Diagnosis is typically made based on a history of significant radiation exposure and suitable clinical findings. An absolute lymphocyte count can give a rough estimate of radiation exposure. Time from exposure to vomiting can also give estimates of exposure levels if they are less than 1000 rad.

The longer that humans are subjected to radiation the larger the dose will be. The advice in the nuclear war manual entitled "Nuclear War Survival Skills" published by Cresson Kearny in the U.S. was that if one needed to leave the shelter then this should be done as rapidly as possible to minimize exposure.

In chapter 12, he states that ""[q]uickly putting or dumping wastes outside is not hazardous once fallout is no longer being deposited. For example, assume the shelter is in an area of heavy fallout and the dose rate outside is 400 roentgen (R) per hour, enough to give a potentially fatal dose in about an hour to a person exposed in the open. If a person needs to be exposed for only 10 seconds to dump a bucket, in this 1/360 of an hour he will receive a dose of only about 1 R. Under war conditions, an additional 1-R dose is of little concern."" In peacetime, radiation workers are taught to work as quickly as possible when performing a task which exposes them to radiation. For instance, the recovery of a lost radiography source should be done as quickly as possible.

The associations between ionizing radiation exposure and the development of cancer are based primarily on the "LSS cohort" of Japanese atomic bomb survivors, the largest human population ever exposed to high levels of ionizing radiation. However this cohort was also exposed to high heat, both from the initial nuclear "flash" of infrared light and following the blast due their exposure to the firestorm and general fires that developed in both cities respectively, so the survivors also underwent Hyperthermia therapy to various degrees. Hyperthermia, or heat exposure following irradiation is well known in the field of radiation therapy to markedly increase the severity of free-radical insults to cells following irradiation. Presently however no attempts have been made to cater for this confounding factor, it is not included or corrected for in the dose-response curves for this group.

Additional data has been collected from recipients of selected medical procedures and the 1986 Chernobyl disaster. There is a clear link (see the UNSCEAR 2000 Report, Volume 2: Effects) between the Chernobyl accident and the unusually large number, approximately 1,800, of thyroid cancers reported in contaminated areas, mostly in children.

For low levels of radiation, the biological effects are so small they may not be detected in epidemiological studies. Although radiation may cause cancer at high doses and high dose rates, public health data regarding lower levels of exposure, below about 10 mSv (1,000 mrem), are harder to interpret. To assess the health impacts of lower radiation doses, researchers rely on models of the process by which radiation causes cancer; several models that predict differing levels of risk have emerged.

Studies of occupational workers exposed to chronic low levels of radiation, above normal background, have provided mixed evidence regarding cancer and transgenerational effects. Cancer results, although uncertain, are consistent with estimates of risk based on atomic bomb survivors and suggest that these workers do face a small increase in the probability of developing leukemia and other cancers. One of the most recent and extensive studies of workers was published by Cardis, "et al." in 2005 . There is evidence that low level, brief radiation exposures are not harmful.

Low-dose exposures, such as living near a nuclear power plant or a coal-fired power plant, which has higher emissions than nuclear plants, are generally believed to have no or very little effect on cancer development, barring accidents. Greater concerns include radon in buildings and overuse of medical imaging.

The International Commission on Radiological Protection (ICRP) recommends limiting artificial irradiation of the public to an average of 1 mSv (0.001 Sv) of effective dose per year, not including medical and occupational exposures. For comparison, radiation levels inside the US capitol building are 0.85 mSv/yr, close to the regulatory limit, because of the uranium content of the granite structure. According to the ICRP model, someone who spent 20 years inside the capitol building would have an extra one in a thousand chance of getting cancer, over and above any other existing risk. (20 yr X 0.85 mSv/yr X 0.001 Sv/mSv X 5.5%/Sv = ~0.1%) That "existing risk" is much higher; an average American would have a one in ten chance of getting cancer during this same 20-year period, even without any exposure to artificial radiation.

Internal contamination due to ingestion, inhalation, injection, or absorption is a particular concern because the radioactive material may stay in the body for an extended period of time, "committing" the subject to accumulating dose long after the initial exposure has ceased, albeit at low dose rates. Over a hundred people, including Eben Byers and the radium girls, have received committed doses in excess of 10 Gy and went on to die of cancer or natural causes, whereas the same amount of acute external dose would invariably cause an earlier death by acute radiation syndrome.

Internal exposure of the public is controlled by regulatory limits on the radioactive content of food and water. These limits are typically expressed in becquerel/kilogram, with different limits set for each contaminant.

Chronic radiation syndrome is a constellation of health effects that occur after months or years of chronic exposure to high amounts of ionizing radiation. Chronic radiation syndrome develops with a speed and severity proportional to the radiation dose received, i.e., it is a deterministic effect of radiation exposure, unlike radiation-induced cancer. It is distinct from acute radiation syndrome in that it occurs at dose rates low enough to permit natural repair mechanisms to compete with the radiation damage during the exposure period. Dose rates high enough to cause the acute form (> ~0.1 Gy/h) are fatal long before onset of the chronic form. The lower threshold for chronic radiation syndrome is between 0.7 and 1.5 Gy, at dose rates above 0.1 Gy/yr. This condition is primarily known from the Kyshtym disaster, where 66 cases were diagnosed, and has received little mention in Western literature. A future ICRP publication, currently in draft, may recognize the condition but with higher thresholds.

In 2013, Alexander V. Akleyev described the chronology of the clinical course or CRS while presenting at ConRad in Munich, Germany. In his presentation, he defined the latent period as being 1-5 years, and the formation coinciding with the period of maximum radiation dose. The recovery period was described as being 3-12 months after exposure ceased. He concluded that "CRS represents a systemic response of the body as a whole to the chronic total body exposure in man." In 2014, Akleyev's book "Comprehensive analysis of chronic radiation syndrome, covering epidemiology, pathogenesis, pathoanatomy, diagnosis and treatment" was published by Springer.

Fluoroscopy may cause burns if performed repeatedly or for too long.

Similarly, Computed Tomography and traditional Projectional Radiography have the potential to cause radiation burns if the exposure factors and exposure time are not appropriately controlled by the operator.

A study of radiation induced skin injuries has been performed by the Food and Drug Administration (FDA) based on results from 1994, followed by an advisory to minimize further fluoroscopy-induced injuries. The problem of radiation injuries due to fluoroscopy has been further investigated in review articles in 2000, 2001, 2009 and 2010.

Radiation burns should be covered by a clean, dry dressing as soon as possible to prevent infection. Wet dressings are not recommended. The presence of combined injury (exposure to radiation plus trauma or radiation burn) increases the likelihood of generalized sepsis. This requires administration of systemic antimicrobial therapy.

Poisoning is a condition or a process in which an organism becomes chemically harmed (poisoned) by a toxic substance or venom of an animal.

Acute poisoning is exposure to a poison on one occasion or during a short period of time. Symptoms develop in close relation to the degree of exposure. Absorption of a poison is necessary for systemic poisoning (that is, in the blood throughout the body). In contrast, substances that destroy tissue but do not absorb, such as lye, are classified as corrosives rather than poisons. Furthermore, many common household medications are not labeled with skull and crossbones, although they can cause severe illness or even death. In the medical sense, toxicity and poisoning can be caused by less dangerous substances than those legally classified as a poison. Toxicology is the study and practice of the symptoms, mechanisms, diagnosis, and treatment of poisoning.

Chronic poisoning is long-term repeated or continuous exposure to a poison where symptoms do not occur immediately or after each exposure. The patient gradually becomes ill, or becomes ill after a long latent period. Chronic poisoning most commonly occurs following exposure to poisons that bioaccumulate, or are biomagnified, such as mercury, gadolinium, and lead.

Contact or absorption of poisons can cause rapid death or impairment. Agents that act on the nervous system can paralyze in seconds or less, and include both biologically derived neurotoxins and so-called nerve gases, which may be synthesized for warfare or industry.

Inhaled or ingested cyanide, used as a method of execution in gas chambers, almost instantly starves the body of energy by inhibiting the enzymes in mitochondria that make ATP. Intravenous injection of an unnaturally high concentration of potassium chloride, such as in the execution of prisoners in parts of the United States, quickly stops the heart by eliminating the cell potential necessary for muscle contraction.

Most biocides, including pesticides, are created to act as poisons to target organisms, although acute or less observable chronic poisoning can also occur in non-target organisms (secondary poisoning), including the humans who apply the biocides and other beneficial organisms. For example, the herbicide 2,4-D imitates the action of a plant hormone, which makes its lethal toxicity specific to plants. Indeed, 2,4-D is not a poison, but classified as "harmful" (EU).

Many substances regarded as poisons are toxic only indirectly, by toxication. An example is "wood alcohol" or methanol, which is not poisonous itself, but is chemically converted to toxic formaldehyde and formic acid in the liver. Many drug molecules are made toxic in the liver, and the genetic variability of certain liver enzymes makes the toxicity of many compounds differ between individuals.

Exposure to radioactive substances can produce radiation poisoning, an unrelated phenomenon.

Early detection is key. Untreated patients usually live 5 to 8 months after diagnosis.

Although not yet formally incorporated in the generally accepted classification systems, molecular profiling of myelodysplastic syndrome genomes has increased the understanding of prognostic molecular factors for this disease. For example, in low-risk MDS, "IDH1" and "IDH2" mutations are associated with significantly worsened survival.

Diagnosis is usually based on repeated complete blood counts and a bone marrow examination following observations of the symptoms. Sometimes, blood tests may not show that a person has leukemia, especially in the early stages of the disease or during remission. A lymph node biopsy can be performed to diagnose certain types of leukemia in certain situations.

Following diagnosis, blood chemistry tests can be used to determine the degree of liver and kidney damage or the effects of chemotherapy on the patient. When concerns arise about other damage due to leukemia, doctors may use an X-ray, MRI, or ultrasound. These can potentially show leukemia's effects on such body parts as bones (X-ray), the brain (MRI), or the kidneys, spleen, and liver (ultrasound). CT scans can be used to check lymph nodes in the chest, though this is uncommon.

Despite the use of these methods to diagnose whether or not a patient has leukemia, many people have not been diagnosed because many of the symptoms are vague, non-specific, and can refer to other diseases. For this reason, the American Cancer Society estimates that at least one-fifth of the people with leukemia have not yet been diagnosed.

Unlike its differentiated counterparts, anaplastic thyroid cancer is highly unlikely to be curable either by surgery or by any other treatment modality, and is in fact usually unresectable due to its high propensity for invading surrounding tissues.

Palliative treatment consists of radiation therapy usually combined with chemotherapy.

New drugs, such as fosbretabulin (a type of combretastatin), bortezomib and TNF-Related Apoptosis Induced Ligand (TRAIL), are however being under investigation "in vitro" and in human clinical studies. Based on encouraging Phase I and II clinical trial results with fosbretabulin, a type of drug that selectively destroys tumor blood vessels, a large, multi-national clinical trial is being undertaken to determine whether the drug can extend the survival of patients with ATC.

The treatment of choice is a large resection or amputation of the affected limb. Radiation therapy can precede or follow surgical treatment. Tumors that have advanced locally or have metastasized can be treated with mono or polychemotherapy, systemically or locally. However, chemotherapy and radiation therapy have not been shown to improve survivorship significantly.

Following observation of the symptoms, the patients need to get complete blood counts and a bone marrow examination. If the patient has leukemia, the morphology and immunophenotype check is needed to make sure the type of leukemia.

The morphology of the blast in BAL is not certain. The cells could display both myeloid lineage and lymphoid or undifferentiated morphology. Therefore, the diagnosis cannot based on the morphology result. The immunophenotype check is the most important basis of the diagnosis of BAL.

Before 2008, the diagnosis of BAL was based on a score system proposed by the European Group for the Immunological Classification of Leukemias (EGIL) which could differentiate from other kinds of acute leukemia. The table shows this method.

If the score of only one lineage is higher than 2, the acute leukemia could be acute myeloid leukemia (AML) or acute lymphoblastic leukemia (ALL). According to the original EGIL scoring system BAL is defined when scores are over two points for both myeloid and T- or B- lymphoid lineages.

In 2008, WHO established a new and strict criteria standard for diagnosis of BAL. The presence of specific T-lymphoid antigens, cytoplasmic CD3 (cCD3), MPO and CD 19 became the most important standard for recognizing the lineage. Other B-lineage markers (CD22, CD79a, CD 10) and monocytic markers are also needed. Table 2 shows the method.

Compared with the EGIL scoring system, the current 2008 WHO criteria applied less but more specific markers to define the lineage of the blasts, and incorporated the intensity of markers expression into the diagnostic algorithm.

The diagnosis of BAL is so difficult that sometimes is misdiagnosed with AML or ALL because the morphology thus the therapy would not have a good effect.

Evidence is conflicting on the prognostic significance of chloromas in patients with acute myeloid leukemia. In general, they are felt to augur a poorer prognosis, with a poorer response to treatment and worse survival; however, others have reported chloromas associate, as a biologic marker, with other poor prognostic factors, and therefore do not have independent prognostic significance.

The role of external beam radiotherapy (EBRT) in thyroid cancer remains controversial and there is no level I evidence to recommend its use in the setting of differentiated thyroid cancers such as papillary and follicular carcinomas. Anaplastic thyroid carcinomas, however, are histologically distinct from differentiated thyroid cancers and due to the highly aggressive nature of ATC aggressive postoperative radiation and chemotherapy are typically recommended.

The National Comprehensive Cancer Network Clinical Practice Guidelines currently recommend that postoperative radiation and chemotherapy be strongly considered. No published randomised controlled trials have examined the addition of EBRT to standard treatment, namely surgery. Radioactive iodine is typically ineffective in the management of ATC as it is not an iodine-avid cancer.

Imbalances in age, sex, completeness of surgical excision, histological type and stage, between patients receiving and not receiving EBRT, confound retrospective studies. Variability also exists between treatment and non-treatment groups in the use of radio-iodine and post-treatment thyroid stimulating hormone (TSH) suppression and treatment techniques between and within retrospective studies.

Some recent studies have indicated that EBRT may be promising, though the number of patients studies has been small.

Clinical trials for investigational treatments are often considered by healthcare professionals and patients as first-line treatment.

Radiation-induced thyroiditis is a form of painful, acute thyroiditis resulting from radioactive therapy to treat hyperthyroidism or from radiation to treat head and neck cancer or lymphoma. It affects 1% of those who have received radioactive iodine (I-131) therapy for Graves' Disease, typically presenting between 5 and 10 days after the procedure. Stored T and T are released as rapid destruction of thyroid tissue occurs, resulting in pain, tenderness, and exacerbation of hyperthyroidism.

Lymphoma Association (UK)

Nodular Lymphocyte Predominant Hodgkin's Lymphoma (NLPHL) Facebook Group

Diagnosis usually occurs at an early stage of disease progression.

The prognosis for BAL patients is not good which is worse than ALL and AML. Medical Blood Institute reported cases of CR rate was 31.6%, with a median remission are less than 6 months

The median survival time is only 7.5 months. The life quality is also low because the immune function of patient is damaged seriously. They have to stay in hospital and need 24h care.

In another study, the results showed that young age, normal karyotype and ALL induction therapy will have a better prognosis than Ph+, adult patients. The study shows median survival of children is 139 months versus 11 months of adults, 139 months for normal karyotype patients versus 8 months for ph+ patients.

The first clue to a diagnosis of AML is typically an abnormal result on a complete blood count. While an excess of abnormal white blood cells (leukocytosis) is a common finding with the leukemia, and leukemic blasts are sometimes seen, AML can also present with isolated decreases in platelets, red blood cells, or even with a low white blood cell count (leukopenia). While a presumptive diagnosis of AML can be made by examination of the peripheral blood smear when there are circulating leukemic blasts, a definitive diagnosis usually requires an adequate bone marrow aspiration and biopsy as well as ruling out pernicious anemia (Vitamin B12 deficiency), folic acid deficiency and copper deficiency.

Marrow or blood is examined under light microscopy, as well as flow cytometry, to diagnose the presence of leukemia, to differentiate AML from other types of leukemia (e.g. acute lymphoblastic leukemia - ALL), and to classify the subtype of disease. A sample of marrow or blood is typically also tested for chromosomal abnormalities by routine cytogenetics or fluorescent "in situ" hybridization. Genetic studies may also be performed to look for specific mutations in genes such as "FLT3", nucleophosmin, and "KIT", which may influence the outcome of the disease.

Cytochemical stains on blood and bone marrow smears are helpful in the distinction of AML from ALL, and in subclassification of AML. The combination of a myeloperoxidase or Sudan black stain and a nonspecific esterase stain will provide the desired information in most cases. The myeloperoxidase or Sudan black reactions are most useful in establishing the identity of AML and distinguishing it from ALL. The nonspecific esterase stain is used to identify a monocytic component in AMLs and to distinguish a poorly differentiated monoblastic leukemia from ALL.

The diagnosis and classification of AML can be challenging, and should be performed by a qualified hematopathologist or hematologist. In straightforward cases, the presence of certain morphologic features (such as Auer rods) or specific flow cytometry results can distinguish AML from other leukemias; however, in the absence of such features, diagnosis may be more difficult.

The two most commonly used classification schemata for AML are the older French-American-British (FAB) system and the newer World Health Organization (WHO) system. According to the widely used WHO criteria, the diagnosis of AML is established by demonstrating involvement of more than 20% of the blood and/or bone marrow by leukemic myeloblasts, except in the three best prognosis forms of acute myeloid leukemia with recurrent genetic abnormalities (t(8;21), inv(16), and t(15;17)) in which the presence of the genetic abnormality is diagnostic irrespective of blast percent. The French–American–British (FAB) classification is a bit more stringent, requiring a blast percentage of at least 30% in bone marrow (BM) or peripheral blood (PB) for the diagnosis of AML. AML must be carefully differentiated from "preleukemic" conditions such as myelodysplastic or myeloproliferative syndromes, which are treated differently.

Because acute promyelocytic leukemia (APL) has the highest curability and requires a unique form of treatment, it is important to quickly establish or exclude the diagnosis of this subtype of leukemia. Fluorescent "in situ" hybridization performed on blood or bone marrow is often used for this purpose, as it readily identifies the chromosomal translocation [t(15;17)(q22;q12);] that characterizes APL. There is also a need to molecularly detect the presence of PML/RARA fusion protein, which is an oncogenic product of that translocation.

Definitive diagnosis of a chloroma usually requires a biopsy of the lesion in question. Historically, even with a tissue biopsy, pathologic misdiagnosis was an important problem, particularly in patients without a clear pre-existing diagnosis of acute myeloid leukemia to guide the pathologist. In one published series on chloroma, the authors stated that 47% of the patients were initially misdiagnosed, most often as having a malignant lymphoma.

However, with advances in diagnostic techniques, the diagnosis of chloromas can be made more reliable. Traweek et al. described the use of a commercially available panel of monoclonal antibodies, against myeloperoxidase, CD68, CD43, and CD20, to accurately diagnose chloroma via immunohistochemistry and differentiate it from lymphoma. Nowadays, immunohistochemical staining using monoclonal antibodies against CD33 and CD117 would be the mainstay of diagnosis. The increasingly refined use of flow cytometry has also facilitated more accurate diagnosis of these lesions.

Diagnosing ALL begins with a thorough medical history, physical examination, complete blood count, and blood smears. While many symptoms of ALL can be found in common illnesses, persistent or unexplained symptoms raise suspicion of cancer. Because many features on the medical history and exam are not specific to ALL, further testing is often needed. A large number of white blood cells and lymphoblasts in the circulating blood can be suspicious for ALL because they indicate a rapid production of lymphoid cells in the marrow. The higher these numbers typically points to a worse prognosis. While white blood cell counts at initial presentation can vary significantly, circulating lymphoblast cells are seen on peripheral blood smears in the majority of cases.

A bone marrow biopsy provides conclusive proof of ALL, typically with >20% of all cells being leukemic lymphoblasts. A lumbar puncture (also known as a spinal tap) can determine whether the spinal column and brain have been invaded. Brain and spinal column involvement can be diagnosed either through confirmation of leukemic cells in the lumbar puncture or through clinical signs of CNS leukemia as described above. Laboratory tests that might show abnormalities include blood count, kidney function, electrolyte, and liver enzyme tests.

Pathological examination, cytogenetics (in particular the presence of Philadelphia chromosome), and immunophenotyping establish whether the leukemic cells are myeloblastic (neutrophils, eosinophils, or basophils) or lymphoblastic (B lymphocytes or T lymphocytes). Cytogenetic testing on the marrow samples can help classify disease and predict how aggressive the disease course will be. Different mutations have been associated with shorter or longer survival. Immunohistochemical testing may reveal TdT or CALLA antigens on the surface of leukemic cells. TdT is a protein expressed early in the development of pre-T and pre-B cells, whereas CALLA is an antigen found in 80% of ALL cases and also in the "blast crisis" of CML.

Medical imaging (such as ultrasound or CT scanning) can find invasion of other organs commonly the lung, liver, spleen, lymph nodes, brain, kidneys, and reproductive organs.

Leukemia is rarely associated with pregnancy, affecting only about 1 in 10,000 pregnant women. How it is handled depends primarily on the type of leukemia. Nearly all leukemias appearing in pregnant women are acute leukemias. Acute leukemias normally require prompt, aggressive treatment, despite significant risks of pregnancy loss and birth defects, especially if chemotherapy is given during the developmentally sensitive first trimester. Chronic myelogenous leukemia can be treated with relative safety at any time during pregnancy with Interferon-alpha hormones. Treatment for chronic lymphocytic leukemias, which are rare in pregnant women, can often be postponed until after the end of the pregnancy.

The outlook in MDS is variable, with about 30% of patients progressing to refractory AML. The median survival rate varies from years to months, depending on type. Stem-cell transplantation offers possible cure, with survival rates of 50% at 3 years, although older patients do poorly.

Indicators of a good prognosis:

Younger age; normal or moderately reduced neutrophil or platelet counts; low blast counts in the bone marrow (< 20%) and no blasts in the blood; no Auer rods; ringed sideroblasts; normal or mixed karyotypes without complex chromosome abnormalities; and "in vitro" marrow culture with a nonleukemic growth pattern

Indicators of a poor prognosis:

Advanced age; severe neutropenia or thrombocytopenia; high blast count in the bone marrow (20-29%) or blasts in the blood;

Auer rods; absence of ringed sideroblasts; abnormal localization or immature granulocyte precursors in bone marrow section;

completely or mostly abnormal karyotypes, or complex marrow chromosome abnormalities and "in vitro" bone marrow culture with a leukemic growth pattern

Karyotype prognostic factors:

- Good: normal, -Y, del(5q), del(20q)

- Intermediate or variable: +8, other single or double anomalies

- Poor: complex (>3 chromosomal aberrations); chromosome 7 anomalies

The IPSS is the most commonly used tool in MDS to predict long-term outcome.

Cytogenetic abnormalities can be detected by conventional cytogenetics, a FISH panel for MDS, or virtual karyotype.