Thrombocytopenia usually has no symptoms and is picked up on a routine full blood count (or complete blood count). Some individuals with thrombocytopenia may experience external bleeding such as nosebleeds, and/or bleeding gums. Some women may have heavier or longer periods or breakthrough bleeding. Bruising, particularly purpura in the forearms and petechiae in the feet, legs, and mucous membranes, may be caused by spontaneous bleeding under the skin.

Eliciting a full medical history is vital to ensure the low platelet count is not secondary to another disorder. It is also important to ensure that the other blood cell types, such as red blood cells and white blood cells, are not also suppressed.

Painless, round and pinpoint (1 to 3 mm in diameter) petechiae usually appear and fade, and sometimes group to form ecchymoses. Larger than petechiae, ecchymoses are purple, blue or yellow-green areas of skin that vary in size and shape. They can occur anywhere on the body.

A person with this disease may also complain of malaise, fatigue and general weakness (with or without accompanying blood loss). Acquired thrombocytopenia may be associated with a history of drug use. Inspection typically reveals evidence of bleeding (petechiae or ecchymoses), along with slow, continuous bleeding from any injuries or wounds. Adults may have large, blood-filled bullae in the mouth. If the person's platelet count is between 30,000 and 50,000/mm, bruising with minor trauma may be expected; if it is between 15,000 and 30,000/mm, spontaneous bruising will be seen (mostly on the arms and legs).

High platelet levels do not necessarily signal any clinical problems, and are picked up on a routine full blood count. However, it is important that a full medical history be elicited to ensure that the increased platelet count is not due to a secondary process. Often, it occurs in tandem with an inflammatory disease, as the principal stimulants of platelet production (e.g. thrombopoietin) are elevated in these clinical states as part of the acute phase reaction.

High platelet counts can occur in patients with polycythemia vera (high red blood cell counts), and is an additional risk factor for complications.

A very small segment of patients report symptoms of erythromelalgia, a burning sensation and redness of the extremities that resolves with cooling and/or aspirin use.

Scientific literature sometimes excludes thrombocytosis from the scope of thrombophilia by definition, but practically, by the definition of thrombophilia as an increased predisposition to thrombosis, thrombocytosis (especially primary thrombocytosis) is a potential cause of thrombophilia. Conversely, secondary thrombocytosis very rarely causes thrombotic complications.

Thrombocytosis (or thrombocythemia) is the presence of high platelet counts in the blood, and can be either primary (also termed essential and caused by a myeloproliferative disease) or reactive (also termed secondary). Although often symptomless (particularly when it is a secondary reaction), it can predispose to thrombosis in some patients. Thrombocytosis can be contrasted with thrombocytopenia, a loss of platelets in the blood.

In a healthy individual, a normal platelet count ranges from 150,000 and 450,000 per mm³ (or microlitre) (150–450 x 10/L). These limits, however, are determined by the 2.5th lower and upper percentile, and a deviation does not necessary imply any form of disease. Nevertheless, counts over 750,000 (and especially over a million) are considered serious enough to warrant investigation and intervention.

Thrombocytopenia is a condition characterized by abnormally low levels of thrombocytes, also known as platelets, in the blood.

A normal human platelet count ranges from 150,000 to 450,000 platelets per microliter of blood. These limits are determined by the 2.5th lower and upper percentile, so values outside this range do not necessarily indicate disease. One common definition of thrombocytopenia requiring emergency treatment is a platelet count below 50,000 per microliter.

Most people with ET are without symptoms referable to ET at the time of diagnosis, which is usually ultimately made after noting an elevated platelet level on a routine complete blood count (CBC). The most common symptoms are bleeding (due to dysfunctional platelets), blood clots (e.g., deep vein thrombosis or pulmonary embolism), headache, nausea, vomiting, abdominal pain, visual disturbances, dizziness, fainting, and numbness in the extremities; the most common signs are increased white blood cell count, reduced red blood cell count, and an enlarged spleen.

Immune thrombocytopenia (ITP) is a type of thrombocytopenic purpura defined as isolated low platelet count (thrombocytopenia) with normal bone marrow and the absence of other causes of thrombocytopenia. It causes a characteristic purpuric rash and an increased tendency to bleed. Two distinct clinical syndromes manifest as an acute condition in children and a chronic condition in adults. The acute form often follows an infection and has a spontaneous resolution within two months. Chronic immune thrombocytopenia persists longer than six months with a specific cause being unknown.

ITP is an autoimmune disease with antibodies detectable against several platelet surface antigens.

ITP is diagnosed by a low platelet count in a complete blood count (a common blood test). However, since the diagnosis depends on the exclusion of other causes of a low platelet count, additional investigations (such as a bone marrow biopsy) may be necessary in some cases.

In mild cases, only careful observation may be required but very low counts or significant bleeding may prompt treatment with corticosteroids, intravenous immunoglobulin, anti-D immunoglobulin, or immunosuppressive drugs. "Refractory ITP" (not responsive to conventional treatment) may require splenectomy, the surgical removal of the spleen. Platelet transfusions may be used in severe bleeding together with a very low count. Sometimes the body may compensate by making abnormally large platelets.

The signs and symptoms of TTP may at first be subtle and nonspecific. Many people experience an influenza-like or diarrheal illness before developing TTP. Neurological symptoms are very common and vary greatly in severity. Frequently reported symptoms include feeling very tired, confusion, and headaches. Seizures and symptoms similar to those of a stroke can also be seen.

As TTP progresses, blood clots form within small blood vessels (microvasculature), and platelets (clotting cells) are consumed. As a result, bruising, and rarely bleeding can occur. The bruising often takes the form of purpura, while the most common site of bleeding, if it occurs, is from the nose or gums. Larger bruises (ecchymoses) may also develop.

The classic presentation of TTP includes a constellation of five medical signs which classically support the clinical diagnosis of TTP, although it is unusual for patients to present with all 5 symptoms. The pentad includes:

- Fever

- Changes in mental status

- Thrombocytopenia

- Reduced kidney function

- Haemolytic anaemia (microangiopathic hemolytic anemia).

High blood pressure (hypertension) may be found on examination.

The following revised diagnostic criteria for essential thrombocythaemia were proposed in 2005. The diagnosis requires the presence of both A criteria together with B3 to B6, or of criterion A1 together with B1 to B6. The criteria are as follows:

- A1. Platelet count > 450 × 10/µL for at least 2 months.

- A2. Acquired V617F JAK2 mutation present

- B1. No cause for a reactive thrombocytosis

- normal inflammatory indices

- B2. No evidence of iron deficiency

- stainable iron in the bone marrow or normal red cell mean corpuscular volume

- B3. No evidence of polycythemia vera

- hematocrit < midpoint of normal range or normal red cell mass in presence of normal iron stores

- B4. No evidence of chronic myeloid leukemia

- But the Philadelphia chromosome may be present in up to 10% of cases. Patients with the Philadelphia chromosome have a potential for the development of acute leukemia, especially acute lymphocytic leukemia.

- B5. No evidence of myelofibrosis

- no collagen fibrosis and ≤ grade 2 reticulin fibrosis (using 0–4 scale)

- B6. No evidence of a myelodysplastic syndrome

- no significant dysplasia

- no cytogenetic abnormalities suggestive of myelodysplasia

Signs include the spontaneous formation of bruises (purpura) and petechiae (tiny bruises), especially on the extremities, bleeding from the nostrils and/or gums, and menorrhagia (excessive menstrual bleeding), any of which may occur if the platelet count is below 20,000 per μl. A very low count (<10,000 per μl) may result in the spontaneous formation of hematomas (blood masses) in the mouth or on other mucous membranes. Bleeding time from minor lacerations or abrasions is usually prolonged.

Serious and possibly fatal complications due to extremely low counts (<5,000 per μl) include subarachnoid or intracerebral hemorrhage (bleeding inside the skull or brain), lower gastrointestinal bleeding or other internal bleeding. An ITP patient with an extremely low count is vulnerable to internal bleeding caused by blunt abdominal trauma, as might be experienced in a motor vehicle crash. These complications are not likely when the platelet count is above 20,000 per μl.

Pancytopenia usually requires a bone marrow biopsy in order to distinguish among different causes.

- anemia: hemoglobin < 13.5 g/dL (male) or 12 g/dL (female).

- leukopenia: total white cell count < 4.0 x 10/L. Decrease in all types of white blood cells (revealed by doing a differential count).

- thrombocytopenia: platelet count < 150×10/L.

Pancytopenia is a medical condition in which there is a reduction in the number of red and white blood cells, as well as platelets.

If only two parameters from the full blood count are low, the term bicytopenia can be used. The diagnostic approach is the same as for pancytopenia.

People with polycythemia vera can be asymptomatic. A classic symptom of polycythemia vera is pruritus or itching, particularly after exposure to warm water (such as when taking a bath), which may be due to abnormal histamine release or prostaglandin production. Such itching is present in approximately 40% of patients with polycythemia vera. Gouty arthritis may be present in up to 20% of patients. Peptic ulcer disease is also common in patients with polycythemia vera; most likely due to increased histamine from mast cells, but may be related to an increased susceptibility to infection with the ulcer-causing bacterium "H. pylori". Another possible mechanism for the development for peptic ulcer is increased histamine release and gastric hyperacidity related with polycythemia vera.

A classic symptom of polycythemia vera (and the related myeloproliferative disease essential thrombocythemia) is erythromelalgia. This is a burning pain in the hands or feet, usually accompanied by a reddish or bluish coloration of the skin. Erythromelalgia is caused by an increased platelet count or increased platelet "stickiness" (aggregation), resulting in the formation of tiny blood clots in the vessels of the extremity; it responds rapidly to treatment with aspirin.

Patients with polycythemia vera are prone to the development of blood clots (thrombosis). A major thrombotic complication (e.g. heart attack, stroke, deep venous thrombosis, or Budd-Chiari syndrome) may sometimes be the first symptom or indication that a person has polycythemia vera.

Headaches, lack of concentration and fatigue are common symptoms that occur in patients with polycythemia vera as well.

Symptoms usually present from the period of birth to early childhood as: nose bleeds, bruising, and/or gum bleeding. Problems later in life may arise from anything that can cause internal bleeding such as: stomach ulcers, surgery, trauma, or menstruation. Abnormality of the abdomen, Epistaxis, Menorrhagia, Purpura, Thrombocytopenia, and prolonged bleeding time have also been listed as symptoms of various Giant Platelet Disorders.

The most important differential diagnosis is disseminated intravascular coagulation, which is characterized with similar features but presence of a low platelet count and microcirculatory thrombosis. Antifibrinolytic treatments are contraindicated in patients with disseminated intravascular coagulation while they are useful in the treatment of primary fibrinogenolysis.

Giant platelet disorders can be further categorized:

- caused by auto-immune disorders, for example Immune thrombocytopenic purpura (ITP), and characterized by low platelet count, but high MPV (Mean-Platelet Volume).

- Caused by glycoprotein abnormalities: Bernard-Soulier syndrome, Velocardiofacial syndrome

- Caused by calpain defect: Montreal platelet syndrome

- Caused by alpha granules defect: Gray platelet syndrome

- Characterized by abnormal neutrophil inclusions: May-Hegglin anomaly, Sebastian syndrome

- With systemic manifestations: Hereditary macrothrombocytopenia with hearing loss, Epstein syndrome, Fechtner syndrome

- With no specific abnormalities: Mediterranean macrothrombocytopenia

- Harris platelet syndrome

Signs and symptoms of neutropenia include fever, painful swallowing, gingival pain, skin abscesses, and otitis. These symptoms may exist because individuals with neutropenia often have infection

Children may show signs of irritability, and poor feeding. Additionally, hypotension has also been observed in individuals who suffer from this condition

Polycythemia vera is an uncommon neoplasm in which the bone marrow makes too many red blood cells. It may also result in the overproduction of white blood cells and platelets.

Most of the health concerns associated with polycythemia vera are caused by the blood being thicker as a result of the increased red blood cells. It is more common in the elderly and may be symptomatic or asymptomatic. Common signs and symptoms include itching (pruritus), and severe burning pain in the hands or feet that is usually accompanied by a reddish or bluish coloration of the skin. Patients with polycythemia vera are more likely to have gouty arthritis. Treatment consists primarily of phlebotomy.

Leukocytosis can be subcategorized by the type of white blood cell that is increased in number. Leukocytosis in which neutrophils are elevated is neutrophilia; leukocytosis in which lymphocyte count is elevated is lymphocytosis; leukocytosis in which monocyte count is elevated is monocytosis; and leukocytosis in which eosinophil count is elevated is eosinophilia.

An extreme form of leukocytosis, in which the WBC count exceeds 100,000/µL, is leukostasis. In this form there are so many WBCs that clumps of them block blood flow. This leads to ischemic problems including transient ischemic attack and stroke.

Leukopenia can be identified with a complete blood count.

Below are blood reference ranges for various types leucocytes/WBCs. The 2.5 percentile (right limits in intervals in image, showing 95% prediction intervals) is a common limit for defining leukocytosis.

Clinical signs and symptoms of complement-mediated TMA can include abdominal pain, confusion, fatigue, edema (swelling), nausea/vomiting and diarrhea. aHUS often presents with malaise and fatigue, as well as microangiopathic anemia. However, severe abdominal pain and bloody diarrhea are unusual. Laboratory tests may also reveal low levels of platelets (cells in the blood that aid in clotting), elevated lactate dehydrogenase (LDH, a chemical released from damaged cells, and which is therefore a marker of cellular damage), decreased haptoglobin (indicative of the breakdown of red blood cells), anemia (low red blood cell count)/schistocytes (damaged red blood cells), elevated creatinine (indicative of kidney dysfunction), and proteinuria (indicative of kidney injury). Patients with aHUS often present with an abrupt onset of systemic signs and symptoms such as acute kidney failure, hypertension (high blood pressure), myocardial infarction (heart attack), stroke, lung complications, pancreatitis (inflammation of the pancreas), liver necrosis (death of liver cells or tissue), encephalopathy (brain dysfunction), seizure, or coma. Failure of neurologic, cardiac, kidney, and gastrointestinal (GI) organs, as well as death, can occur unpredictably at any time, either very quickly or following prolonged symptomatic or asymptomatic disease progression. For example, approximately 1 in 6 patients with aHUS initially will present with proteinuria or hematuria without acute kidney failure. Patients who survive the presenting signs and symptoms endure a chronic thrombotic and inflammatory state, which puts many of them at lifelong elevated risk of sudden blood clotting, kidney failure, other severe complications and premature death.

Leukopenia () is a decrease in the number of white blood cells (leukocytes) found in the blood, which places individuals at increased risk of infection.

Neutropenia, a subtype of leukopenia, refers to a decrease in the number of circulating neutrophil granulocytes, the most abundant white blood cells. The terms "leukopenia" and "neutropenia" may occasionally be used interchangeably, as the neutrophil count is the most important indicator of infection risk. This should not be confused with agranulocytosis.

Thrombotic thrombocytopenic purpura (TTP) is a rare disorder of the blood-coagulation system, causing extensive microscopic clots to form in the small blood vessels throughout the body, resulting in low platelet counts. These small blood clots, called thrombi, can damage many organs including the kidneys, heart, brain, and nervous system. In the era before effective treatment with plasma exchange, the fatality rate was about 90%. With plasma exchange, this has dropped to 10% at six months. Because the disease generally results from antibodies that activate the immune system to inhibit the ADAMTS13 enzyme, agents that suppress the immune system, such as glucocorticoids, rituximab, cyclophosphamide, vincristine, or ciclosporin, may also be used if a relapse or recurrence follows plasma exchange. Platelets are not transfused unless the patient has a life-threatening bleed, since the transfused platelets would also quickly be consumed by thrombi formation, leading to a minimal increase in circulating platelets.

Most cases of TTP arise from autoantibody-mediated inhibition of the enzyme ADAMTS13, a metalloprotease responsible for cleaving large multimers of von Willebrand factor (vWF) into smaller units. The increase in circulating multimers of vWF increases platelet adhesion to areas of endothelial injury, particularly where arterioles and capillaries meet, which in turn results in the formation of small platelet clots called thrombi. As platelets are used up in the formation of thrombi, this then leads to a decrease in the number of overall circulating platelets, which may then cause life-threatening bleeds. The reason why the antibodies form is generally unknown for most patients, though it can be associated with some medications and autoimmune diseases such as HIV and Lupus, as well as pregnancy.

A rarer form of TTP, called Upshaw–Schulman syndrome, or "Inherited TTP," results from an autosomal recessive gene that leads to ADAMTS13 dysfunction from the time of birth, resulting in persisting large vWF multimers, which in turn results in the formation of thrombi (small platelet clots).

Red blood cells passing the microscopic clots are subjected to shear stress, which damages their membranes, leading to rupture of red blood cells within blood vessels, which in turn leads to anaemia and schistocyte formation. The presence of these blood clots in the small blood vessels reduces blood flow to organs resulting in cellular injury and end organ damage. Current therapy is based on support and plasmapheresis to reduce circulating antibodies against ADAMTS13 and replenish blood levels of the enzyme.

Leukocytosis is very common in acutely ill patients. It occurs in response to a wide variety of conditions, including viral, bacterial, fungal, or parasitic infection, cancer, hemorrhage, and exposure to certain medications or chemicals including steroids.

For lung diseases such as pneumonia and tuberculosis, WBC count is very important for the diagnosis of the disease, as leukocytosis is usually present.

The mechanism that causes leukocytosis can be of several forms: an increased release of leukocytes from bone marrow storage pools, decreased margination of leukocytes onto vessel walls, decreased extravasation of leukocytes from the vessels into tissues, or an increase in number of precursor cells in the marrow.

Certain medications, including corticosteroids, lithium and beta agonists, may cause leukocytosis.

The clinical hallmark is haemorrhagic bullae on the mucosa of the oronasopharynx. Haemorrhage from ruptured bullae, epistaxis or gastrointestinal bleeding is severe and may cause shock and death.

Onyalai is an acute disease that results in the development of hemorrhagic lesions on oral, nasal, and subconjunctival mucous membranes and skin, including on the soles of the feet. The patient initially is not in distress, which may result in a delay of diagnosis. As the disease progresses, hematuria, melena and menorrhagia may develop. Bleeding usually persists for approximately eight days, and may recur. Approximately 80 percent of cases will develop chronic thrombocytopenia. Periodic episodes of acute hemorrhage are possible and may be severe, leading to shock and death.

Neutropenia or neutropaenia is an abnormally low concentration of neutrophils (a type of white blood cell) in the blood. Neutrophils make up the majority of circulating white blood cells and serve as the primary defense against infections by destroying bacteria, bacterial fragments and immunoglobulin-bound viruses in the blood. Patients with neutropenia are more susceptible to bacterial infections and, without prompt medical attention, the condition may become life-threatening (neutropenic sepsis).

Neutropenia can be acute (temporary) or chronic (long lasting). The term is sometimes used interchangeably with "leukopenia" ("deficit in the number of white blood cells").