3. Pain in the lower abdomen due to inflammation of the Fallopian tubes.
4. Pain during sex.
5. Bleeding between periods (in some cases, which indicate that the infection has spread to the uterus.)
6. In infants, there are usually no symptoms at birth, but later may result in Pneumonia when the baby is 2-3 weeks old.

Adverse effects Chlamydia not detected and left untreated can lead to serious complications. Advanced chlamydia can cause infection of the appendix, heart and liver. In women, it can cause pelvic inflammatory disease in which the fallopian tube may be damaged leading to infertility and may cause Ectopic Pregnancy. It can also cause eye infections. In addition, men risk an infection of the epididymis which may cause infertility.

Test Testing is quick and effective. One of the most common ways of testing for Chlamydia is to collect a cell sample from the infected area (cervix or penis) with a cotton swab, which is sent to a laboratory for evaluation and results.

Treatment
Chlamydia can be cleared with a range of antibiotics taken for 1-3 weeks. All sexual partners must be screened and treated to prevent re-infection. Pregnant women may be treated with erythromycin. They should have follow up tests done if they have failed or forgot to take the pills or had unprotected sex during treatment.

AIDS

2008-08-23T01:16:00.000-07:00

AIDS( Acquired Immune Deficiency Syndrome) is a condition linked to HIV, the Human Immunodeficiency Virus that affects the natural functioning of the body's immune system. It attacks the 'T-cells' which are vital for the body's ability to fight off disease. The virus is found in blood and body fluids such as semen and vaginal secretions. The virus is transmitted mainly by sexual intercourse but can also be passed on when secretions containing HIV is transferred to a body of a non-infected person. One should check for HIV when he/she has contracted one of several diseases indicating a significant breakdown in the immune system.

Symptoms
Symptoms of HIV infection may develop from three weeks to three months after the infection. Thus it is impossible to ever truly know if a partner is infected or not. Infection may initially cause symptoms such as high fever, fatigue, night sweats and swollen glands, dry cough unrelated to smoking or flu, persistent diarrhea or bloody stools, weight loss, fungal infections, vomiting etc. The symptoms vary greatly from person to person. In later stages, further serious infections such as Herpes, Meningitis, Pneumonia and Cancers occur.

Tests
The only reliable way to determine whether or not you are infected with HIV is to have a blood test for HIV done. If you have HIV antibodies in your blood, it means that you have an HIV infection or you are HIV-Positive. Sometimes a person can be an asymptomatic carrier of the virus. They may have the virus but show no symptoms and remain well but eventually after a long period say 8-10 years they succumb to the dieease

How the virus is transmitted

The virus can be transmitted by:-
1. Having sex with an infected person.
2. Sharing a needle i.e. shooting drugs with someone who's infected.
3. Being born when the mother is infected, or drinking the breast milk of an infected woman.
4. Getting a transfusion of infected blood or through contact of blood.

All these can increase the chances of infection. Infection cannot be transmitted by shaking hands, hugging or sharing a toilet seat or towel with an infected person. Sexually active man can minimize the risk of contracting HIV by avoiding numerous casual relationship and always practicing safe sex.

Treatment
There is no effective vaccine against Human Immunodeficiency Virus and hence no complete cure for the disease. Intense research is going on to restore the immune system to normalcy in HIV patients and to find and effective vaccine. Asymptomatic carriers may be treated with anti-retroviral therapy to delay the onset and lessen the impact of HIV infections. Drugs used include Zidovudine ( ZDU) and Dideoxyinosine (DDI) but both have a range of toxic side effects. Other treatment is for the infections and cancers that may arise due to HIV which improve the quality of life of AIDS victims.

Sexually Transmitted Diseases (STDs)

2008-08-23T00:55:00.000-07:00

Sexually transmitted diseases, or STDs, are infections that can be transferred from one person to another through sexual contact and also by contact with infected blood or secretions. Most STDs are curable if diagnosed and treated in their early stages, but some of them are very dangerous that they can even cause death. Some can also lead to related conditions such as pelvic inflammatory disease, cervical cancer, and complications in pregnancy. Most STDs can be avoided by practicing safe sex by limiting your partners, using condoms etc.

Some Snaps Of STDs

AIDS Chlamydia
Crabs Genital Warts
Gonorrhea Genital Herpes
Syphilis Non-Specific Urethritis

Publish Post

Sexually transmitted diseases,pregnancy,cancer,yoga,

Frequent urination

2008-08-23T00:47:00.000-07:00

Why do I have to go to the loo so often?

Frequent trips to the toilet are a hallmark of pregnancy. Having to pee a lot is especially common during the first and last trimester. In fact, it's one of the usual early signs of pregnancy, part of all the hormonal changes your body goes through. Later on, your growing uterus shrinks your bladder's capacity just as you are producing more urine. Even when your bladder is empty, the pressure on it can make it feel full. Also, pregnant women sometimes have trouble emptying their bladder completely, another reason for the extra pit stops.

Any hints on how to spend less time on the loo?

Not really. You can try drinking almost nothing for the hour or two before bedtime to cut down on night-time trips. (But keep drinking at least 8 to 10 glasses of water during the day.) Even that may not work, though. One mother's interpretation: "It's nature's cruel way of training you for the many nights of interrupted sleep once your baby arrives!"

When does it signal a potential problem?

Talk to your doctor if you feel pain or burning when you urinate - or a sense of urgency while being able to produce only a few drops at a time. You may have a urinary tract infection and, if this is left untreated, it can lead to a kidney infection, which in turn increases your risk of

When will it stop?

You can expect all this to die down soon after your baby's born. For the first few days postnatal, you'll urinate greater quantities and even more often as your body gets rid of the extra fluid you retained during pregnancy. But after a few days, your need to urinate will be back to what it was before you were pregnant.

'Do-it-yourself abortion pills' online womens Buying

2008-08-23T00:36:00.000-07:00

Women living in over 70 countries where abortion is restricted are using the Internet to buy do-it-yourself medication for abortions, according to a new research.

Women in Northern Ireland and over 70 countries with restrictions have used one of the main websites, Women on Web, the study has found.

The British Journal of Obstetrics and Gynaecology review of 400 customers found nearly 11 percent had needed a surgical procedure after taking the medication, reports BBC.

The website claims that it can help reduce the problems linked with unsafe abortions. But anti-abortion campaigners called the development of such sites "very worrying indeed".

The research into those who had used 'Women on Web' found that about 8 percent did not end up using the medication they had ordered. Almost 11 percent went on to need a surgical procedure - either because the drugs had not completed the abortion or because of excessive bleeding.

In the study, almost 200 women answered questions about their experiences 58 percent said they were just grateful to have been able to have had an abortion in this way, while 31 percent had felt stressed but found the experience acceptable.

'Women on Web' posts the drugs only to countries where abortion is heavily restricted, and to women who declare they are less than nine weeks' pregnant.

Vaginal spotting or bleeding

2008-08-22T23:49:00.000-07:00

Is spotting normal during pregnancy?
Spotting is light bleeding from the vagina similar to, but lighter than, a period. It varies in colour from red to brown. While it's not exactly normal, light bleeding or spotting during pregnancy -- particularly during the first three months -- is fairly common. Usually it turns out to be caused by something minor or "just one of those things".

What should I do if I notice spotting?
Call your doctor straightaway, even if it eventually stops within the first day. Spotting may not always indicate a serious problem, but your doctor will be able to assess if it is a sign of some other underlying problem or complication. You'll probably need an examination or an ultrasound scan to rule out any complications and to make sure you and your baby are fine.

Be specific about your symptoms. Do tell your doctor:
• if the discharge was light pink, brown or bright red.
• if the flow was light, heavy or accompanied by clots or tissue.

• if you experienced pain, dizziness, fever or chills.

• if you have had to use sanitary napkins to soak the discharge, do let your doctor know how many.

All this information provides a fairly good indication of how heavy or light the bleeding has been, and your doctor will be able to advise you accordingly.

What causes spotting?
There are many causes for spotting early in pregnancy. For instance, when the fertilised egg attaches itself to the wall of the uterus, you may experience some implantation bleeding, which is usually light and lasts a day or two.

Spotting also takes place if you have a vaginal infection (such as a yeast infection or bacterial vaginosis) or a sexually transmitted infection (such as trichomoniasis, gonorrhoea, chlamydia, or herpes).

Spotting may also be due to a somewhat irritated or inflamed cervix (you may bleed a bit after sex, an internal examination or a cervical smear, for instance). A cervical polyp, or a benign growth may also cause spotting.

But spotting can also be an early sign of miscarriage or an ectopic pregnancy, especially if accompanied by abdominal pain or cramping.

Bleeding can also signal a molar pregnancy -- a relatively rare condition in which abnormalities in the fertilised egg at conception make it impossible for the embryo to develop or survive.

First trimester bleeding may also be a sign of an underlying problem with the placenta. Research shows a link between early pregnancy bleeding and an increased risk of later complications, such as preterm delivery or placental abruption, particularly if the bleeding is heavy.

And in the third trimester bleeding or spotting can signal a condition called placenta previa, placenta abruptio (whereby the placenta separates from the uterus), or premature labour.

If you notice spotting after 37 weeks, it's most likely to be just a sign that the cervix is beginning to soften, maybe even dilate in preparation for labor, and you may observe a blood-tinged mucus discharge. You should still report any bleeding or spotting at this point to your doctor.

As scary as all this may sound, spotting is more often a harmless mystery. About 20 weeks into her first pregnancy, a BabyCenter mum discovered she was spotting. Her doctor was concerned so he suggested that she give up exercising, stop having sexual intercourse and avoid lifting heavy objects for three weeks.

After a week the spotting stopped. Her doctor never figured out why it had happened and she delivered a healthy baby boy at full-term.

What pregnant women crave

2008-08-22T23:25:00.000-07:00

If you guessed pickles and ice cream, you're only half right!

What do pregnant women crave? A survey on our sister site in America showed that if today's dear husband were rushing out to the shops to satisfy his pregnant wife's middle-of-the-night urges, he'd probably bring back ice cream - without the pickles. When women were asked what they longed to eat while pregnant, most of them (almost 40 per cent) said 'something sweet'. Slightly fewer (33 per cent) opted for salty snacks. Fans of spicy food came in third (17 per cent). Trailing behind (at 10 per cent) were those who craved citrus fruit, green apples and other lip-puckering tart or sour foods.

Pickled onions, anyone?

The yearning for a particular type of food is an undeniable part of carrying a baby; about 85 per cent of women report at least one food craving during pregnancy. And not all of these cravings can be neatly catalogued -- or stomached. American readers confessed to wanting pickles wrapped in cheese, salsa spooned straight out of the jar and yes, even steak fat. And where in the spectrum of sweet, salty, spicy, and sour does one woman's passion for black olives on Sara Lee cheesecake lie? One user told us she ate a steady diet of pickled onions, which she can't bear the sight of, now that her baby's arrived. Aubergine, particularly on pizza, was another reader's obsession.

Many of these cravings seem to come out of nowhere, with a ferocity that is overpowering. "Over the entire ninth month period," one new mum said, "I had a real, all-out craving for peaches. I couldn't get enough of them, up to five pounds a day!"

Where do cravings come from? The extreme hormonal changes women go through during pregnancy can have a powerful impact on taste and smell. (This would help explain why women going through menopause can also experience strong food cravings and aversions.) But the bottom line is that no one really knows for sure. Some experts are sceptical that food cravings can be attributed simply to hormones.

What could a longing for cigarette butts mean?

As to what a particular craving signifies, the answer depends on whom you ask. Some nutritionists and healthcare practitioners believe that certain cravings may be meaningful. For example, cravings for ice and bizarre substances such as laundry starch and cigarette butts have been linked to an iron deficiency (even though none of these items contain significant amounts of iron). In fact, a number of US readers reported consuming large quantities of ice during their pregnancies, a craving they had never had before.

Some alternative medicine practitioners believe that a craving for chocolate may be triggered by a shortage of B vitamins. Some women may need more essential fatty acids in their diet; when they start taking flax oil, their food cravings disappear. Similarly, a craving for red meat seems like a transparent cry for protein. And the reader who consumed great quantities of peaches may have been responding to her body's need for beta carotene.

Still, the link between what your body needs and what you crave seems weak. If it were strong we would all be craving broccoli and fresh fruit, rather than the chocolate and crisps most of us desire occasionally.

It's possible that what you really need is a hug

In the end, the experts our sister site consulted agreed that you should pay attention to your pregnancy cravings -- but not necessarily give in to them. Usually a healthy diet can meet all our nutritional needs but some experts think food also satisfies an emotional need. If we are not feeling emotionally fulfilled, maybe we need a hug rather than a hamburger.

Other ways to curb unhealthy cravings? Eat breakfast every day (skipping breakfast can make cravings worse), get plenty of exercise and make sure you have a wide ranging and healthy diet.

Top 10 Signs Of Pregnancy

2008-08-22T23:08:00.000-07:00

If you're extremely tuned in to your body's rhythms, you may begin to suspect you're pregnant soon after conception. But most women won't experience any early pregnancy symptoms until the fertilised egg attaches itself to the uterine wall, several days after conception. Others may notice no signs of pregnancy for weeks and begin to wonder "Am I pregnant?" only when they miss a period. Below is a list of some of the first signs of impending motherhood. You may experience all, some, or none of these symptoms of pregnancy:

1. Food cravings. Yes, it's a cliché, but food cravings sometimes can be a sign of pregnancy. Don't rely on them as a sure symptom (it may be all in your head, or even a sign that your body is low on a particular nutrient), but if cravings are accompanied by some of the other symptoms on this list, start counting the days from your last period.

2. Darkening of your areolas. If the skin around your nipples gets darker, you may have successfully conceived, though this may also signal a hormonal imbalance unrelated to pregnancy or be a leftover effect from a previous pregnancy.

3. Implantation bleeding or cramping. 3. About eight days after ovulation, you may experience implantation spotting, a slight staining of a pink or brown colour, as well as some cramping. This is caused by the egg burrowing into the endometrial lining. You might also see some spotting around the time you expect your period.

4. Frequent urination. Once the embryo implants and begins producing the hormone human chorionic gonadotropin (hCG), you may find yourself going to the bathroom more often.

5. Fatigue. Feeling tired? No, make that exhausted. High levels of the hormone progesterone can make you feel as if you've run a marathon when all you've done is put in a day at the office. Fatigue is a hallmark of early pregnancy, though probably not a surefire symptom on its own.

6. Tender, swollen breasts. If you're pregnant, your breasts will probably become increasingly tender to the touch, similar to the way they feel before your period, only more so. Once your body grows accustomed to the hormone surge, the pain will subside.

7. Altered sense of taste. You may notice that your sense of taste changes. Some women say they have a metallic taste in their mouth, others that they cannot stand the taste of coffee, tea, or a food they usually like.

8. Morning sickness. If you're lucky, morning sickness won't hit you until a few weeks after conception. (A lucky few escape it altogether.) But as early as a couple of days following conception, you may begin feeling nauseated and queasy. And not just in the morning, either -- pregnancy-related nausea can be a problem morning, noon, or night.

9. A missed period. If you're usually pretty regular and your period is late, it's worth trying a pregnancy test. A missed period is the surest sign of pregnancy in a woman of childbearing age who usually has regular periods.

And finally...

10. A positive home pregnancy test. If you've waited to test until at least the first day of a missed period and a blue line appears in the test window, you're most likely to be in the family way. Make an appointment with your doctor to confirm the good news, and head on over to our pregnancy area. Congratulations!

Bone Marrow Cancer - II

2008-08-21T07:17:00.000-07:00

Acute Myeloid Leukaemia

What is Acute Myeloid Leukaemia

Acute Myeloid Leukaemia is a type of leukaemia which arises from the precursors of the myeloid cells which would subsequently, in normal circumstances, evolve into normal white cells. Bone marrow is found inside most of the bones in the body. By adulthood, a large proportion of bone marrow has become relatively inactive. Generally speaking, it is the marrow inside the vertebra, ribs and pelvis, which is responsible for producing the blood cells in adults. In times of crisis or when these areas of bone marrow are damaged, marrow activity may switch on in the other bones. The bone marrow is a collection of cells inside a connective tissue and fatty stroma. Stem cells are the ultimate origin of the other cells. Stem cells differentiate to form 3 main types of 'progenitor' cells. Each of these cells is then responsible to produce red cells, white cells and megakaryocytes (which produce platelets). There are a number of proteins, which stimulate production of blood cells. These include erythropoietin, (EPO) granulocyte-macrophage colony stimulating factor (GM-CSF), granulocyte-CSF (G-CSF), Interleukin 3, 5 and 6 (IL-3, IL-5, IL-6). Generally speaking, these proteins interact with receptors on the surface of the primitive bone marrow cells and stimulate them to produce the adult cells.

Who gets Acute Myeloid Leukaemia?

Acute Myeloid Leukaemia is uncommon and occurs at any time of life, with average incidence of acute myeloid leukaemia being 2.3 per 100,000 people per year. Acute Myeloid Leukaemiausually occurs (80%) in adults with the majority of cases of acute myeloid leukaemia occurring in people over the age of 60, with sex incidence being equal. However, acute myeloid leukaemia can occur in children, especially if there is a predisposition for the leukaemia.

Predisposing Factors

The cause of most cases of acute myeloid leukaemia is unknown. Acute myeloid leukaemia often occurs on the background of another haematological (blood or bone marrow) condition, such as:

Myelodysplastic syndromes.
Chronic myeloid leukaemia.
Myelofibrosis.
Polycythaemia rubra vera.
Essential thrombocythaemia.
Severe aplastic anaemia. Acute myeloid leukaemia also occurs in individuals exposed to:
Previous radiotherapy or nuclear irradiation.
Previous chemotherapy with alkylating agents or certain other chemotherapy agents and certain organic chemicals such as Benzene and Toluene. Certain individuals may inherit a predisposition to acute myeloid leukaemia such as those with Fanconi's anaemia or Down's syndrome.

Progression

The acute myeloid leukaemia tumour spreads by expansion within the marrow space and the marrow of the bones in the body.

Probable Outcomes

In acute myeloid leukaemia the most important prognostic factor is the attainment of complete remission (CR). This is defined as remission of the leukaemia (evidenced by disappearance of the blast cells) and attainment of near normal platelet and white cell levels. Being of an older age at diagnosis (older than 60) and the presence of medical problems other than the AML also influences prognosis of acute myeloid leukaemia. The duration of the complete remission (CR) and the rapidity with which it is attained are other important factors. Patients are likely to have better prognoses if the blast cells disappear early with treatment, and there is a more prolonged remission. Around 65-75% of patients achieve CR with that chemotherepeutic regime - the others don't because of a drug resistant leukaemia or fatal complications of bone marrow toxicity with the drugs. Infectious complications are the main cause of death.

How is Acute Myeloid Leukaemia Diagnosed?

General investigations (full blood count) may show anaemia (often severe). White cell counts can be low or very high, or just slightly high. More importantly, abnormal leukaemic blast cells are found in more than 95% of patients in peripheral blood. Platelet counts are usually low.

How is Acute Myeloid Leukaemia treated?

Treatment against acute myeloid leukaemia: The aim of acute myeloid leukaemia treatment is to destroy the leukaemic cells as completely as possible and achieve complete remission. Before acute myeloid leukaemia treatment, replacement of various blood components (e.g. platelets, red cells) may be required to prevent bleeding or severe anaemia. Following induction of chemotherapy, it is usual for patients to receive consolidative treatment sometimes followed by maintenance therapy. The usual induction therapy involves cytarabine and an anthracyclene (e.g. daunorubicin). The addition of etoposide or other agents does not increase the CR rate but may increase CR duration. Standard post-remission therapy includes either high dose chemotherapy or stem cell transplantation - patients receive their own stem cells collected while in remission (autologous) or another person's stem cells (allogenic) - the latter has more complications but greater success rate. In the occurrence of a relapse - certain acute myeloid leukaemia patients, notably younger patients, may benefit from stem cell transplantation (from a suitable donor if one is found). This rescues approximately 20% of relapsed patients with AML. Your Haematologist will be able to advise you as to the suitability of this acute myeloid leukaemia treatment for you.

Monitoring: Improvement in acute myeloid leukaemia symptoms is an important measurement. Specific monitoring may be by monitoring the level of blast cells in the peripheral blood. An accurate picture of what is happening in the bone marrow can be achieved by a bone marrow aspiration.

Acute myeloid leukaemia: Treatment of the Symptoms: The acute myeloid leukaemia symptoms that may require attention are infection, bleeding and anaemia. Anaemia may be treated with blood transfusion. Acute myeloid leukaemia patients may require platelet transfusions. Bacterial infections due to low neutrophil counts usually require urgent treatment with intravenous antibiotics. Care should also be taken to treat more unusual infections such as candida (thrush) in the mouth. Particularly during chemotherapy, the destruction of the leukaemic cells can produce large amounts of uric acid and prophylactic treatment with Allopurinol is mandatory. Information on other types of

leukaemia:

Acute Myeloid Leukaemia References

Braunwald, Fauci, Kasper, Hauser, Longo, Jameson. Harrison's Principles of Internal Medicine. 15th Edition. McGraw-Hill. 2001
Cotran RS, Kumar V, Collins T. Robbins Pathological Basis of Disease Sixth Ed. WB Saunders Company 1999.
Kumar P, Clark M. Clinical Medicine. Fourth Ed. WB Saunders, 1998.

Regimens Used in the Treatment of This Disease:

Treatments Used in This Disease:

Bone Marrow Transplant

Drugs/Products Used in the Treatment of This Disease:

Cytarabine (DBL)
(Cytarabine)
Etoposide Injection
(Etoposide)
Adriamycin Solution
(Doxorubicin hydrochloride)
Daunorubicin Injection
(Calcipotriol)
Glivec
(Imatinib mesylate)
Ledertrexate
(Methotrexate)
Zavedos
(Idarubicin hydrochloride)

Bone Marrow Cancer - I

2008-08-21T06:53:00.000-07:00

Myelodysplastic syndrome (MDS)

What is Myelodysplastic syndrome

Myelodysplastic syndrome (MDS) describes a group of bone marrow disorders that are characterised by a defect in stem cells. The bone marrow is the tissue located in the centre of long bones in the body and is responsible for producing most of the cells in the body. Stem cells are the precursor cells that divide and grow to produce each of the particular cell lineages. Haemopoetic stem cells produce cells in the blood of three classes- white blood cells (leukocytes), red blood cells (erythrocytes), and platelets (thrombocytes). In Myelodysplastic syndrome (MDS) the stem cells become mutant and are no longer able to divide effectively into each of the blood cells. The normal bone marrow gradually becomes replaced with the mutant cells and there is a fall in each of the different cells within the bloodstream. Patients with this disorder therefore typically have anaemia, neutropenia and thrombocytopenia (low platelets). The latter two can predispose to infection and bleeding. The abnormal cells in the bone marrow can also transform and cause syndromes also pose a risk of transformation to Acute Myeloid Leukaemia (AML).

Who gets Myelodysplastic syndrome?

The true incidence of Myelodysplastic syndrome (MDS) is difficult to estimate as it has only recently been regarded as a distinct class of disorders and controversies exist regarding its classification. However, MDS is now considered as common as Acute Myeloid Leukaemia (AML) and more cases are beginning to be recognised. MDS is most common in elderly patients as they are more prone to bone marrow damge but it can occur in any ae group. The overall incidence is thought to be around 0.5-4 cases per one million people per year.

Predisposing Factors

The risk of MDS increases with age where patients usually older than 50 years get the primary form (no known exposure) of the disorder. The second type of MDS is acquired following drug treatments or radiotherapy that damage the bone marrow. This type accounts for most cases under fifty years of age and arises 2-8 years following the damaging treatment. Certain genetic defects (such as Down syndrome), cigarette smoking, benzene exposure and DNA repair disorders can also increase your risk of this condition. Males are affected slightly more common than females in all age groups.

Progression

The mechanism of development of MDS is not known. The course of the disease is variable, but serious complications of bone marrow failure, and transformation into acute myeloblastic leukaemia commonly occur. Patients may also get infections (due to reduced neutrophils that normally fight diseases) and bleeding problems (due to reduced platelets). The therapy-related form of the disease is normally much worse and rapidly progresses to cause a fall in red blood cells, neutrophils and platelets within the bloodstream.

Probable Outcomes

The median survivial in primary (non-therapy related) MDS varies from 9 to 29 months, although some individuals in good prognostic groups live for 5 years or more. Overall, progression to AML occurs in around 30%. Other causes of death include bleeding and infection due to the reduction in platelets and neutrophils respectively. Patients with therapy-related MDS have a much worse outlook and most only survive for 4-8 months following the diagnosis.

How Will Myelodysplastic syndrome Affect Me?

The signs and symptoms of this disorder are quite non-specific and a significant proportion of patients may have no symptoms at all. These patients are sometimes diagnosed by routine blood tests for other disorders, that happen to identify abnormal or reduced numbers of certain cells in the peripheral blood. If symptoms do occur, the most common are fatigue, weakness, reduced exercise tolerance and dizziness which is caused by the underlying anaemia (reduction in oxygen carrying red blood ceels in the blood). You may also notice symptoms of infection such as fever, cough or discomfort urinating as your body is more prone to bacterial and other infections due reduced neutrophils. Reduced platelets can cause easy bruising and bleeding from the gums or nose. If you have any of the above symptoms you should talk to your doctor. They will ask you a more detailed history about your symptoms and any possible predisposing factors to the disorder (such as certain chemotherapy drugs).

Clinical Examination

Your doctor will carefully examine you and may identify several particular signs that suggest the diagnosis of MDS. Often you will appear pale due to anaemia of the doctor may detect a rapid heart rate or signs of heart failure. Signs of infection include fever, rigors, chills, sweating and increased heart rate. Your doctor will also carefully examine your skin, gums and nose for signs of bleeding. They may also take a urine or stool sample to determine the presence of blood. In addition, they will gently feel your stomach and may identify a big spleen which is associated with a particula, advanced type of the disease.

How is Myelodysplastic syndrome Diagnosed?

The most common test performed is a full blood count that shows low haemoglobin (oxygen carrying protein), low red cell count, low white cell count, high monocytes, and low platelets. These abnormalities may occur alone or in combination but later stages of disease are characterised by deficiencies in all cell types. The cells also have abnormal shapes and appearances that help the doctor make the diagnosis. In addition, a bone marrow biopsy (sample of bone marrow) is often taken to confirm the diagnosis as this can visualise the actual abnormal precursor cells.

How is Myelodysplastic syndrome treated?

Treatment of MDS largely aims to control the symptoms of the underlying cellular deficiencies and reduce progression of disease without causing severe side effects. Patients with mild disease and less than 5% blasts cells (abnormal precursors) in the bone marrow, will usually be managed conservatively with red cell and platelet transfusions and antibiotics for infections, as they are needed. Patients with more severe disease and more than 5% blast cells in the bone marrow, will require more aggressive treatment. A number of options are available, including: supportive care only, low-dose chemotherapy, intensive chemotherapy, and bone marrow transplantation. The choice of treatment will depend on your age, risk of disease and current performance status. Note that many of the treatments for MDS are fairly new and still under investigation. The mainstay of treatment for all patients is therefore to focus on prompt treatment of infection, bleeding complications and anaemia. Information on other types of leukaemia:

Myelodysplastic syndrome References

Besa E, Woermann U. Myelodysplastic Syndrome, eMedicine, Web MD, 2006. Available [online] at URL: http://www.emedicine.com/med/topic2695.htm
Cotran RS, Kumar V, Collins T. Robbins Pathological Basis of Disease, Sixth Ed. WB Saunders Company 1999. p 678.
Doll D, Landaw S. Clinical manifestations and diagnosis of the myelodysplastic syndromes, UpToDate, 2006.
Estey E, Schrier S. Treatment and prognosis of the myelodysplastic syndromes, UpToDate, 2006.
Kumar P, Clark M. Clinical Medicine. Fifth Ed. WB Saunders, 2002. p 390
Longmore, Wilkinson, Rajagopalan. Oxford Handbook of Clinical Medicine. 6th Edition. Oxford University Press. 2004.
Murtagh J. General Practice, 3rd Ed. McGraw-Hill, Australia, 2003.

Treatments Used in This Disease:

Bone Marrow Transplant

Drugs/Products Used in the Treatment of This Disease:

Vidaza
(Azacitidine)

Bone Cancer - V

2008-08-19T21:36:00.000-07:00

Metastases to the Bone :

What is Metastases to the Bone

Metastases is the term used to describe the spread of cancer from its site of origin to another location in the body. Bone is one of the most common locations in the body to which cancer metastasises. Any type of cancer can spread to the bone.The most common metastasising cancers are those of the breast, lung, kidney, thyroid and prostate.

Who gets Metastases to the Bone?

Bone metastases are common, however, its true incidence is unknown, as it is dependent on the prevalence of certain types of cancers in the community which predispose to bone metastases.

Predisposing Factors

Bone metastases are found more commonly in middle-aged to elderly people; they are uncommon in children. The major cancer types which tend to metastasize to bone include multiple myeloma, breast, prostate, lung, kidney, and thyroid cancers. However, a number of factors are involved - the probability of bone metastasis can be assessed only by knowing the prevalence of the cancer and its preference for bone in a particular ethnic group.

Progression

Bone metastases results in injury to bone tissue. There are two types of bone lesions: lytic lesions, which destroy bone material, and blastic lesions, which fill up bone with extra cells. Normal bone is in a constant state of remodelling - being broken down and rebuilt. Cancer cells that have spread to the bone disrupt this balance between the activity of cells that break down bone (osteoclasts) and cells that make bone (osteoblasts).

Bone metastases may be found anywhere in the skeleton, but generally occur in the central parts. More than 90% of all metastases are found in the back, pelvis, upper leg, ribs, upper arm, and skull. Complications of bone metastases include pain, increased risk of fracture, raised calcium levels in the blood, and a decreased blood cell count.

Probable Outcomes

Once cancer has spread to the bone, prognosis tends to be poor and treatment is generally aimed at minimising symptoms and improving quality of life. Bone metastases often have a significant impact on a patient's quality of life by causing reduced mobility and pain, and complications such as high calcium levels, bone marrow suppression and fractures.

How is Metastases to the Bone Diagnosed?

Tests which may be done if bone metastases are suspected include:

Blood tests.
ECG (if the patient has an irregular heartbeat).
X-rays.
Whole body bone scan looking for metastases.
CT scan / MRI scan to assess local disease.

How is Metastases to the Bone treated?

The goal of treatment for bone metastases is to relieve pain and reduce the risk of fracture. Treatment may consist of surgery, radiation therapy, pain medications, and/or bisphosphonate drugs.

Surgery may be required if there is immediate risk of fracture. Metal rods, plates, screws, wires, nails, or pins can be inserted to stabilise the bone at risk.
Radiation Therapy: For metastatic lesions without immediate risk of fracture, radiation is effective for reducing localised bone pain and progression of the cancer.
Medications: A groups of drugs called 'bisphosphonates' have been shown to reduce the risk of fractures caused by metastatic bone lesions, as well as treating bone pain and controlling raised calcium levels. Painkillers may be required if bone pain is interfering with the patient's quality of life.

Metastases to the Bone References

Hetzel M, et al. Reliability of symptoms to determine use of bone scans to identify bone metastases in lung cancer: prospective study. BMJ 2004;328:1051-1052
Kmietowicz Z. Patients with bone metastases need better care. BMJ 1998;317:1547
Peh W. Bone metastases. eMedicine 2002.
[available online @ http://www.emedicine.com/radio/topic88.htm]
Walling A. Effect of Bisphosphonate Therapy on Bone Metastases, Am F Phys.
[available online @ http://www.aafp.org/afp/20040301/tips/20.html]

Drugs/Products Used in the Treatment of This Disease:

Bonefos
(Sodium clodronate)
Zometa
(Zoledronic acid)

Bone Cancer - IV

2008-08-19T21:27:00.000-07:00

Bone Cancer (Chondrosarcoma of Cartilage)

What is Bone Cancer

Chondosarcoma of Cartilage is characterised by one or more tumours of the cartilage.

Cartilage is a highly specialised avascular form of connective tissue. It consists of chondrocytes and the extracellular matrix that they produce. It is solid and firm but also pliable - rendering cartilage a highly resilient tissue.

Cartilage is a key tissue in the development and maintenance of most bones in the body. During foetal development, the long bones of the body develop from cartilage models. In adults, cartilage forms the articular surface of many joints and the rings of the trachea. There are three different types of cartilage classified on the basis of the extracellular matrix: hyaline, elastic and fibrocartilage.

Who gets Bone Cancer?

This type of bone cancer is uncommon, accounting for only 20% of primary bone malignancies (0.2% of total). Chondrosarcomas are a group of tumours ranging from slow-growing non-metastasising lesions to high grade malignancies and occurs with increasing age. Peak incidence of chondrosarcoma is in the 4th to 6th decades. However, the clear cell and mesenchymal variants can occur in younger patients with sex incidence being a 2:1 male predominance.

Geographically, this bone cancer tumour is found worldwide.

Predisposing Factors

Increasing age, being of the male sex and the presence of a pre-existing enchondroma (benign tumours of hyaline cartilage occurring within the medullary cavity) - although only 10% of chondrosarcomas arise in these pre-existing lesions.

Progression

This type of bone cancer tumour spreads by direct extension into adjacent tissues with characteristic scalloping on x-rays due to the nodular growth patterns of the lesions. When metastases occur, they tend to be to the lungs and other bones.

Other sites can include regional lymph nodes (more common in mesenchymal chondrosarcoma), skin and soft tissues.

Probable Outcomes

A crucial prognostic factor in bone cancer is tumour grade. The majority of conventional chondrosarcomas tend to be of low grade and are thus associated with an improved prognosis. Ten year survival rates are 83% for grade I, 64% for grade II and 29% for grade III.

Tumour size also plays an important role in bone cancer prognosis with smaller lesions behaving less aggressively than larger bone cancer tumours (irrespective of grade). Therefore, early bone cancer diagnosis and bone cancer treatment are associated with an improved prognosis. Unfortunately, these tumours often present as gross, unresectable masses.

How is Bone Cancer Diagnosed?

General investigations into bone cancer may show anaemia or low platelet count if bone marrow is involved. Abnormal alkaline phosphatase levels may also be found.

How is Bone Cancer treated?

Most chondrosarcoma are resistant to chemotherapy, so treatment of these bone cancer tumours revolves around wide surgical excision where clinically possible.

Chemotherapy is advocated in the treatment of the histological variants, mesenchymal and dedifferentiated tumours, but its role in the treatment of conventional chondrosarcoma remains to be defined.

Radiotherapy is used in bone cancer patients where the primary tumour is not resectable.

Improvement in bone cancer symptoms is an important measurement. Specific monitoring may be by serial imaging to detect any recurrence or metastatic spread.

The bone cancer symptoms that may require attention are somatic pain from bone metastases, visceral pain from lung metastases and neurogenic pain if nerve tissue is compressed. Coughing and breathlessness from lung involvement may require specific treatment.

(Source: David Dalley, St Vincent's Hospital).

Bone Cancer References

[1] Flemming DJ, Murphey MD: Enchondroma and chondrosarcoma. Semin Musculoskelet Radiol 2000; 4(1): 59-71
[2] Healey JH, Lane JM: Chondrosarcoma. Clin Orthop 1986 Mar; (204): 119-29
[3] Murphey MD, Flemming DJ, Boyea SR, et al: Enchondroma versus chondrosarcoma in the appendicular skeleton: differentiating features. Radiographics 1998 Sep-Oct; 18(5): 1213-37; quiz 1244-5

Drugs/Products Used in the Treatment of This Disease:

Mobic
(Meloxicam)
Orudis
(Ketoprofen)

Bone Cancer- III

2008-08-19T01:55:00.000-07:00

Osteosarcoma (Osteogenic sarcoma) :

What is Osteosarcoma

Osteosarcoma is a type of bone cancer.

The bones of the body are a specialised form of connective tissue that form the majority of the human skeleton. They are comprised of calcium, phosphate and magnesium within a framework of type I collagen. The size of the skeleton does not tend to increase beyond puberty (when fusion of the skeletal growth plates occur) but bone is a highly metabolically active tissue undergoing constant resorption, formation and remodelling.

The Three major functions of bone can be seen as:

Mechanical- support of tissues, attachment of muscles and enabling movement of the body;

Metabolic- the bone forms the major storage reservoir for calcium and phosphate in the body; and

Protective- bones provide the protective casing for vital internal organs and also for the bone marrow.

Who gets Osteosarcoma?

It is is rare, accounting for less than 0.2% of new malignancies each year. However, it is the most common primary malignant bone tumour. The vast majority of bony malignancies are metastatic. More than 75% occur in patients younger than 20 years (with peaks at 10-14 for girls and 15-18 for boys) but a second smaller peak also occurs in the elderly with sex incidence being a twice as common in males.

Geographically, the tumour is found worldwide.

Predisposing Factors

Genetic factors play a fundamental role in the development of osteosarcoma. Heritable mutations in the p53 germline are associated with the autosomal recessive Li Fraumeni syndrome of familial cancers and patients with mutations in the Rb gene (associated with the development of retinoblastoma) are also at a high risk of developing osteosarcoma. Osteosarcoma also arises with increased frequency in patients with osteogenesis imperfecta.

Other predisposing factors include: Areas of rapid bone growth (as suggested by the location of tumours at sites of maximal bone growth and in regions of Paget's disease); and radiation (especially post-radiotherapy for a solid organ tumour in childhood).

Progression

This type of tumour spreads by vascular invasion and haematogenous dissemination. Lung and distant bone metastases are the most common sites for spread.

Probable Outcomes

Prior to the development of chemotherapeutic techniques the prognosis from osteosarcoma was universally poor, with a 5 year survival rate of less than 20%. However, a localised osteosarcoma is now associated with a 5 year survival rate of approximately 60%.

How is Osteosarcoma Diagnosed?

General investigations may show anaemia or low platelet count if bone marrow is involved. Abnormal alkaline phosphatase levels may be detected.

How is Osteosarcoma treated?

Treatment for osteosarcoma revolves around surgical excision and chemotherapy. Surgery takes the form of either amputation or, in less advanced cases, limb salvage procedures where local resection is performed. Sometimes chemotherapy is used preoperatively in the hope that a non-resectable tumour requiring amputation can be shrunk and a local resection performed. The introduction of combination chemotherapy techniques and of limb sparing surgical procedures have dramatically reduced the mortality and morbidity of osteosarcoma.

Improvement in symptoms is an important measurement. Specific monitoring may be by serial CT and radioisotope bone scanning for the detection of recurrent disease. The chest should also be monitored with serial x-rays as it may be possible to resect even multiple secondaries from an osteogenic sarcoma.

The symptoms that may require attention are somatic pain from bone metastases, visceral pain from liver or lung metastases and neurogenic pain if nerve tissue is compressed. Coughing and breathlessness from lung involvement may require specific treatment.

Osteosarcoma is radioresistant, and as such, radiation therapy has no role in routine management.

(Source: David Dalley: St Vincent's Hospital).

Regimens Used in the Treatment of This Disease:

Bone Cancer-II

2008-08-19T01:49:00.001-07:00

Ewings Sarcoma:

What is Ewings Sarcoma

Ewings sarcoma is a primary malignant "small round cell" tumour of bone. The small cells that make up the tumour resemble those of lymphoma or neuroblastoma, and current evidence suggests that the tumour cells are related to nerve cells (have a neural phenotype).

Who gets Ewings Sarcoma?

Ewings sarcoma constitutes approximately 10-15% of all bone sarcomas. It is the bone tumour with the youngest age predilection - being common in adolescence, and has a peak incidence in the second decade of life.

Predisposing Factors

Ewings sarcomas arise in teenage years when bone growth is most rapid. It is believed that the rapid bone growth predisposes to the development of the cancer. In approximately 85% of Ewings sarcomas there is a specific genetic cause.

Progression

The disease can be very aggressive, hence it is considered a systemic disease. Local growth is often accompanied by systemic metastasis (spreading) - to lung, other bones, and bone marrow.

Probable Outcomes

Ewings sarcoma is a curable disease, even with the presence of metastatic disease, especially in children under the age of 11. Patients with lesions in the distal arm (below the elbow) or distal leg (below the calf) have a 5-year survival rate of 80% with effective treatment.

How is Ewings Sarcoma Diagnosed?

Blood Tests: Serum alkaline phosphatase is usually raised, and hypercalcaemia may be present with widespread disease.

X-ray: The plain radiograph may show characteristic "onion peel" periosteal reaction with a generous soft tissue mass.

How is Ewings Sarcoma treated?

The treatment of Ewings sarcoma usually involves chemotherapy and surgery, with or without radiotherapy.

Systemic chemotherapy is often used before surgery - involving doxorubicin, cyclophosphamide, etoposide, vincristine, and dactinomycin.

Local treatment of the tumour (often after chemotherapy) involves surgical resection, usually with limb salvage or radiation therapy.

Analgesics and anti-inflammatory drugs are important for pain relief.

Ewings Sarcoma References

Braunwald, Fauci, Kasper, Hauser, Longo, Jameson. Harrison's Principles of Internal Medicine. 15th Edition. McGraw-Hill. 2001
Cotran RS, Kumar V, Collins T. Robbins Pathological Basis of Disease Sixth Ed. WB Saunders Company 1999.
Kumar P, Clark M. Clinical Medicine. Fourth Ed. WB Saunders, 1998.

Regimens Used in the Treatment of This Disease:
- Dacarbazine
Drugs/Products Used in the Treatment of This Disease:
- Doxorubicin Hydrochloride Injection (DBL)
  (Doxorubicin hydrochloride)
- Doxorubicin Hydrochloride Injection USP
  (Doxorubicin hydrochloride)
- Etoposide Injection
  (Etoposide)
- Cycloblastin
  (Cyclophosphamide)
- Holoxan
  (Ifosfamide)

Bone Cancer - I

2008-08-18T22:36:00.000-07:00

Endochondroma (chondroma, Ollier's disease) :

What is Endochondroma

Chondroma is a benign (does not spread throughout body) tumour of cartilage. When chondromas form within the medullary cavity within the bone they are called endochondromas. Olliers disease is a syndrome when a person suffers from many endochondromas.

Who gets Endochondroma?

Chondromas mainly affects people between the age of 10 and 30 years. There is an equal incidence of chrondomas between males and females.

Predisposing Factors

Olliers disease is caused by an inborn genetic error that causes abnormal endochondral bone formation. The cause of single endochondromas is unknown.

Progression

Endochondromas have the potential to become malignant chondrosarcomas. In Olliers disease 30% of patients have malignant transformation. Overall 1% of endochondromas undergo malignant transformation. Tumours closer to the midline are more likely to become malignant.

Probable Outcomes

Prognosis for a benign single endochondroma is excellent. See information available on chondrosarcomas for malignant transformation.

How is Endochondroma Diagnosed?

A plain x-ray is the most effective way to diagnose endochondroma.

How is Endochondroma treated?

Single asymptomatic lesions are followed up with x-rays. If lesions enlarge or become painful a bone biopsy may be needed to examine for malignancy.

Regular review and monitor of Olliers disease is required to recognise malignant transformation. Pathological fractures are allowed to heal and the tumour is removed by curettage, and bone grafting may occur.

Endochondroma References

Wheeless textbook of orthopaedics: http://www.wheelessonline.com/index.htm
www.bonetumor.org

Blood Cancer -IV

2008-08-18T22:29:00.000-07:00

Tumour Lysis Syndrome :

What is Tumour Lysis Syndrome

Tumour lysis syndrome is the name given to a collection of metabolic abnormalities that occur following the initiation of cytotoxic chemotherapy.

Who gets Tumour Lysis Syndrome?

This potentially lethal syndrome is most likely to occur in patients with bulky, rapidly proliferating tumours that are responsive to therapy. The

most common malignancies it is associated with are leukaemias, high-grade non-hodgkin's lymphoma and Burkitt lymphoma, although it has been associated with other haematological and solid malignancies. Clinically, tumour lysis syndrome occurs in about 6% of patients being treated for non-hodgkin's lymphoma, but laboratory parameters consistent with it are seen in up to 42% of patients.

Predisposing Factors

The cells that make up cancer are often numerous and rapidly proliferating. There are therefore large numbers of them to be killed, and chemotherapy aims to do this quickly. As such large numbers are killed at the same time, their contents are rapidly and simultaneously released into the bloodstream. As a result, tumour lysis syndrome may occur and usually does so within 1-5 days of chemotherapy. Very occasionally, tumour lysis syndrome occurs spontaneously, with no exposure to chemotherapy agents.

Progression

Tumour lysis syndrome causes a triad of hyperkalaemia, hyperphosphataemia and hyperuricaemia and leads to acute renal failure.

Probable Outcomes

Morbidity and mortality are related to acute renal failure, cardiac arrhythmias (due to hyperkalaemia) and metabolic acidosis. Tumour lysis syndrome is often predictable, and close monitoring of at-risk patients usually allows for effective treatment or even prevention.

How is Tumour Lysis Syndrome Diagnosed?

Recognition of at-risk patients and the prevention of tumour lysis syndrome are the most important aspects of management. Pre-treatment hyperuricaemia and high lactate dehydrogenase levels represent a high tumour load, and therefore an increased risk for developing tumour lysis syndrome. Patients with pre-ex

isting renal impairment are also at higher risk.

All patients at high risk of tumour lysis syndrome should have electrolytes and kidney function monitored prior to chemotherapy and for 48-72 hours following therapy. This way any abnormalities will be detected early and renal failure may be prevented.

How is Tumour Lysis Syndrome treated?

Allopurinol, urinary alkalinisation and aggressive hydration aim to reduce plasma uric acid levels and prevent renal failure. Rasburicase can be used if allopurinol is ineffective. Prophylaxis may also include limiting of potassium and phosphate intake.

Due to the unpredictability of chemotherapy, tumour lysis syndrome may still occur despite aggressive prophylaxis. If signs develop, monitoring should continue at least twice daily. The appearance of renal failure in a patient with cancer does not immediately indicate tumour lysis syndrome. As mentioned earlier, there are many other causes of renal impairment in cancer patients. However, the appearance of all the aforementioned electrolyte disturbances plus renal failure, relatively soon after chemotherapy drugs have been administered, strongly suggests tumour lysis syndrome.

If prevention has been unsuccessful or was not instituted, tumour lysis syndrome requires aggressive treatment. Therapy is aimed at maximising excretion of released intracellular products and minimising production of uric acid. Patients may require treatment in an oncology unit or ICU due to the need for continuous monitoring and specialist treatment. Laboratory results must be given priority and reviewed quickly to allow for rapid detection and correction of electrolyte imbalances. Regular cardiac monitoring using ECG should also be carried out, in order to detect any rhythm abnormalities should they occur. A coagulation profile should also be performed as part of early monitoring.

Each electrolyte imbalance should be corrected individually, and the most important to address is the hyperuricaemia. Allopurinol is used, and can be given intravenously if the patient cannot tolerate it orally. If renal impairment is already obvious, dose reduction may be necessary. Rasburicase may be a useful alternative to allopurinol. It is faster, safe for use in children, and may reduce the need for dialysis.

Urine alkalinisation should be performed to reduce uric acid precipitation. Sodium bicarbonate can be given intravenously to alkalinise urine. This prevents crystallisation of uric acid, and a pH of 7.0 is a reasonable aim. Care must be taken with this treatment, as calcium phosphate crystallises at an alkaline pH and an adjustment too far in that direction should be avoided. Regular urinary pH measurements should be used to guide alkalinisation therapy.

Good urine flow helps prevent uric acid precipitation, but care should be taken not to fluid overload patients whose renal function is deteriorating. Hydration helps to correct electrolyte imbalances by diluting extracellular fluid. It also increases renal blood flow and encourages natural excretion of electrolytes. High-risk patients should be well hydrated prior to and during treatment, using intravenous fluids. This should be continued maintaining urine output of 3L/day unless the patient shows cardiac signs of volume overload. Proper fluid management is vital in preventing fluid overload and hypertensive complications. Diuretics should only be used in well hydrated patients showing signs of volume overload.

Hyperkalaemia should be aggressively treated and monitored. Dietary potassium should be restricted, and potassium immediately removed from all intravenous fluids. Intravenous insulin + glucose helps redistribute potassium into the intracellular space. IV calcium gluconate can be used for cardio-protection if potassium levels exceed 6.5mmol/L. Potassium wasting diuretics should be used with caution as they may worsen renal precipitation. Oral potassium exchange resins should be given immediately, as this will outlast shorter-term treatments. Should all of these treatments fail to reduce potassium levels, dialysis is indicated.

Oral phosphate binders (eg: aluminium hydroxide) should be used to control hyperphosphataemia. Hypocalcaemia usually resolves as phosphate levels are corrected. Hypocalcaemia should not be actively corrected (with calcitriol) unless Chvostek and TrousseauÃ¢â‚¬â„¢s signs are positive.

Dialysis may be indicated if the above measures fail to keep uric acid or phosphate levels below 10mg/dL. Haemodialysis is preferred, and may need to be repeated depending on results of ongoing monitoring. Dialysis helps prevent renal failure, and its preparation should be considered early in the course of the syndrome.

The prognosis of tumour lysis syndrome is excellent with adequate treatment, with renal failure returning to normal when uric acid levels drop below 10mg/dL.

Tumour Lysis Syndrome References

Kindly Supplied by Virtual Nursing Education.

Drugs/Products Used in the Treatment of This Disease:

Fasturtec
(Rasburicase rys)

Blood Cancer -III

2008-08-18T22:22:00.000-07:00

Hyponatraemia :

What is Hyponatraemia

Hyponatraemia is defined as low levels of sodium in the serum, that is less than 135mmol/L (normal range is between 135mmol/L and 145mmol/L). Sodium is the predominant positively charged ion (cation) in the body's extracellular fluid. Severe hyponatraemia is when the serum sodium levels are below 125mmol/L.

Who gets Hyponatraemia?

Hyponatraemia occurs in approximately 1% of hospitalised patients. Incidence rates can be much higher in cancer patients, for example between 15-50% in small cell lung cancer. Decreased serum sodium levels in cancer patients usually occur due to fluid overload, which is caused by inappropriate levels of hormone that prevents excretion of free water (antidiuretic hormone - ADH). This is known as the syndrome of inappropriate secretion of ADH (SIADH), and is easily the most common cause of hyponatraemia in cancer patients.

Predisposing Factors

Malignant illness can cause hyponatraemia in a variety of ways. These include:

Decreased kidney (renal), adrenal or thyroid function (insufficiency)
Factors relating to medical treatment (iatrogenic factors)
SIADH
Central nervous system (CNS) lesions, lung disease or nausea causing physiologic increases in ADH secretion.
Adaptive circulatory mechanisms such as low blood pressure, heart failure or liver cirrhosis.

SIADH is the most common cause of hyponatraemia in patients with cancer.

Other Mechanisms that can cause hyponatraemia include:

Increased thyroid hormones (hyperthyroidism) and adrenal insufficency.
Excessive salt excretion (salt-wasting) in drug-induced kidney damage, adrenal insufficiency or use of specific medications that increase urine excretion (thiazide diuretics).
Chemotherapy.
Chemotherapy and associated nausea and vomiting.
Overhydration with fluids containing less sodium than normal blood (hypotonic fluids).

Progression

Hyponatraemia is usually caused by an excess of total body water relative to sodium levels. It is most often caused by water retention combined with excessive administration of fluids.

Water retention usually occurs as a result of increased ADH secretion due to a reduced volume of blood within the vessels (intravascular volume). This decreased intravascular volume may be due to excessive swelling when the body's fluid has shifted outside of the blood vessles (oedematous state) or true volume depletion (e.g. from blood loss).

The syndrome of inappropriate ADH secretion (SIADH) involves the inability of the kidney to dilute urine even though the plasma has become less concentrated. It is defined as an inappropriately high urine concentration (osmolality) at the same time as decreased serum osmolality.

Probable Outcomes

Hyponatraemia results in primarily brain-related (neurological) symptoms. If serum sodium levels fall quickly, brain swelling (cerebral oedema), fits (seizures), coma and even death may result. Fortunately, serum sodium can be easily monitored, and this complication can be prevented in many patients.

How is Hyponatraemia Diagnosed?

As the early stages of hyponatraemia may be asymptomatic, laboratory findings are useful in making the diagnosis. Diagnosis of SIADH is made by finding low serum sodium and low serum concentration (osmolality) (<280>20 mmol/L) in a patient with normal intravascular volume.

Kidney, liver, heart, adrenal and thyroid function must all be normal for the diagnosis of SIADH to be made.

How is Hyponatraemia treated?

Treatment depends on patient symptoms and the underlying cause of the hyponatraemia. Life-threatening situations must be treated supportively; an airway tube (intubation) may be necessary and medications to stop fits (anticonvulsant medications) should be considered in patients with seizures. Low sodium (hypotonic) IV fluids should be avoided, as these worsen the condition.

Serum sodium must be corrected at the appropriate rate; asymptomatic patients require slow (0.5mmol/L/hr) replacement, whereas patients who show symptoms require more rapid intervention (1-2mmol/L/hr). This rapid correction is only indicated for the first 1-3 hours of treatment, with the remainder of correction (aim is to increase serum sodium levels by 12-15mmol/L) occurring over 24 hours.

Most cases of hyponatraemia due to SIADH develop gradually, and gradual correction is appropriate unless there are neurological symptoms. The central nervous system reacts to hyponatraemia in a specific way. If levels change too quickly, nerve cell swelling and damage may occur. Slow sodium replacement is required to prevent fluid shifting rapidly from the cells, which can cause a specific type of damage to the brain (cerebral pontine myelinolysis). Treatment of the underlying cancer may or may not be successful in reducing the ectopic ADH secretion, and this is not considered treatment enough on its own.

The other important factor in the management of hyponatraemia is fluid management. If the cause is decreased blood volume, this must be addressed appropriately. Administration of normal saline (salt water with the same sodium concentrations as blood) corrects both the fluid loss and the low sodium levels, whilst suppressing ADH secretion and encouraging free water excretion. Salt and water restriction are appropriate in cases of hyponatraemia due to oedematous states. This must be accompanied by treatment of the underlying cause of the oedema.

Because SIADH is a state of excess free water, it is treated initially by limiting the total free water intake. If limiting free water is unsuccessful, a specific type of antibiotic (demeclocycline, a tetracycline antibiotic), can be used to inhibit the activity of ADH on the kidney, but it is relatively slow to take action. Treatment with 3% saline +/- a medication to increase fluid excretion (diuretic - frusemide) is recommended if CNS symptoms are present. If the syndrome is chronic, frusemide or salt tablets may be used for long term treatment. The underlying tumour must also be treated.

Hyponatraemia References

Kindly Supplied by Virtual Nursing Education.

Blood Cancer-II

2008-08-18T21:41:00.000-07:00

Neutropaenic sepsis :

What is Neutropaenic sepsis

Neutropaenic sepsis is a systemic infection that occurs in the setting of decreased blood neutrophils (granulocytes).

A decrease in neutrophils increases the risk of infection, and once microorganisms have entered the body, reduces the body's ability to fight the infection.

Many microorganisms, including some that don't usually cause infections, may proliferate in these patients and cause disseminated infection.

Who gets Neutropaenic sepsis?

Up to 48.3% of neutropaenic cancer patients suffer infections and 21% of patients with cancer who experience neutropaenic fever will suffer serious complications. Neutropaenic sepsis carries an overall 4-30% mortality rate in cancer patients.

Predisposing Factors

Cancer patients may suffer neutropaenia as a result of their disease, for example leukaemia, but the most common causes are chemotherapy and radiotherapy. Most chemotherapy agents are myelosuppressive, meaning they suppress bone marrow function and thus production of white blood cells including neutrophils.

Progression

Neutropaenia increases the susceptibility of the body to bacterial infection. Patients with neutropaenia alone (i.e. no other white blood cell deficits) are not at increased risk of parasitic or viral infections. Prolonged neutropenia also increases the risk of systemic fungal infection.

The most common infections seen in neutropaenic patients are skin infections, including ulcers, abscesses and rashes that are slow to heal. Signs of infection such as warmth and swelling may be absent, as these are usually mediated by neutrophils.

Neutropaenic sepsis is when an infection enters the blood, often from a skin or gastrointestinal source, and becomes systemic. This is dangerous as many organ systems may be affected and the infection can worsen quickly.

Neutropaenic patients are susceptible to infections with the following bacteria: Staphylococci, Streptococci, Enterococci, Pseudomonas aeruginosa, Aeromonas hydrophila, Bacillus species, Corynebacteria and Enterobacteriaciae. Fungi from the species Candida, Aspergillus and Fusarium can also cause infection.

Probable Outcomes

With early detection and treatment, there is rarely a progression to sepsis and the patient fully recovers.

How is Neutropaenic sepsis Diagnosed?

Signs and Symptoms of Sepsis:

increased heart rate
decreased blood pressure
pale, clammy skin
rapid, shallow breathing
general weakness

If the sepsis becomes severe and the patient goes into septic shock, they may suffer the above symptoms more seriously, as well as:

decreased urine output
breathing difficulties requiring oxygen, intubation or even mechanical ventilation
altered blood clotting (uncontrolled clots and bleeds)
disorientation and confusion
jaundice
changes in blood sugar resulting in hyperglycaemic or hypoglycaemic coma

However, with early detection and treatment, neutropaenic fever rarely progresses to sepsis and the patient fully recovers.

How is Neutropaenic sepsis treated?

Empirical antibiotic therapy is vital to the treatment of a neutropaenic patient who becomes febrile. This is particularly useful in preventing deaths due to gram-negative organisms, but treatment covering both gram-positive and gram-negative organisms is required. There is no doubt as to the value of empirical antibiotics, but debate continues as to the best regime. Currently the Therapeutic Guidelines recommend gentamicin + ceftazidime or ticarcillin/clavulanic acid. Monotherapy with ceftazidime, cefepime, meropenem or imipenem has also proven effective. All of these drugs should be used at maximum recommended dosage. Vancomycin is indicated if a resistant gram-positive organism is isolated. Ideally, each patient should be approached individually, with attention paid to recent infections and antibiotic exposure, when deciding on an empirical antibiotic regime.

Neutropaenic sepsis References

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Blood Cancer-I

2008-08-18T21:24:00.000-07:00

Disseminated Intravascular Coagulation
What is Disseminated Intravascular Coagulation

Disseminated intravascular coagulation (DIC) is a disorder that affects the blood clotting cascade. This disorder occurs when your body's clotting mechanisms are activated inappropriately. DIC can occur in the short or long term, and is the end complication of a variety of diseases such as cancers and some infections. Clots form throughout the whole body, instead of localizing only to the site of injury. Eventually, all the blood clotting factors are used up and unavailable to be used when needed at actual sites of injury. In the image on the right severe bleeding has occured in an infant, leading to gangrene within the affected limb.

Who gets Disseminated Intravascular Coagulation?

Disseminated intravascular coagulation often presents with a subacute thrombotic picture in cancer patients, and is associated with high mortality rates when this acutely develops into the haemorrhagic form.

Disseminated intravascular coagulation occurs in 7-10% of patients with malignant disease. Adenocarcinomas and leukaemias are the most common cancer associations.

Predisposing Factors

About 50% of individuals with disseminated intravascular coagulation are patients with complications from pregnancy. Widespread infection and trauma are responsible for the majority of the remaining cases.

There are many causes of disseminated intravascular coagulation. These can be classified as acute or chronic, systemic or localized. The disorder may be the result of single or multiple conditions.

Acute DIC:

Infectious:

Bacterial (eg: gram-negative infections, meningococcal disease)
Viral (eg, HIV,
cytomegalovirus [CMV], varicella)
Fungal (eg, histoplasma)
Parasitic (eg, malaria )

Malignant disease:

Those originating in cells of the bloodstream (eg, acute myelocytic leukemias)
Spread of cancers

Obstetric:

Placental abruption (early separation of a normal placenta from the wall of the uterus
Eclampsia (a serious complication of pregnancy characterized by convulsions.)

Trauma

Burns

Surgery

Acute liver failure

Snake bites

Transfusion reactions of blood

Chronic DIC:

Malignancies

Leukaemia

Obstetric:

Retained products of conception (eg - dead fetus, post miscarriage).

Vascular:

Rheumatoid arthritis

Inflammatory:

Ulcerative colitis,
Crohn's disease (inflammatory conditions affecting the bowels).

Progression

Disseminated intravascular coagulation begins with over-activation of your body's coagulation system and excessive clotting. The excessive clotting is usually stimulated by a substance that enters the blood, with possible causes as listed above. As the clotting factors and platelets are consumed, there are less clotting factors available to be used at real sites of bleeding and excessive bleeding occurs. The results of this process (ie. abnormal small clots (microthrombi) and/or bleeding) are found in many organs and tissues. Significant changes may occur in some of your body's organs such as the kidney, lungs, brain, adrenals or placenta.

Probable Outcomes

The prognosis for disseminated intravascular coagulation varies according to each individual patient. It depends on the cause of your disseminated intravascular coagulation.

How Will Disseminated Intravascular Coagulation Affect Me?

If you are affected by disseminated intravascular coagulation, some of the following symptoms may be experienced;

Symptoms of infection - fevers, cough, shortness of breath, pain, rash, behaviour changes, sick contacts and recent travel.

If you are young and affected by disseminated intravascular coagulation, a birth history may be relevant -

Events occurring just before, around and after birth - ie. course of pregnancy, prenatal testing, any neonatal illnesses may be important.
Risk factors for infection around the time of your birth (fever in your mother, premature rupture of the membranes, your mother's status for a particular bacteria called group B streptococcus and antibiotics given around the time of birth).

Depending on your condition, age and many other factors, your doctor may ask about symptoms such as -

Abnormal or increased bruising
Lethargy (tiredness)
Recent illness, infections.
Loss of weight
Drug use
Pregnancy history
Family history suggestive of an inherited clotting disorder or cancers
Ongoing medical problems including; cancers, problems with blood vessels and inherited or acquired problems affecting the immune system.

Clinical Examination

When your doctor examines you, he or she may find the following signs. There may be no bleeding at all, to widespread bleeding at different sites of the body.

Bleeding may occur from the mouth, nose, sites of injections, or from virtually any site.
There may be widespread bruising.
Abnormal clots may block off vessels to vital organs. Any organ may be involved but the skin, brain and kidney are most commonly affected. Respiratory symptoms such as shortness of breath or extreme respiratory difficulty may occur if the lungs are involved.
Neurologic signs such as convulsions (due to abnormal electrical activity in the brain causing things such as abnormal movements, spasms, or changes in behaviour) and coma (a state of unconsciousness) may be present.

How is Disseminated Intravascular Coagulation Diagnosed?

The doctor may decide to do some of the following tests, to help determine the reason for and the severity of your disseminated intravascular coagulation.

In severe cases with increased bleeding, some of these tests may be performed:

Blood film - this is a smear of the blood taken,which may show broken, fragmented red blood cells.
Decreased platelets (platelets are a type of blood cell which have a key role in normal blood clotting. They clump together during clotting processes, to plug holes in damaged blood vessels).
Increased prothrombin time (PT) - this test measures the clotting time of plasma (the liquid portion of the blood).
Increased activated partial thromboplastin time (APTT) - this measures the time it takes for clots to form by various pathways in the body.
High levels of fibrin degredation products (FDPs). These are proteins that are produced when clots are broken up by the body.
Decreased fibrinogen. (A protein produced by the liver which helps stop bleeding by helping blood clots form).
Decreased amounts of factors that help the blood clot;
- Factors V, VIII, X, XIII
- Protein C.

In mild cases without bleeding, the following test results may be present:

Increased synthesis of clotting factors and platelets may result in a normal PT, APTT, TT and platelet counts, although FDPs will be raised.

There is no single diagnostic test for disseminated intravascular coagulation. This condition is suggested by the following combination: a clinical picture consistent with disseminated intravascular coagulation, low levels of platelets, prolonged PT and APTT, and presence of FDPs.

How is Disseminated Intravascular Coagulation treated?

If you are affected by disseminated intravascular coagulation, the doctor's first step is to treat the underlying cause of your disease, where possible. For example - if infection is the underlying cause, you may be given appropriate antibiotics.
You may also be given supportive treatment like fluids and your urine output monitored with a urinary catheter.
The next step is to replace missing blood components. If your platelet levels are low, platelet transfusions are appropriate. If plasma coagulation factors are decreased, they may be replaced with fresh frozen plasma. If fibrinogen levels are low, the doctor might consider transfusion with cryoprecipitate, which is a substance rich in fibrinogen.
Doctors might consider heparin therapy in your treatment, which is a controversial issue. Heparin helps stop clotting, working by stopping enzymes that potentiate clotting. However, in some patients, bleeding can be accelerated.
Thus heparin therapy is probably is best reserved for patients with evidence of ischemia (insufficient blood supply) of the digits and cyanosis.
Surgical treatment is limited to treating certain underlying causes - eg. removal of a cancer.

Disseminated Intravascular Coagulation References

Furlong MA, Furlong BR. Disseminated Intravascular Coagulation 2005 E-medicine [serial online]. 2005 [cited 24th April 2006]. Available from URL: http://www.emedicine.com/emerg/topic150.htm
Longmore M, Wilkinson I, Torok E. Oxford Handbook of clinical Medicine. New York; Oxford University Press, 2001.
Kumar V, Abbas A K & Fausto N. Robbins & Cotran Pathologic Basis of Disease. China: Elseiver Saunders; 2005.
Kumar P, Clark M. Clinical Medicine United Kingdom: WB Saunders; 2002.

Drugs/Products Used in the Treatment of This Disease:
- Heparin Injection BP (DBL)
  (Heparin sodium)

Bladder Cancer-II

2008-08-18T11:19:00.000-07:00

Bladder Cancer (Squamous Cell Carcinoma of the Bladder)What is Bladder Cancer
Squamous Cell Carcinoma of the Bladder is a rarer type of bladder cancer. The majority of bladder cancers are transitional cell carcinomas that arise in the urinary tract epithelium and can also occur in parts of the kidney, ureter and urethra (tubes carrying urine from the kidney and urinary bladder respectively).

The bladder functions as a waste storage system for urine. Urine is produced by the kidneys as they filter the blood. The urine then travels down the ureters into the bladder. The bladder expands and once it reaches a certain maximum volume, the urge to pass urine increases until urine is passed.

The bladder is made up of an elastic type tissue which contains a layer of muscle. The bladder is lined with epithelium called transitional cells which are tall, thin cells that protect the underlying bladder from the urine contained therein.

Because the bladder is lined with transitional epithelium, the usual type of cancer affecting the bladder is transitional cell carcinoma. However, in response to chronic irritation the epithelial lining of the bladder can gradually change to squamous (similar to the skin). With further exposure to irritative or carcinogenic agents - bladder cancer can develop.

Who gets Bladder Cancer?

Bladder cancer on the whole is the most common malignancy affecting the urinary system. The majority of cases are transitional cell carcinomas affecting the tall epithelial cells lining the bladder. Squamous cell carcinoma accounts for only 3 to 7% of bladder cancers in Western countries, but in certain countries where parasites are very common (especially schistosomiasis) it is found much more frequently. The parasites cause chronic irritation of the blad

der causing the cells to change their shape to try to protect the bladder. Over time the cells can change to become neoplastic or cancerous. In these countries up to 70% of bladder cancers are the squamous type. The incidence of bladder cancer increases with age and 80% of patients are found to be between 50 and 80 years.

Men: bladder cancer is much more common in men and is the fourth most common cancer. In Australia approximately 554 men die from bladder cancer each year. However, sq

uamous cell carcinoma accounts for only a small percentage.

Women: Bladder cancer is the tenth most common cancer in women. Approximately 250 Australian women die from bladder cancer each year. However, squamous cell carcinoma accounts for only a small percentage.

Predisposing Factors

bladder cancer is almost exclusively found in bladders exposed to chronic irritation and infection. It is primarily a bladder disease of developing countries and is twice as common in white people compared to blacks. In African countries, Schistosoma haematobium is a parasitic infection of the bladder transmitted by freshwater snails and is acquired when people bathe in s

low-moving freshwater rivers and lakes. The eggs of the parasite cause chronic inflammation of the bladder and ureters - and more frequently leads to obstructive kidney disease, but can also cause bladder cancer.

In the United States chronic inflammation of the bladder is more often due to long-term indwelling urinary catheters or other instrumentation, and bladder stones.

Progression

Bladder cancer initially spreads to involve larger areas of the mucosa of the bladder, with deeper invasion later. Finally metastatic spread to other organs via the blood stream and lymphatics can occur. At the time of discovery most bladder tumours are deeply invasive.

Probable Outcomes

Bladder cancer generally has poorer prognosis than transitional cell carcinoma. The reason for this is probably that most bladder tumours are discovered late. The bladder cancer prognosis hence depends on the stage of the bladder tumour at the time of bladder cancer diagnosis. Women tend to have a poorer bladder cancer prognosis than men.

How Will Bladder Cancer Affect Me?

Bladder tumours classically present with painless haematuria (blood in the urine). They can also present with symptoms simulating urinary tract infections such as frequency, dysuria, urgency. Blood in the urine does not always indicate bladder cancer, and cystitis (inflammation of the bladder) is a much commoner cause. However, all patients should be assumed to have cancer (and be appropriately investigated) until proven otherwise.

Pain can also result from local nerve involvement.

If a ureter is obstructed patients can also develop pyelonephritis (inflammation of the kidney and its pelvis with fever and flank pain) or hydronephrosis (obstruction and dilation of the upper urinary tract).

Clinical Examination

With bladder cancer there is normally little to find on examination, unless the bladder tumour is widespread. Your doctor will carefully examine your abdomen, pelvis and urinary tract.

Haematuria (blood in the urine) may be obvious on urinary examination, or microscopic haematuria (only visible under the microscope) on urinalysis may be the only sign in 2% of incidents.

Visit our information on Anatomy and Physiology of the Renal System.

How is Bladder Cancer Diagnosed?

Bladder cancer investigations tend to involve basic blood tests such as FBP (full blood picture) which may reveal anaemia due to chronic blood loss. A mid-stream urine sample (MSU) may reveal red blood cells or malignant cells.

Imaging of the urinary tract will be preformed such as Ultrasound and intravenous pylogram followed by CT and/or MRI. These rule out pathology in other parts of the urinary tract and can be used to visualise the urothelium. Cytoscopy (visualisation of the bladder with a camera) and biopsy are important investigations to obtain a tissue daignosis.

How is Bladder Cancer treated?

Bladder cancer treatment options depend on the stage of the cancer.

Surgical resection of part of the bladder, or the whole bladder (radical cystectomy) may be performed with curative intent in early bladder cancer. Radical cystectomy is a major procedure and is usually reserved for cases where more conservative approaches are not likely to succeed and a cure is possible. A conduit or reservoir (using ileum- the final segment of the small intestines) can then be fashioned, which connects the ureters to the ileum or the urethra, or the anterior abdominal wall for the drainage of urine. A uretero-ileal conduit is the more widely used.

In males radical cystectomy also involves removal of the bladder, prostate, seminal vesicles, and proximal urethra, and often causes impotence (erectile dysfunction) post-surgery unless the nerves responsible for erectile function are preserved.

In females radical cystectomy includes removal of the bladder, urethra, uterus, fallopian tubes, ovaries, anterior vaginal wall, and surrounding fascia.

Local (intravesical) or systemic chemotherapy and/or radiotherapy can also be used for bladder cancer treatment.

Chemotherapy protocols include:

MVAC- a combination of 4 drugs: Methotrexate (IV days 1,15,22), Vinblastine (IV days 1,15,22), Doxorubicin (IV day 2) and Cisplatin (IV over 2 hours day 2). Cycle is repeated every 28 days.
For bladder cancer patients unlikely to tolerate MVAC because of renal function, age or performance status: Cisplatin (day 1) and Gemcitabine (days 1+8) are used.
Concomitant chemotherapy/radiotherapy: with Cisplatin (5days) and Normal Saline hydration for the first and fourth weeks of radical radiation.

Bladder Cancer References

AIHW, Cancer Survival in Australia 2001. Australian Institute of Health and Welfare and Australasian Association of Cancer Registries 2001, Canberra, AIHW cat. no. CAN 13.
Bochner B, Epidemiology and etiology of bladder cancer, UpToDate, 2005.
Braunwald, Fauci, Kasper, Hauser, Longo, Jameson. Harrison's Principles of Internal Medicine. 15th Edition. McGraw-Hill. 2001.
Cotran RS, Kumar V, Collins T. Robbins Pathological Basis of Disease Sixth Ed. WB Saunders Company 1999.
Kumar, Clark. Clinical Medicine. 5th Edition. Saunders. 2002.
Longmore, Wilkinson, Rajagopalan. Oxford Handbook of Clinical Medicine. 6th Edition. Oxford University Press. 2004.
Steinberg G, Kim H, Bladder cancer, eMedicine, Web MD, 2005. Available [online] at URL: http://www.emedicine.com/med/topic2344.htm.

Regimens Used in the Treatment of This Disease:

Treatments Used in This Disease:

Drugs/Products Used in the Treatment of This Disease:

Doxorubicin Hydrochloride Injection (DBL)
(Doxorubicin hydrochloride)
Doxorubicin Hydrochloride Injection USP
(Doxorubicin hydrochloride)
Mitomycin C Kyowa
(Mitomycin)
Roferon-A
(Interferon alfa-2a)
Thiotepa
(Thiotepa)

Bladder Cancer-I

2008-08-18T11:10:00.000-07:00

Bladder Cancer (Transitional cell carcinoma of the Bladder)

What is Bladder Cancer

A type of bladder cancer is Transitional cell carcinoma of the Bladder.

The bladder functions as a waste storage system for urine. Urine is produced by the kidneys as they filter the blood, and then travels down the ureters into the bladder. The bladder expands and once it reaches a certain maximum volume, the urge to pass urine increases until urine is passed.

The bladder is made up of an elastic type tissue which contains a layer of muscle. The bladder is lined with epithelium called transitional cells which are tall, thin cells that protect the underlying bladder from the urine contained therein. The membrane that the epithelium sits on is called the basal membrane.

Who gets Bladder Cancer?

Bladder cancer is a relatively uncommon disease.
Bladder cancer incidence increases with increasing age.
Bladder cancer is twice as common in males as it is in females.
Bladder cancer is seen worldwide, but is more common in certain parts of Africa and the Mediterranean due to an infection caused by Schistoma (a parasite in that region).
90% of bladder tumours are of the transitional cell carcinoma type.

Predisposing Factors

Cigarette smoking predisposes people to bladder cancer. Smoking cigarettes increases a persons risk of developing bladder cancer approximately 5 fold.

Industrial exposure to certain chemicals such as analine in the dye industry increases the risk. Other organic chemicals used in rubber and other manufacturing processes can also increase the risk.

Exposure to the chemotherapy agent Cyclophosphamide (occasionally used in younger people to treat either lymphoma or autoimmune diseases) is associated with a higher risk of developing bladder cancer.

Chronic irritation of the bladder appears to provoke development of bladder cancer. The bladder can be irritated by reoccurring infections and bladder stones. In certain parts of Africa and in the Mediterranean area, a parasitic infection called schistosomiasis causes irritation of the lining of the bladder. The parasites that burrow into the bladder appear to stimulate the tumour.

Progression

This type of bladder cancer tumour spreads by different mechanisms, depending on the type.

Superficial transitional cell carcinoma (or superficial bladder cancer, bladder warts) tend to spread only within the bladder unless they are left untreated for a long period of time. They may spread along the lining of the bladder but not penetrate deeply into the bladder unless left.

Invasive bladder cancer spreads via the lymphatics to the regional lymph nodes in either the groin or pelvis and then upwards into the abdomen. Blood borne spread is to the bones, lung, liver and occasionally brain.

Probable Outcomes

Superficial bladder cancer has an extremely good prognosis with a vast majority (greater than 90%) of people being alive and well after 5 years, with a majority of them being cured.

Invasive bladder cancer however is different. If invasive bladder cancer is diagnosed early, the cure rate is still greater than 50% but if the tumour spreads to the regional lymph nodes this reduces survival to less than 50% over 5 years. Distant metastases is a bad sign as it means that the disease has spread and is obviously at a late stage in the tumours development.

How is Bladder Cancer Diagnosed?

General investigations into bladder cancer may show anaemia, especially if haematuria (presence of blood in the urine) has been significant and prolonged. A raised alkaline phosphatase level may indicate either liver or bone involvement and in some cases the serum calcium may be raised in bone metastases. Abnormal kidney function (e.g raised creatinine or urea) may indicate that the bladder tumour, whether superficial or deep, is causing some blockage of the ureters where they enter the bladder.

How is Bladder Cancer treated?

Radiotherapy has an important role in treating specific problems due to bladder tumours. In particular, painful bone metastases usually respond well to doses of radiation.

Superficial Bladder Cancer:

Superficial bladder tumours can be managed very effectively by repeated resection. After removal of these bladder tumours the surgeon will normally check inside the bladder on a regular basis from that point forward. Superficial bladder tumours tend to come back intermittently and may require resection on a repeated basis.

Invasive Bladder Cancer:

Invasive bladder cancer requires a more aggressive approach. In the early stages, the disease can be resected surgically either by partial or complete removal of the bladder (cystectomy). This can be fairly major surgery which will require the creation of an ileal conduit.

If the disease has spread to the regional lymph nodes these may need to be removed during the same operation. If the bladder cacner tumour is found in the regional nodes, bladder cancer treatment may then be surgery plus radiotherapy or radiotherapy alone.

A number of chemotherapy agents are active against bladder cancer and these may be given intravenously or instilled directly into the bladder (intra-vesical): Intravesical BCG.

1) Chemotherapy protocols include:

MVAC
Methotrexate 30mg/m2 IV bolus days 1,15,22
Vinblastine 3mg/m2 IV bolus days 1,15,22 (vesicant)
Doxorubicin 30mg/m2 IV bolus day 2 (vesicant)
Cisplatin 70mg/m2 IV over 2 hours day 2
- (Repeat every 28 days) Restage every 3 cycles

2) For bladder cancer patients unlikely to tolerate MVAC because of renal function, age or performance status:
- Cisplatin 70 mg/m2 day 1 (or substitute carboplatin AUC 5)
- Gemcitabine 1250 mg/m2 days 1+8

3) Concomitant chemo/radiotherapy.
- Cisplatin 20mg/m2/daily x 5days with 1 litre N Saline hydration.
- Cover during week 1 and 4 of radical radiation concomitantly.

Bladder Cancer References

eMEDiCINE.
Shah I; Gupta CL; Gupta R; Bardwajs Department of Urology, Acharya Shri Chander College of Medical Sciences and Hospital, Sidhra, Jammu, Jammu-180006 (India) Transitional cell carcinoma of bladder in young patients JK-Practitioner. 2001 Jul-Sep; 8(3): 181-2.
Warde P, Gospodarowicz MK: New approaches in the use of radiation therapy in the treatment of infiltrative transitional-cell cancer of the bladder. World J Urol 1997; 15(2): 125-33.

Regimens Used in the Treatment of This Disease:
Symptoms of This Disease:
- Dysuria (and Urine Frequency)
- Blood in urine
Treatments Used in This Disease:
- Intravesical BCG (Bacillus Calmette-Guerin vaccine for immunotherapy)
Drugs/Products Used in the Treatment of This Disease:
- Mitomycin C Kyowa
  (Mitomycin)

Anus Cancer

2008-08-18T10:59:00.000-07:00

Anal Cancer

(Squamous Cell Carcinoma of the Anus)

What is Anal Cancer

The main type of anal cancer is Squamous Cell Carcinoma of the Anus.

The anus is a canal that connects the lower part of the large intestine (rectum) to the outside of the body. It allows the faeces to pass from the large intestine during a bowel movement. Faeces are formed in the longest part of the large intestine (colon), stored in the rectum, and pass through the anus. Squamous cell carcinoma of the anus forms from the lining of the anal canal. They are the most common type of anal cancer.

Who gets Anal Cancer?

Anal cancer is fairly rare. In young people anal cancer is more common in men. The average age for anal cancer sufferers is 60 years of age.

Predisposing Factors

Many people believe anal cancer is caused by the Human Papilloma Virus. Predisposing factors include:

Smoking.

HIV

Lowered immunity.

Increased sexual activity.

Fistulas (abnormal openings).

Progression

Anal cancer spreads by local invasion initially, and then via the lymphatics - with inguinal, pelvic, para-aortic and iliac nodes being the most common sites of early anal cancer spread.

Probable Outcomes

Anal cancer prognosis depends upon the size of the anal tumour, where the anal tumour is and whether it has spread to the lymph nodes.

How is Anal Cancer Diagnosed?

Signs of anal cancer are checked through routine blood tests for anaemia and infection.

How is Anal Cancer treated?

Anal cancer treatment depends upon the stage of the anal cancer and the level of local and extended involvement. Anal surgery is generally conducted, either local resection or an abdominoperineal resection.

Radiotherapy and chemotherapy are employed if the cancer is in any of the later stages.

Chemotherapy for anal cancer typically involves:

Mitomycin C 10 mg/m2 IV day 1 only
5-Fluorouracil 800 mg/m2/day continuous infusion days 1-4 and 43-46

Initial phase 4 week 36 Gy
A 2 week break
Second phase 1/2 to 2 weeks (varies) 14.4-18 Gy
(Some radiation oncologists do not have the break. In week 5, 5FU is infused)

Regimens Used in the Treatment of This Disease:

Drugs/Products Used in the Treatment of This Disease:

Fluorouracil Injection BP
(Fluorouracil)
Mitomycin C Kyowa
(Mitomycin)

Adrenal Gland Cancer

2008-08-18T10:52:00.000-07:00

Adrenal Gland Cancer (Adenocarcinoma of the Adrenal Gland/Adrenocorticol carcinoma)

What is Adrenal Gland Cancer

Adenocarcinoma is a malignant (one that can spread throughout the body) cancer of the adrenal glands. The adrenal glands are paired organs that sit on top of the kidneys in the back of the upper abdomen. The adrenal cortex (the outer layer of the adrenals) is part of the endorcrine system. It secretes hormones to deal with stress (glucocorticoids), hormones to deal with water, salt and blood pressure control (aldosterone) and also some sex hormones. Some cancers of the adrenal gland also produce these hormones, which in excessive amounts cause a distinctive set of symptoms.

Who gets Adrenal Gland Cancer?

Adrenal gland cancer (Adrenocorticol carcinomas) is rare (1 in 2,000,000 of all cancers). They occur at any age including childhood, however the median age is 44 years.

Predisposing Factors

The cause of adrenal gland cancer unknown.

Progression

Adrenal gland cancer (Adrenocorticol carcinomas) tend to metastasise or spread early on. This occurs through the blood and lymph. Distant growth often occurs within the lungs and other internal organs. Metastases within bones is rare.

Probable Outcomes

Adrenal gland cancer prognosis depends upon the size of the tumour and how successful surgery is in removing it. Many drenal gland cancer tumours have spread beyond the adrenals by the time they are diagnosed.

How is Adrenal Gland Cancer Diagnosed?

Blood and urine testing for hormone levels is used in the detection of adrenal gland cancer

How is Adrenal Gland Cancer treated?

Adrenal gland cancer treatment is based on a combination of surgery, chemotherapy and radiotherapy depending on the stage and spread of tumour. Adrenal gland cancer surgery will remove adrenals and any surrounding lymph nodes or tissues that are affected by the cancer (an Adrenalectomy). Chemotherapy uses the drug Mitotane to target the adrenal gland specifically. Radiotherapy is used to combat aggressive tumours.

Drugs/Products Used in the Treatment of This Disease:

Mitotane
(Mitotane)