IMPORTANT COMMUNICATE FOR ALL READERS OF FRANK'S BLOGS.

Engineer: FRANK SHARP FROM DATE 01/12/2014 IS FIGHTING AGAINST DEATH CAUSED BY:

DIAGNOSED CONSOLIDATED Acute myeloid leukemia (AML M3) RAR ALPHA BCR3 HIGH RISK, also known as acute myelogenous leukemia or acute nonlymphocytic leukemia (ANLL).

NOTE: THIS POST  MAY  HAVE DELICATE CONTENTS IF FEEL BAD SWITCHOVER PLEASE.









 NOTE HERE PHOTOGRAPHED MY  EXTREME HIGH SIXTIME EMORRAGIC PISS  (4:30AM) IN ONLY 4 HOURS. (IT'S ONLY BLOOD) + MOUTH EMORRAGIC SESSIONS + INTERNAL AUDITIVE CHANNELS FLOODED BY BLOOD AND PNEUMONIA STRANGE BREATHINGS combined with other many correlated aspect diffcult to explain like:
looking pale and feeling tired and breathless, which is due to anaemia caused by a lack of red blood cells,unusual bleeding caused by too few platelets - this may include bruising (bruises may appear without any apparent injury),bleeding gums,  feeling generally unwell and run down.



Background:
Acute myeloid leukemia (AML) is a cancer of the myeloid line of blood cells, characterized by the rapid growth of abnormal white blood cells that accumulate in the bone marrow and interfere with the production of normal blood cells. AML is the most common acute leukemia affecting adults, and its incidence increases with age. Although AML is a relatively rare disease, accounting for approximately 1.2% of cancer deaths in the United States,
its incidence is expected to increase as the population ages.

Leukemia is a cancer of the blood. Leukemia begins when normal blood cells change and grow uncontrollably. Acute myeloid leukemia (AML) is a disorder of the process that normally produces neutrophils, red blood cells, and/or platelets, which are types of normal blood cells. AML may sometimes be called acute myelogenous leukemia, acute myelocytic leukemia, or acute nonlymphocytic leukemia. Unlike chronic leukemia, acute leukemia develops quickly and generally needs immediate treatment. AML occurs in people of all ages but is most common in adults older than 65.

The symptoms of AML are caused by replacement of normal bone marrow with leukemic cells, which causes a drop in red blood cells, platelets, and normal white blood cells. These symptoms include fatigue, shortness of breath, easy bruising and bleeding, and increased risk of infection. Several risk factors and chromosomal abnormalities have been identified, but the specific cause is not clear. As an acute leukemia, AML progresses rapidly and is typically fatal within weeks or months if left untreated.

In AML, damage to the genetic material or DNA, called acquired mutations, in the blood-forming cells cause problems with the normal development of the blood cells. This causes the build-up of many immature cells called myeloblasts or blasts. Blasts do not act like fully developed, healthy blood cells and do not help a person’s immune system work. These acquired mutations and the large number of blasts also reduces the production of healthy red blood cells, which carry oxygen, and platelets, cells that help the blood to clot. Therefore, people with AML are usually anemic because they do not have enough red blood cells, are more likely to get infections because they do not have enough mature neutrophils, and bruise or bleed easily because of a low numbers of platelets.

AML is usually found in the blood and bone marrow, the spongy, red tissue in the inner part of the large bones, but it can sometimes also spread to other parts of the body, such as the brain, skin, and gums. Occasionally, AML cells can form a solid tumor called a myeloid sarcoma or chloroma that can develop anywhere in the body.

HERE IN PHOTO ON OF MY 24H INFUSION STATIONS GROUP FEEDING LIFE SUPPORT

AML has several subtypes; treatment and prognosis varies among subtypes. Five-year survival varies from 15–70%, and relapse rate varies from 33–78%, depending on subtype. AML is treated initially with chemotherapy aimed at inducing a remission; patients may go on to receive additional chemotherapy or a hematopoietic stem cell transplant. Recent research into the genetics of AML has resulted in the availability of tests that can predict which drug or drugs may work best for a particular patient, as well as how long that patient is likely to survive................................

As seen above and right I  have placed by surgery a necessary  PICC  device , A PICC  It's a peripherally inserted central catheter (PICC line) is a form of intravenous access that can be used for a prolonged period of time. A PICC is inserted in a peripheral vein, such as the basilic vein (large vein in upper arm) and then advanced through increasingly larger veins, toward the heart until the tip rests in the distal superior vena cava (large vein that carries blood into the heart).PICCs can remain in situ for extended periods of time, from seven days to 12 months, although little information is available with respect to viability timeframes. They are used in both the hospital and community settings. PICCs can be used for intravenous delivery of total parenteral nutrition (TPN), chemotherapy, antibiotics or other medications, and can also be used for blood sampling if the lumen is 4 French or larger in size (Arrow and Bard manufacturers guidelines). To maintain patency, PICC management should include regular flushing with normal saline and "locking" with heparin or normal saline when not in use.

SEE HERE THAT I NEED FREQUENT BLOO TRANSFUSIONS.


AML is not a single disease. It is the name given to a group of leukaemias that develop in the myeloid cell line in the bone marrow. Some years ago doctors from America, France and Britain decided to classify AML into eight different sub-types based on the appearance of the leukaemic cells under the microscope. Each sub-type provides information on the type of blood cell involved and the point at which it stopped maturing properly in the bone marrow. This is known as the French-American-British (FAB) classification system.

The current World Health Organisation’s classification system for AML uses additional information, obtained from more specialised laboratory techniques, like genetic studies, to classify AML more precisely. This information also provides more reliable information regarding the likely course (prognosis), of a particular subtype of AML, and the best way to treat it..

You make millions of blood cells every day. Each type of cell has an expected lifespan. For example, red blood cells normally last about 120 days. Some white blood cells last just hours or days - some last longer. Every day millions of blood cells die and are broken down at the end of their lifespan. There is normally a fine balance between the number of blood cells that you make, and the number that die and are broken down. Various factors help to maintain this balance. For example, certain hormones in the bloodstream and chemicals in the bone marrow called growth factors help to regulate the number of blood cells that are made.

The most important factor in predicting prognosis in AML is the genetic make-up of the leukaemic cells. Certain cytogenetic


Morphology

AML is first described by its morphology, or what the cancerous cells look like under the microscope. AML is classified by the type of normal, immature white blood cell it most closely resembles.

Most patients with AML have a subtype called myeloid leukemia, which means the cancer is in the cells that normally produce neutrophils. Other patients have a type of AML called monoblastic or monocytic leukemia. In monocytic leukemia, the cells look like white blood cells called monocytes. Leukemia cells can also be a mixture of myeloblastic and monocytic cells.

Sometimes AML seems to come from cells that produce red blood cells, called erythroid, or platelets, called megakaryocytic. Acute promyelocytic leukemia (APL) is a unique subtype of AML where the cancer cell stops maturing when the cell is at a stage called the promyelocyte or progranulocyte stage. APL is associated with a translocation between chromosomes 15 and 17 [t(15;17)].

Flow cytometry is a blood test that can identify particular proteins on the surface of abnormal cells and is sometimes used to find the difference among these subtypes.

The classification system from the World Health Organization (WHO) includes these major groups:

 AML with recurrent genetic abnormalities, meaning with specific chromosomal changes
 AML with multilineage dysplasia, or abnormalities in how the blood cells look
 AML, related to therapy that is damaging to cells, also called therapy-related myeloid neoplasm
 AML that is not otherwise categorized

The French-American-British (FAB) classification is an older system for describing AML, but it is still commonly used and is listed below for reference.

M0: Myeloblastic without differentiation
M1: Myeloblastic with little or no maturation
M2: Myeloblastic with maturation
M3: Promyelocytic (MINE)
M4: Myelomonocytic
M4eo: Myelomonocytic with eosinophils
M5a: Monocytic without differentiation (monoblastic)
M5b: Monocytic with differentiation
M6: Erythroleukemic
M7: Megakaryocytic


Other cytogenetic changes are associated with an average or intermediate prognosis, while others still are associated with a poor, or unfavourable prognosis. It is important to note that in most cases of AML, neither ‘good’ or ‘bad-risk’ cytogenetic changes are found. People with ‘normal’ cytogenetics are also regarded as having an average prognosis.

Some subtypes of AML are associated with specific symptoms. For example, in some subtypes of AML, leukaemic cells can spread from the blood stream into other parts of the body such as the gums, causing swelling and discomfort. Acute promyelocytic leukaemia (APML or M3) is associated with bleeding and abnormalities in blood clotting.
How common is it ?

HERE PICTURED MINE EXTREME NEED OF NEW PLATELETS TRANSFUSION

Each year in Australia around 900 people are diagnosed with AML. Overall AML is rare, accounting for 0.8% of all cancers diagnosed, at a rate of 3.7 per 100,000 of the population.
changes are associated with a more favourable prognosis than others. This means that they are more likely to respond well to treatment, and may even be cured. Favourable cytogenetic changes include: a translocation between chromosome 8 and 21 t(8;21), inversion of chromosome 16; inv(16) and a translocation between chromosome 15 and 17; t(15;17). This final change is found in a subtype of AML called acute promyelocytic leukaemia (APML or M3). APML is treated differently to other types of AML, and usually has the best overall prognosis.

 Most signs and symptoms of AML are caused by the replacement of normal blood cells with leukemic cells. A lack of normal white blood cell production makes the patient susceptible to infections; while the leukemic cells themselves are derived from white blood cell precursors, they have no infection-fighting capacity. A drop in red blood cell count (anemia) can cause fatigue, paleness, and shortness of breath. A lack of platelets can lead to easy bruising or bleeding with minor trauma.

HERE IN PHOTO MY HOSPITAL BED WHICH IS MY 24H longtime LOCATION


The early signs of AML are often vague and nonspecific, and may be similar to those of influenza or other common illnesses. Some generalized symptoms include fever, fatigue, weight loss or loss of appetite, shortness of breath, anemia, easy bruising or bleeding, petechiae (flat, pin-head sized spots under the skin caused by bleeding), bone and joint pain, and persistent or frequent infectionS.

 Treatment needs to begin soon after AML is diagnosed, as it progresses very quickly. The type of treatment used will depend on a number of factors including the sub-type of AML, the genetic make-up of the leukaemic cells, general health and age.

Chemotherapy is the main form of treatment for AML. Initially, the aim of treatment is to destroy leukaemic cells and induce a remission. This means that there is no evidence of leukaemic cells in the blood and bone marrow and that normal blood cell production and normal blood counts are restored. Once a remission has been achieved, more chemotherapy is given in an effort to prevent the leukaemia from returning (relapsing). This is called post-remission or consolidation therapy.


HERE IN PHOTO SOME OTHER CHEMICAL AND PHARMACOLOGICAL INFUSIONS 24H


Chemotherapy is usually given as a combination of drugs, usually over a period of a week or so. In most cases the drugs are given as infusions through a special line called a central venous catheter, which will be inserted before treatment begins.

People with a sub-type of AML called acute promyelocytic leukaemia (APML), may also be treated with a non-chemotherapy drug called all-trans retinoic acid (ATRA), a derivative of vitamin A, which helps make the leukaemic cells either mature properly, or die.

Occasionally, a stem cell transplant may be used. This increases the chance of cure for some people with AML.

 All treatments can cause side-effects. The type and severity of side effects will vary between individuals, depending on the type of treatment used and how each individual responds to it. In general, more intensive treatment is associated with more severe side-effects. It is important that symptoms are reported immediately to your doctor or nurse, as in most cases they can be treated and are reversible.

AML affects the ability of the bone marrow to produce adequate numbers of blood cells and platelets, and chemotherapy reduces this ability even further. Blood counts generally fall within a week of treatment and may take some time to recover, depending on the type and doses of drugs used. During this time, you are likely to need antibiotics and other drugs to treat, or prevent infection. You are also likely to need blood transfusions to treat severe anaemia, and platelet transfusions to reduce the risk of bleeding.

In AML, the myeloid stem cells usually become a type of immature white blood cell called myeloblasts (or myeloid blasts). The myeloblasts in AML are abnormal and do not become healthy white blood cells. Sometimes in AML, too many stem cells become abnormal red blood cells or platelets. These abnormal white blood cells, red blood cells, or platelets are also called leukemia cells or blasts. Leukemia cells can build up in the bone marrow and blood so there is less room for healthy white blood cells, red blood cells, and platelets. When this happens, infection, anemia, or easy bleeding may occur. The leukemia cells can spread outside the blood to other parts of the body, including the central nervous system (brain and spinal cord), skin, and gums.

Other possible side-effects of chemotherapy include:


 feeling sick - nausea and/or vomiting
 feeling tired and weak
 hair loss and thinning
 mouth problems such as mucositis or ulcers
 diarrhoea or constipation
 skin problems sych as dryness, rash or sensitivity to sunlight
 fertility problems.


Outlook for  AML
Your age when you were diagnosed plays a big part in your likely outcome. Generally, the younger you are, the more likely your treatment is to work well. This is partly because leukaemia behaves in different ways in different people. And partly because younger people are better able to cope physically with the very intensive treatments that are more likely to cure leukaemia. But specialists and researchers are working on ways of adapting the very intensive treatments so they are also suitable for older people.

Of all adults diagnosed with acute myeloid leukaemia, on average around a quarter (25%) will live for at least 5 years. Younger adults tend to do much better than older people. For example, more than half (50%) of the people under 45 diagnosed with AML will live for at least 5 years. Some of these people will be cured. But in others the AML will come back. Unfortunately, we can’t tell in advance who has been cured and who will relapse.

In people over 65 years of age the outlook tends not to be so good and around 12 out of 100 people (12%) are alive for more than 5 years.

It may sound harsh to ask the question, “Can I survive this?” But it’s a question on the minds of most people facing a diagnosis of leukemia. And hearing the answer can be just as hard as asking the question.

But should be noticed this list here below:

(Here pictured The only Frank's picture on the web taken in hospital after termination of 2nd cycle of hard chemiotherapy........(The mask is to protect me to get outside crap .............and more.................

Points to remember:

- I never smoked.

- I never drunk.

- Worked a lot (many people said ways too much)

- I have a very very  bad family  (Parents mainly + brother  + sister worst persons to encounter in a life and recently confirmed to be socially dangerous at my risk)

- I have a very unfortunate life, which was/is constantly creating against me anykind of unecessary increasing beastly difficulties of any kind of type !

- I don't actually have a job and don't have chances to have one in the future if I survive this.

- I have already a such called other phisical invalidity collected years ago on a job plus this new crap of todays, which will develop more issues after time.

- I live actually in a country which is populated by the most selfish, ignorant, unhelpful bastards of the world confirmed another time by some hospital nurse (male) crappy behaviour against me which landed him to be rightfully beaten by me !!!!.

- I never loved life starting from child (this because of people and family combined behaviour and many earlier health factors).

EDIT OF 05/2/2015:
- SUCCESSFULLY (FOR NOW)SURPASSED 2 CYCLE OF HARD CHEMOTHERAPY WITH DISCRETE SIDE EFFECTS MAINLY  CONCENTRATED IN:

 Cancer and cancer treatment often cause a variety of side effects CLICK FOR INFOS.

- AND.................... SURPRISINGLY PARENTS AND SOME PEOPLE ARE CREATING MORE ISSUES.........THAN  THE
 CANCER ITSELF AND HIS CURE !!!!!!!!!!!!!!!!


EDIT OF 12/3/2015:

- FRANK DID HIS FURTHER HARD TREATMENTS WITH HARD CHEMOTHERAPY COMPATIBLE WITH HIS HIGH RISK.
- GOT A PNEUMONIA INFECTION BUT POINTLY STOPPED BEFORE FURTHER DANGER INCOMING.
- GOT FEWER
- GOT FURTHER EARING DISEASE.
- GOT SEVERAL ISSUES IN EATING UNTIL STOPPED EATING, NOW SUPPLYED ARTIFICIALLY, BUT RECOVERABLE.
- LOST 17KG OF WEIGHT.
- LOST HIS OWN BIG WELL KNOWN POWER.
- LOST SLEEP,...........BY AGES.
- ALMOST 24HR IN BED.

EDIT OF 15/4/2015:

- FRANK DID HIS FURTHER 4th HARD TREATMENTS WITH HARD
 CHEMOTHERAPY COMPATIBLE WITH HIS HIGH RISK.
- GOT A PNEUMONIA INFECTION BUT POINTLY STOPPED
BEFORE FURTHER DANGER INCOMING.
- GOT FEWER
- GOT FURTHER EARING DISEASE.
- GOT SEVERAL ISSUES IN EATING UNTIL STOPPED EATING,
 SUPPLYED ARTIFICIALLY, BUT RECOVERABLE.
- LOST 19KG OF WEIGHT.
- LOST HIS OWN BIG WELL KNOWN POWER.
- LOST SLEEP,...........BY AGES.
- ALMOST 24HR IN BED.

EDIT OF 16/4/2015:

- FRANK DID HIS 5th FURTHER HARD TREATMENTS WITH HARD CHEMOTHERAPY
COMPATIBLE WITH HIS HIGH RISK.
- GOT A MORE PNEUMONIA INFECTION BUT POINTLY STOPPED BEFORE FURTHER
DANGER INCOMING.
- GOT FEWER
- GOT MORE FURTHER EARING DISEASE.
- GOT SEVERAL ISSUES IN EATING UNTIL STOPPED EATING,
THEN SUPPLYED ARTIFICIALLY, BUT RECOVERED AFTER
- LOST 23KG OF WEIGHT.
- LOST HIS OWN BIG WELL KNOWN POWER.
- LOST SLEEP,...........BY AGES.
- ALMOST 24HR IN BED.

EDIT OF 19/4/2015:

FRANK RETURNED TO HOME FOR AN UNDEFINED TIME COMBINED WITH MANDATORY MORE THERAPY ASSISTED BY HOSPITAL AND ADVANCED MANDATORY CONTINUOS  MEDICAL ASSITANCE.

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....................TO BE CONTINUED...............
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I have many several difficulties like walking ,looking, speaking, writing. thinking, sleeping.....eating.....drinking....memory....coordination........

REGARDS, 

ELECTRONIC, PROFESSOR, ENGINEER  FRANK SHARP.

 

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