Platelets- Anatomy, Structure, Functions, Disorders

Last updated: June 14, 2026Reviewed date: June 14, 2026Reading time: 24 min read
Patient Tools

Read, save, and share this guide

Use these quick tools to make this medical article easier to read, print, save, or share with a family member.

Patient Mode

Understand this article easily

Switch between simple English and easy Bangla patient notes. This is for education and does not replace a doctor consultation.

Platelets, or thrombocytes, are the smallest blood cells, colorless cell fragments in our blood that form clots and stop or prevent bleeding. Typically around 2μm in diameter and anucleated, with an average lifespan of 7 to 10 days in humans. The platelet is a circulating anuclear...

For severe symptoms, danger signs, pregnancy, child illness, or sudden worsening, seek urgent medical care.

বাংলা রোগী নোট এখনো যোগ করা হয়নি। পোস্ট এডিটরে “RX Bangla Patient Mode” বক্স থেকে সহজ বাংলা সারাংশ যোগ করুন।

এই তথ্য শিক্ষা ও সচেতনতার জন্য। এটি ডাক্তারি পরীক্ষা, রোগ নির্ণয় বা প্রেসক্রিপশনের বিকল্প নয়।

Article Summary

Platelets, or thrombocytes, are the smallest blood cells, colorless cell fragments in our blood that form clots and stop or prevent bleeding. Typically around 2μm in diameter and anucleated, with an average lifespan of 7 to 10 days in humans. The platelet is a circulating anuclear fragment of a bone marrow megakaryocyte, 3 to 4 μm in diameter, with limited synthetic capability. The mean normal platelet...

Key Takeaways

  • This article explains Structure of Platelets in simple medical language.
  • This article explains Platelets Overviews in simple medical language.
  • This article explains Functions of Platelets in simple medical language.
  • This article explains Platelet Formation in simple medical language.
Educational health guideWritten for patient understanding and clinical awareness.
Reviewed content workflowUse writer and reviewer profiles for stronger trust.
Emergency safety firstUrgent warning signs are highlighted below.

Seek urgent medical care if you notice

These warning signs are general safety guidance. Local emergency numbers and clinical judgment should always come first.

  • Fever with very low white blood cells or known immune suppression.
  • Unusual bruising, persistent bleeding, black stools, or severe weakness.
  • Shortness of breath, fainting, confusion, or rapidly worsening fatigue.
1

Emergency now

Use emergency care for severe, sudden, rapidly worsening, or life-threatening symptoms.

2

See a doctor

Book a professional medical evaluation if symptoms persist, worsen, recur often, affect daily activities, or occur in a high-risk patient.

3

Learn safely

Use this article to understand possible causes, tests, treatment options, prevention, and questions to ask your clinician.

Before reading

RX Patient Tools

Use these quick guides before reading the article, or return to them when you need help preparing questions for a doctor.

Start here Choose the right pathway for symptoms, reports, medicines, or urgent warning signs. Disease article roadmap Read this topic step by step: meaning, symptoms, warning signs, diagnosis, treatment, prevention, and follow-up. Treatment planner Prepare questions about treatment choices, benefits, risks, side effects, and follow-up. Family & caregiver guide Organize symptoms, reports, medicines, questions, and follow-up safely. Nutrition & diet guide Prepare food, hydration, supplement, and medicine-timing questions safely. Prevention guide Organize risk factors, protective habits, screening, and warning signs. Recovery guide Prepare a safe plan for activity, rehabilitation, warning signs, and follow-up.
Definition

Platelets, or thrombocytes, are the smallest blood cells, colorless cell fragments in our blood that form clots and stop or prevent bleeding. Typically around 2μm in diameter and anucleated, with an average lifespan of 7 to 10 days in humans. The platelet is a circulating anuclear fragment of a bone marrow megakaryocyte, 3 to 4 μm in diameter, with limited synthetic capability. The mean normal platelet count is between 250,000 and 260,000 cells/mm3, although there is a wide range of accepted normal values in most laboratories that extend as low as 150,000 to as high as 400,000/mm3. Platelets are made in our bone marrow, the sponge-like tissue inside our bones. Bone marrow contains stem cells that develop into red blood cells, white blood cells, and platelets.

Platelets are small blood cells with several physiological purposes; the best studied is thrombosis activation. Through their clotting activity and activation of the coagulation cascade, they are crucial to maintaining adequate blood volume in those with vascular injury. The initiation of this activity begins with tissue injury and results in the release and binding of several glycoproteins, growth factors, and clotting factors. The complexity of these processes allows for many pharmacologic targets, which provides several options when it comes to antithrombotic therapy.

Platelet Count (PLT)

Just as it sounds, this is the actual number of platelets you have (per microliter of blood).

  • Low range: Less than 150,000 platelets per microliter
  • Normal range: 150,000 to 450,000 platelets per microliter1
  • Elevated range: 500,000 to 1,000,000 platelets per microliter

If your platelet count falls below 50,000, you may experience prolonged bleeding times.

Structure of Platelets

Platelets form by the fragmentation of megakaryocytes within the bone marrow. Megakaryocytes duplicate in the marrow without dividing, resulting in the production of giant cells. Within these giant cells, organelles organize into discrete domains, which will eventually become individual platelets, separated by a network of invaginating plasma membranes. These megakaryocytes are positioned next to the sinusoidal walls, such that shearing forces from circulating blood fragment the megakaryocyte cytoplasm into individual platelets and sweep these new platelets into the bloodstream.

Platelets circulate in the blood in discoid form but undergo significant structural changes following activation, mediated by actin and myosin within the cytoplasm. The platelets transform from discoid forms into compact spheres with dendritic extensions, which allow platelet adhesion. A variety of membrane-bound glycoprotein receptors facilitates the adhesion and aggregation of platelets.

As described above, platelets are anuclear but do contain RNA, ribosomes, mitochondria, and various granules, which are important in enacting platelet function. There are three distinct types of platelet granule

  • α-granules: the most abundant and largest secretory granules. They contain most of the platelet factors involved in hemostasis, including p-selectin, von Willebrand Factor, and fibrinogen
  • Dense granules: the smallest granules, which are visible on electron microscopy as dense bodies. They contain ADP and serotonin, as well as high levels of calcium
  • Lysosomes: contain hydrolytic enzymes including acid phosphatase and arylsulfatase

An ‘open canalicular system’ formed of deep surface membrane invaginations facilitates the secretion of granules. This system also has a key role in the transport of membrane receptors, allowing them to cluster, stabilize platelet adhesion sites, and amplify signals.

Structurally a platelet is divided into three zones

Peripheral zone – this zone is primarily involved in the adhesion and aggregation function

  • Glycocalyx – This is the thick carbohydrate-rich structure found on the exterior surface of platelets and serves as the site of the first contact during the hemostatic response by platelets, and it is made up of major and minor glycoproteins. GP-Ib-IX-V complex involved in adhesion at the site of vascular injury. GPIIb-IIIa is involved in aggregation by attachment through fibrinogen to other platelets.
  • Unit membrane – It is made of a lipid bilayer and open canalicular system, which serves a vital role in the acceleration of coagulation through the anionic phospholipid, phosphatidylserine, provided by the surface of activated platelets when clotting is initiated which converts prothrombin to thrombin.
  • The submembrane area – It plays a vital role in transmitting signals from the surface to organelles in the cytoplasm regulating signal processes of platelet activation.

Sol-gel zone – This is the matrix that is made of microtubules and microfilament, which plays a vital role in platelet structure and its support. This zone is responsible for various shape changes on activation during hemostasis and during ex vivo storage. Organelles are embedded within this matrix.

Organelle zone

  • Alpha-granules which stores fibrinogen fibronectin FV vWF, PDGF cytokines, chemokines, TG-beta-1, and VEGF
  • Dense- granules stores calcium ATP, ADP, serotonin, and pyrophosphate
  • Mitochondria- Are the powerhouse of platelets
  • Glycogen
  • Lysosome and peroxisome

When a platelet is activated, secretions from the α and dense granules are involved in further platelet activation and aggregation. Secretions also have immune-mediated effects.

Platelets Overviews

Platelets, also called thrombocytes, are membrane-bound cell fragments that are essential for clot formation during wound healing.

Key Points

Platelets, also called thrombocytes, are derived from megakaryocytes, which are derived from stem cells in the bone marrow.

Platelets circulate in the blood and are involved in hemostasis, leading to the formation of blood clots and blood coagulation.

Platelets lack a nucleus but do contain some organelles, such as mitochondria and endoplasmic reticulum fragments.

If the number of platelets in the blood is too low, excessive bleeding can occur. However, if the number of platelets is too high, blood clots can form ( thrombosis ), which may obstruct blood vessels.

Platelets are a natural source of growth factors involved in wound healing, coagulants, and inflammatory mediators.

Key Terms

  • extracellular matrix: All the connective tissues and fibers that are not part of a cell, but rather provide support.
  • platelet: A small, colorless, disc-shaped particle found in the blood of mammals. It plays an important role in the formation of blood clots.

Platelets, also called thrombocytes, are membrane-bound cell fragments derived from the fragmentation of larger precursor cells called megakaryocytes, which are derived from stem cells in the bone marrow. Platelets are important for the blood clotting process, making them essential for wound healing.

Platelet Structure and Distribution

Platelets are irregularly shaped, have no nucleus, and typically measure only 2–3 micrometers in diameter. Platelets are not true cells but are instead classified as cell fragments produced by megakaryocytes. Because they lack a nucleus, they do not contain nuclear DNA. However, they do contain mitochondria and mitochondrial DNA, as well as endoplasmic reticulum fragments and granules from the megakaryocyte parent cells. Platelets also contain adhesive proteins that allow them to adhere to fibrin mesh and the vascular endothelium, as well as to a microtubule and microfilament skeleton that extends into filaments during platelet activation. Less than 1% of whole blood consists of platelets. They are about 1/10th to 1/20th as abundant as white blood cells.

Platelets- Anatomy, Structure, Functions, Disorders

Platelet: Image from a light microscope (40×) from a peripheral blood smear surrounded by red blood cells. One platelet can be seen in the upper left side of the image (purple) and is significantly smaller in size than the red blood cells (stained pink) and the two large neutrophils (stained purple).

Functions of Platelets

Platelets circulate in blood plasma and are primarily involved in hemostasis (stopping the flow of blood during injury), by causing the formation of blood clots, also known as coagulation. The adhesive surface proteins of platelets allow them to accumulate on the fibrin mesh at an injury site to form a platelet plug that clots the blood. The complex process of wound repair can only begin once the clot has stopped bleeding.

Platelets secrete many factors involved in coagulation and wound healing. During coagulation, they release factors that increase local platelet aggregation (thromboxane A), mediate infection, or irritation, often causing pain, swelling, heat, or redness. সহজ বাংলা: শরীরের প্রদাহ; ব্যথা, ফোলা বা লালভাব হতে পারে।" data-rx-term="inflammation" data-rx-definition="Inflammation is the body’s response to injury, infection, or irritation, often causing pain, swelling, heat, or redness. সহজ বাংলা: শরীরের প্রদাহ; ব্যথা, ফোলা বা লালভাব হতে পারে।">inflammation (serotonin), and promote blood coagulation through increasing thrombin and fibrin (thromboplastin). They also release wound healing-associated growth factors including platelet-derived growth factor (PDGF), which directs cell movement; TGF beta, which stimulates the deposition of extracellular matrix tissue into a wound during healing; and vascular endothelial growth factor (VEGF), which stimulates angiogenesis, or the regrowth of blood vessels. These growth factors play a significant role in the repair and regeneration of connective tissues. Local application of these platelet-produced healing-associated factors in increased concentrations has been used as an adjunct to wound healing for several decades.

or

Platelets have a crucial role in thrombus formation and hemostasis. Platelets circulate in the blood in a quiescent discoid form but may become activated by contact with damaged blood vessel walls. Following blood vessel damage, substances in the exposed subendothelial extracellular matrix such as collagen and von Willebrand factor may bind to platelet surface receptors. Platelets will adhere to sites of injury, and receptor binding will lead to platelet activation.

As described above, platelets undergo a structural transformation at this point and begin to secrete granule contents to promote platelet aggregation and platelet plug formation. Activated platelets release factors such as ADP, thromboxane A2, and thrombin, which can promote activation of other nearby platelets in a positive feedback mechanism. Activation also leads to the surface expression of glycoprotein IIb-IIIa. This protein binds to fibrinogen, allowing cross-linking of platelets and mediating platelet aggregation. A final change during activation is the expression of phosphatidylserine, which generates a negative charge on platelet surfaces. This negative charge allows clotting factor complexes to assemble on the surface, as part of the secondary hemostasis response.

The above processes ultimately lead to the production of a thrombus: a structure formed of aggregated, activated platelets, combined with a mesh of cross-linked fibrin and entrapped erythrocytes and leukocytes. This thrombus restores the structural integrity of the damaged vessel wall and prevents blood loss while the vessel heals.

There is additional growing evidence of the role of platelets in inflammatory and immune responses. Leukocytes are recruited to thrombi via interactions with platelet P-selectin, and platelet α-granules contain a range of pro-inflammatory cytokines. Antiplatelet medications have been found to affect immunity and may even reduce mortality related to infection and sepsis.

Platelets- Anatomy, Structure, Functions, Disorders

Platelets: A blood slide of platelets aggregating, or, clumping together. The platelets are the small, bright purple fragments.

If the number of platelets is too low, excessive bleeding can occur and wound healing will be impaired. However, if the number of platelets is too high, blood clots can form (thrombosis), which may obstruct blood vessels and result in ischemic tissue damage caused by a stroke, myocardial infarction, pulmonary embolism, or the blockage of blood vessels to other parts of the body. Thrombosis also occurs when blood is allowed to pool, which causes clotting factors and platelets to form a blood clot even in the absence of an injury.

Platelet Formation

Platelets are membrane-bound cell fragments derived from megakaryocytes, which are produced during thrombopoiesis.

Key Points

Megakaryocytes are produced from stem cells in the bone marrow by a process called thrombopoiesis.

Megaryocytes create platelets by releasing protoplatelets that break up into numerous smaller, functional platelets.

Thrombopoiesis is stimulated and regulated by the hormone thrombopoietin.

Platelets have an average life span of five to ten days.

Old platelets are destroyed by phagocytosis. The spleen holds a reservoir of additional platelets.

Abnormal numbers of platelets result from problems in thrombopoiesis. This is associated with various disorders and potential pathological complications.

Key Terms

  • megakaryocyte: A large cell found in bone marrow that is responsible for the production of platelets.
  • Thrombopoietin: A hormone produced by the liver or kidneys that stimulates megakaryocyte differentiation and platelet release.
  • bone marrow: The fatty vascular tissue that fills the cavities of bones; the place where new blood cells are produced.

Platelets are small, clear, irregularly-shaped cell fragments produced by larger precursor cells called megakaryocytes. Platelets are also called thrombocytes because they are involved in the blood clotting process, which is necessary for wound healing. Platelets are continuously produced as a component product of hematopoiesis (blood cell formation).

Thrombopoiesis

Platelets are produced during hematopoiesis in a sub-process called thrombopoiesis, or the production of thrombocytes. Thrombopoiesis occurs from common myeloid progenitor cells in the bone marrow, which differentiate into promegakaryocytes and then into megakaryocytes. Megakaryocytes stay in the bone marrow and are thought to produce protoplatelets within their cytoplasm, which are released in cytoplasmic extensions upon cytokine stimulus. The protoplatelets then break up into hundreds of platelets that circulate throughout the bloodstream, while the remaining nucleus of the ruptured megakaryocyte is consumed by macrophages.

Megakaryocyte and platelet production is regulated by thrombopoietin, a hormone produced by the liver and kidneys. Thrombopoietin stimulates the differentiation of myeloid progenitor cells into megakaryocytes and causes the release of platelets. Thrombopoietin is regulated by a negative feedback mechanism based on platelet levels in the body so that high levels of platelets result in lower levels of thrombopoietin, while low levels of platelets result in higher levels of
thrombopoietin.

Each megakaryocyte produces between 5,000 and 10,000 platelets before its cellular components are fully depleted. Altogether, around 10^11 platelets are produced each day in a healthy adult. The average lifespan of a platelet is just 5 to 10 days. Old platelets are destroyed by macrophage phagocytosis in the spleen and by Kupffer cells in the liver. Up to 40% of platelets are stored in the spleen as a reserve, released when needed by sympathetically-induced splenic muscle contractions during severe injury.

Platelets- Anatomy, Structure, Functions, Disorders

Hematopoiesis: Myeloid progenitor cells differentiate into promegakaryocytes, and megakaryocytes, which release platelets.

Implications of Platelet Formation

Balanced thrombopoiesis is important because it directly influences the amount of platelets in the body and their associated complications. If the number of platelets is too low, excessive bleeding can occur, even from minor or superficial injuries. If the number of platelets is too high, blood clots can form (thrombosis) and travel through the bloodstream, which may obstruct blood vessels and result in ischemic events. These include stroke, myocardial infarction, pulmonary embolism, or infarction of other tissues.

An abnormality or disease of the platelets is called a thrombocytopathy, which could be either a low number of platelets (thrombocytopenia), a decrease in function of platelets (thrombasthenia), or an increase in the number of platelets (thrombocytosis). In any case, issues with the number of circulating platelets is often due to issues in thrombopoietin feedback regulation, but may also be associated with genetic characteristics and certain medications and diseases. For example, thrombocytopenia often occurs in leukemia patients. Cancerous myeloid cells crowd out healthy ones in the bone marrow, causing impaired thrombopoiesis.

Disorders of Platelets

The three broad categories of platelet disorders are “not enough”; “dysfunctional”; and “too many”.[rx]:vii

Thrombocytopenia

  • Immune thrombocytopenias (ITP) – formerly known as immune thrombocytopenic purpura and idiopathic thrombocytopenic purpura
  • Splenomegaly
    • Gaucher’s disease
  • Familial thrombocytopenia[rx]
  • Chemotherapy
  • Babesiosis
  • Dengue fever
  • Onyalai
  • Thrombotic thrombocytopenic purpura
  • HELLP syndrome
  • Hemolytic–uremic syndrome
  • Drug-induced thrombocytopenic purpura (five known drugs – most problematic is heparin-induced thrombocytopenia (HIT)
  • Pregnancy-associated
  • Neonatal alloimmune associated
  • Aplastic anemia
  • Transfusion-associated
  • Pseudothrombocytopenia
  • idiopathic thrombocytopenic purpura
  • Gilbert’s syndrome[rx]

Altered platelet function

  • Congenital
    • Disorders of adhesion
      • Bernard–Soulier syndrome
    • Disorders of activation
      • Disorders of granule amount or release
      • Hermansky–Pudlak syndrome
      • Gray platelet syndrome
      • ADP receptor defect
      • Decreased cyclooxygenase activity
      • Storage pool defects, acquired or congenital
    • Disorders of aggregation
      • Glanzmann’s thrombasthenia
      • Wiskott–Aldrich syndrome
  • Acquired
    • Disorders of adhesion
      • Paroxysmal nocturnal hemoglobinuria
      • Asthma
      • Samter’s triad (aspirin-exacerbated respiratory disease/AERD)[58]
      • Cancer
      • Malaria
      • Decreased cyclooxygenase activity

Thrombocytosis and thrombocythemia

  • Reactive
    • Chronic infection
    • Chronic inflammation
    • Malignancy
    • Hyposplenism (post-splenectomy)
    • Iron deficiency
    • Acute blood loss
  • Myeloproliferative neoplasms – platelets are both elevated and activated
    • Essential thrombocytosis
    • Polycythemia vera
  • Associated with other myeloid neoplasms
  • Congenital

What Causes Low Platelets?

A low platelet count occurs when:

  • A person’s bone marrow is damaged and unable to make enough of its own platelets. This can be caused by certain cancers, such as Leukemia – and it can also be caused by cancer treatments.
  • Platelets have been lost due to severe bleeding, such as following a traumatic injury or during surgery.
  • Platelets have been destroyed by autoimmune diseases, certain medicines, infections, or other conditions.
  • The patient’s spleen, which filters the bloodstream, removes too many platelets.

Symptoms of low platelets include bruising easily and unusual bleeding, such as excessive bleeding from a small cut or blood in urine or stool.

Bone marrow problems

Your bone marrow is the spongy tissue inside the bone. It’s where all the components of blood, including platelets, are produced. If your bone marrow isn’t producing enough platelets, you’ll have a low platelet count. The causes of low platelet production include:

  • aplastic anemia
  • vitamin B-12 deficiency
  • folate deficiency
  • iron deficiency
  • viral infections, including HIV, Epstein-Barr, and chickenpox
  • exposure to chemotherapy, radiation, or toxic chemicals
  • consuming too much alcohol
  • cirrhosis
  • leukemia
  • myelodysplasia

Platelet destruction

Each platelet lives about 10 days in a healthy body. A low platelet count can also be a result of the body destroying too many platelets. This can be due to the side effects of certain medications, include diuretics and anti-seizure medications. It can also be a symptom of:

  • hypersplenism, or an enlarged spleen
  • an autoimmune disorder
  • pregnancy
  • a bacterial infection in the blood
  • idiopathic thrombocytopenic purpura
  • thrombotic thrombocytopenic purpura
  • hemolytic uremic syndrome
  • disseminated intravascular coagulation

Causes of High Platelet Count

If the body has too many platelets in circulation, you may develop a condition called thrombocytosis.

The following factors may contribute to high platelet count:3

  • Primary bone marrow disorder – Essential thrombocytosis is a condition in which the megakaryocytes in the bone marrow produce too many platelets, increasing the risk of blood clots.
  • Chronic inflammation in the body – Inflammatory conditions such as rheumatoid arthritis (RA) and inflammatory bowel disease (IBD) may result in elevated platelet counts as high levels of inflammation may cause the bone marrow to produce more white blood cells and platelets to combat cellular damage.
  • Infection – Bone marrow cells increase the production of white blood cells and platelets to help fight infection, causing an elevation in platelet count.
  • Iron deficiency anemia – Reactive or secondary thrombocytosis may result when the body is undergoing a breakdown of red blood cells and the bone marrow cells go into overproduction to meet needs.
  • Spleen removal – Up to one-third of platelets are stored in the spleen at any time, and so removal of this organ will cause an increase in platelet concentration in the bloodstream. This is generally a temporary condition, however.
  • Cancer – High platelet counts can also be seen in cancer, especially with gastrointestinal cancer, as well as lymphoma, lung, ovarian, and breast cancer. This is thought to be due to the inflammation associated with the malignancy stimulating the production of platelets in the bone marrow.

In addition, a temporary increase in the platelet count can happen after major surgery or trauma.

What are the symptoms of a low platelet count?

Whether or not you experience symptoms depends on your platelet count.

Mild cases, such as when a low platelet count is caused by pregnancy, usually don’t cause any symptoms. More severe cases may cause uncontrollable bleeding, which requires immediate medical attention.

If you have a low platelet count, you may experience:

  • red, purple, or brown bruises, which are called purpura
  • a rash with small red or purple dots called petechiae
  • nosebleeds
  • bleeding gums
  • bleeding from wounds that lasts for a prolonged period or doesn’t stop on its own
  • heavy menstrual bleeding
  • bleeding from the rectum
  • blood in your stool
  • blood in your urine

In more serious cases, you may bleed internally. Symptoms of internal bleeding include:

  • blood in the urine
  • blood in the stool
  • bloody or very dark vomit

Talk to your doctor immediately if you experience any signs of internal bleeding.

Rarely, this condition may lead to bleeding in your brain. If you have a low platelet count and experience headaches or any neurological problems, tell your doctor right away.

We believe in health equity—the equal opportunity for everyone to live their healthiest life. Join us in transforming health outcomes through the power of storytelling.

How is a low platelet count diagnosed?

If your doctor suspects a low platelet count, they’ll first perform a physical examination. During the exam, your doctor will check your body for any unusual bruising or evidence of petechiae, which is a sign of capillary bleeding that often accompanies a low platelet count.

Your doctor may also feel your abdomen to check for an enlarged spleen, which can cause a low platelet count. You may also be asked if you have any family history of bleeding disorders since these types of disorders can run in families.

Blood tests

To diagnose this condition, your doctor needs to do a complete blood count test. This test looks at the number of blood cells in your blood. It’ll tell your doctor if your platelet count is lower than it should be. A typical platelet count will range between 150,000 and 450,000 platelets per mL blood.

Your doctor may also wish to have your blood tested for platelet antibodies. These are proteins that destroy platelets. Platelet antibodies can be produced as a side effect to certain drugs, such as heparin, or for unknown reasons.

Your doctor may also order blood-clotting tests, which include partial thromboplastin time and prothrombin time. These tests simply require a sample of your blood. Certain chemicals will be added to the sample to determine how long it takes your blood to clot.

Ultrasound

If your doctor suspects that your spleen is enlarged, they may order an ultrasound. This test will use sound waves to make a picture of your spleen. It can help your doctor determine if your spleen is the proper size.

Bone marrow aspiration and biopsy

If your doctor suspects that there’s a problem in your bone marrow, they may order a bone marrow aspiration. During an aspiration, your doctor will use a needle to remove a small amount of bone marrow from one of your bones.

A bone marrow biopsy may also be ordered. Your doctor will use a needle to take a sample of your core bone marrow, usually from the hipbone. It may be performed at the same time as a bone marrow aspiration.

What is the treatment for a low platelet count?

The treatment for a low platelet count depends on the cause and severity of your condition. If your condition is mild, your doctor may wish to hold off on treatment and simply monitor you.

Your doctor may recommend that you take measures to prevent your condition from worsening. This could include:

  • avoiding contact sports
  • avoiding activities with a high risk of bleeding or bruising
  • limiting alcohol consumption
  • stopping or switching medications that affect platelets, including aspirin and ibuprofen

Medicines

You may need one or more medicines to treat a low or high platelet count.

Medicines to treat high platelet count

  • Anagrelide: This medicine can lower platelet counts in people who have a high risk of complications such as serious blood clots. This medicine may cause anemia and scarring of your bone marrow.
  • Aspirin: This medicine helps prevent blood clots. Aspirin can raise your risk of bleeding.
  • Hydroxyurea: This is used to reduce platelet counts. Possible side effects include making fewer blood cells, skin wounds, problems with your digestive system, and fever.
  • Interferon-a and pegylated interferon: These medicines help reduce platelet counts. Side effects include extreme tiredness, flu-like symptoms, and confusion.

Medicine to treat low platelet count

  • Anti-D immunoglobulin: This medicine is used to increase platelet counts in some people who have immune thrombocytopenia. Possible side effects include flu-like symptoms, low hemoglobin  levels, and a breakdown of your red blood cells.
  • Corticosteroids: These medicines help increase platelet counts. Corticosteroids include prednisone, prednisolone, and dexamethasone. This may be the first treatment your provider recommends for a low platelet count. Possible side effects include diabetes, insomnia, high blood pressure, digestive problems, mood changes, and slow growth in children.
  • Fondaparinux: This is used to treat heparin-induced thrombocytopenia (HIT). This medicine may cause bleeding, anemia, insomnia, dizziness, low blood pressure, and confusion.
  • Immunosuppressors: These medicines stop your immune system from destroying your platelets. They are used to treat immune thrombocytopenia when corticosteroids do not work. Examples of this type of medicine include azathioprine, cyclophosphamide, cyclosporine, danazol, and dapsone. These medicines may increase your risk for infection. Other, less serious side effects can include loss of appetite, nausea, vomiting, increased hair growth, and hand trembling. These effects get better and may go away as the body adjusts to the medicine.
  • Intravenous immunoglobulin (IVIG): This is used to increase your platelet count and treat major bleeding in immune thrombocytopenia. IVIG is also used to treat HIT. Complications may include serious allergic reactions and damage to your kidneys or lungs.
  • Rituximab: This is an antibody treatment that may be used to treat immune thrombocytopenia or thrombotic thrombocytopenic purpura. This medicine may raise your risk of infections.
  • Thrombopoetin receptor agonist (TPO-RA) such as romiplostim and eltrombopag: These increase platelets in immune thrombocytopenia. They are used most often after other treatments have not worked. Possible side effects include low platelets, damage to the liver, venous thromboembolism, cataracts, bruising, and nosebleeds.

Procedures

You may need one or more of the following procedures to treat your platelet disorder.

  • Plasma exchange: This is used to treat thrombotic thrombocytopenic purpura. In this procedure, the liquid part of your blood (plasma) is replaced with donor plasmas using a machine that collects the cells in your blood.
  • Plasma infusion: This is used to treat thrombotic thrombocytopenic purpura that is caused by your body not making enough of a protein called ADAMTS13. A plasma infusion helps replace the missing protein.
  • Platelet transfusion: This procedure is used to quickly increase your platelet count when you are having serious bleeding. Possible complications include risk of infectious disease, allergic reaction, and difficulty with future transfusions. If you have HIT, a platelet transfusion can raise your risk of forming blood clots.
  • Plateletpheresis: This is used to treat life-threatening clotting in people who have high platelet counts. This procedure removes platelets from your blood and returns the liquid part of your blood (plasma) to your bloodstream.
  • Bone marrow transplant: This procedure can help treat life-threatening types of platelet disorders. It is used to treat conditions that occur when the stem cells in your bone marrow do not make enough platelets.
  • Surgery to remove your spleen (splenectomy): Your spleen is an organ in your upper left abdomen that stores platelets. Removing your spleen helps raise your platelet count. This helps treat a low platelet count. Possible complications include bleeding, infection, and blood clots.

What health problems can platelet disorders cause?

Platelet disorders can cause the following complications:

  • Bleeding from your nose and gums
  • Menstrual bleeding lasting more than 7 days, called menorrhagia
  • Bleeding in your brain or your digestive system
  • Blood clots, which can block blood flow to your limbs and organs, such as your lungs and brain
  • Blood or bone marrow cancer
  • Bone marrow failure
  • Heart attack or decreased blood flow to your heart
  • Pregnancy complications

If you think that you are or someone else is having symptoms of serious bleeding, a heart attack, or stroke, call 9-1-1 immediately. Every minute matters.

Manage your condition

To help prevent complications, your healthcare provider may ask you to take the following steps to help prevent complications.

  • See your provider for ongoing medical care. You may need routine tests to monitor your platelet levels. You may also need ongoing treatment to keep your platelet count in the normal range. If you are pregnant, your provider will monitor your condition to make sure that your platelet count is not too low or too high. Learn more about how platelet disorders can affect your pregnancy.
  • Take all medicines as prescribed. If you are taking medicines to lower your platelet count, tell your provider or dentist about them before any surgery or dental procedures. These medicines thin your blood and may increase bleeding during these procedures.
  • Watch for symptoms of bleeding. Symptoms can appear suddenly or over time. Platelet disorders can cause bleeding in almost any part of the body. Bleeding can lead to a medical emergency and should be treated quickly. Tell your provider right away if you have any symptoms.
  • Tell your provider if you have any symptoms of an infection, such as a fever. This is very important for people who have had their spleens removed, because removing your spleen raises your risk of an infection. People who have had their spleens removed may need vaccines to prevent certain infections. Talk to your provider about vaccines, including pneumococcal and meningococcal vaccines.
  • Avoid medicines that may lower your platelet count or stop your platelets from working properly. Two examples of such medicines are aspirin and ibuprofen. These medicines may thin your blood too much. Be careful when using over-the-counter medicines, as many contain aspirin or ibuprofen. Tell your provider about all the medicines you take, including over-the-counter medicines, vitamins, supplements, and herbal remedies.
  • Make healthy lifestyle changes. If you smoke, quit. Smoking can raise your risk of a blood clot. Also, get treatment for other health conditions that can raise the risk of a blood clot.
  • Avoid injuries that can cause bruising and bleeding.
    • Do not take part in contact sports, such as boxing, football, or karate. These sports can lead to injuries that can cause bleeding. Other sports, such as skiing or horseback riding, also put you at risk for injuries that can cause bleeding. Ask your provider about physical activities that are safe for you.
    • If your child has thrombocytopenia, ask your child’s healthcare provider whether you need to restrict your child’s activities.
    • Take safety precautions, such as using a seatbelt while riding in a car and wearing gloves when working with knives and other tools.
    • Invasive dental procedures may cause serious bleeding. Get regular dental care and practice oral hygiene to help prevent gum bleeding and lower the chance of needing such procedures.

References

Doctor visit helper

Prepare before seeing a doctor

A simple rural-patient checklist to help you explain symptoms clearly, ask better questions, and avoid unsafe self-treatment.

Safety note: This is not a prescription or diagnosis. For severe symptoms, pregnancy danger signs, children with serious illness, chest pain, breathing difficulty, stroke-like weakness, or major injury, seek urgent care.

Which doctor may help?

Start with a registered doctor or the nearest qualified health center.

What to tell the doctor

  • Write when the problem started and how it changed.
  • Bring old prescriptions, investigation reports, and current medicines.
  • Write allergies, pregnancy status, diabetes, kidney/liver disease, and major past illnesses.
  • Bring one family member if the patient is weak, elderly, confused, or a child.

Questions to ask

  • What is the most likely cause of my symptoms?
  • Which danger signs mean I should go to hospital quickly?
  • Which tests are necessary now, and which can wait?
  • How should I take medicines safely and what side effects should I watch for?
  • When should I come for follow-up?

Tests to discuss

  • Vital signs: temperature, pulse, blood pressure, oxygen saturation
  • Basic physical examination by a clinician
  • CBC, urine test, blood sugar, or imaging only when clinically needed

Avoid these mistakes

  • Do not use antibiotics, steroid tablets/injections, or strong painkillers without proper medical advice.
  • Do not hide pregnancy, kidney disease, ulcer, allergy, or blood thinner use.
  • Do not delay emergency care when danger signs are present.

Medicine safety and first-aid guide

This section is for patient education only. It does not replace a doctor, pharmacist, or emergency care.

Safe first steps

  • Avoid heavy lifting, sudden bending, and prolonged bed rest.
  • Use comfortable posture and gentle movement as tolerated.
  • Discuss physiotherapy, X-ray, or MRI only when clinically needed.

OTC medicine safety

  • For mild back pain, pain-relief medicine may be discussed with a doctor or pharmacist.
  • Avoid repeated painkiller use if you have kidney disease, stomach ulcer, uncontrolled blood pressure, or are taking blood thinners.

Avoid these mistakes

  • Do not start antibiotics without a proper medical decision.
  • Do not use steroid tablets or injections casually for quick relief.
  • Do not delay emergency care because of home remedies.

Get urgent help if

  • Back pain with leg weakness, numbness around private area, loss of urine/stool control, fever, cancer history, or major injury needs urgent care.
Medicine names, dose, and timing must be decided by a qualified clinician or pharmacist after checking age, pregnancy, allergy, other diseases, and current medicines.

For rural patients and family caregivers

Patient health record and symptom diary

Write your symptoms, medicines already taken, test results, and questions before visiting a doctor. This note stays on your device unless you print or copy it.

Doctor to discuss: Medicine doctor / pediatrician for children / qualified clinician
Tests to discuss with doctor
  • Temperature chart and hydration assessment
  • CBC with platelet count if fever persists or dengue/other infection is possible
  • Urine test, malaria/dengue tests, chest evaluation, or blood culture only when clinically indicated
Questions to ask
  • What is the most likely cause of my symptoms?
  • Which warning signs mean I should go to emergency care?
  • Which tests are really needed now?
  • Which medicines are safe for my age, pregnancy status, allergy, kidney/liver/stomach condition, and current medicines?
  • Do I need antibiotics, or is this more likely viral?

Emergency warning signs such as chest pain, severe breathing difficulty, sudden weakness, confusion, severe dehydration, major injury, or loss of bladder/bowel control need urgent medical care. Do not wait for online information.

Safe pathway to proper treatment

Care roadmap for: Platelets- Anatomy, Structure, Functions, Disorders

Use this simple roadmap to understand the next safe steps. It is educational and does not replace examination by a doctor.

Go to emergency care if you notice:
  • Severe or rapidly worsening symptoms
  • Breathing difficulty, chest pain, fainting, confusion, severe weakness, major injury, or severe dehydration
Doctor / service to discuss: Qualified healthcare provider; specialist depends on symptoms and examination.
  1. Step 1

    Check danger signs first

    If danger signs are present, seek emergency care and do not wait for online information.

  2. Step 2

    Record the symptom story

    Write when symptoms started, severity, medicines already taken, allergies, pregnancy status, and test results.

  3. Step 3

    Visit a qualified clinician

    A doctor, nurse, or qualified healthcare provider can examine you and decide which tests or treatment are needed.

  4. Step 4

    Do only useful tests

    Do tests after clinical assessment. Avoid unnecessary tests, random antibiotics, or repeated medicines without diagnosis.

  5. Step 5

    Follow up and return early if worse

    If symptoms worsen, new warning signs appear, or treatment is not helping, return for review quickly.

Rural patient practical tips
  • Take a written symptom diary and all previous prescriptions/test reports.
  • Do not hide medicines already taken, even herbal or over-the-counter medicines.
  • Ask which warning signs mean urgent referral to hospital.

This roadmap is for education. A real diagnosis and treatment plan requires history, examination, and clinical judgment.

RX Patient Help

Ask a health question safely

Write your symptom story. A health professional or site editor can review it before any answer is prepared. This box is not for emergency care.

Emergency first: Severe chest pain, breathing trouble, unconsciousness, stroke signs, severe injury, heavy bleeding, or rapidly worsening symptoms need urgent local medical care now.

Frequently Asked Questions

Platelet Count (PLT) Just as it sounds, this is the actual number of platelets you have (per microliter of blood). Low range: Less than 150,000 platelets per microliter Normal range: 150,000 to 450,000 platelets per microliter1 Elevated range: 500,000 to 1,000,000 platelets per microliter If your platelet count falls below 50,000, you may experience prolonged bleeding times. Structure of Platelets Platelets form by the fragmentation of megakaryocytes within the bone marrow. Megakaryocytes duplicate in the marrow without dividing, resulting in the production of giant cells. Within these giant cells, organelles organize into discrete domains, which will eventually become individual platelets, separated by a network of invaginating plasma membranes. These megakaryocytes are positioned next to the sinusoidal walls, such that shearing forces from circulating blood fragment the megakaryocyte cytoplasm into individual platelets and sweep these new platelets into the bloodstream.[rx] Platelets circulate in the blood in discoid form but undergo significant structural changes following activation, mediated by actin and myosin within the cytoplasm. The platelets transform from discoid forms into compact spheres with dendritic extensions, which allow platelet adhesion. A variety of membrane-bound glycoprotein receptors facilitates the adhesion and aggregation of platelets.[rx] As described above, platelets are anuclear but do contain RNA, ribosomes, mitochondria, and various granules, which are important in enacting platelet function.[rx] There are three distinct types of platelet granule α-granules: the most abundant and largest secretory granules. They contain most of the platelet factors involved in hemostasis, including p-selectin, von Willebrand Factor, and fibrinogen[rx] Dense granules: the smallest granules, which are visible on electron microscopy as dense bodies. They contain ADP and serotonin, as well as high levels of calcium Lysosomes: contain hydrolytic enzymes including acid phosphatase and arylsulfatase[rx] An ‘open canalicular system’ formed of deep surface membrane invaginations facilitates the secretion of granules.[rx] This system also has a key role in the transport of membrane receptors, allowing them to cluster, stabilize platelet adhesion sites, and amplify signals.[rx] Structurally a platelet is divided into three zones Peripheral zone - this zone is primarily involved in the adhesion and aggregation function Glycocalyx - This is the thick carbohydrate-rich structure found on the exterior surface of platelets and serves as the site of the first contact during the hemostatic response by platelets, and it is made up of major and minor glycoproteins. GP-Ib-IX-V complex involved in adhesion at the site of vascular injury. GPIIb-IIIa is involved in aggregation by attachment through fibrinogen to other platelets. Unit membrane - It is made of a lipid bilayer and open canalicular system, which serves a vital role in the acceleration of coagulation through the anionic phospholipid, phosphatidylserine, provided by the surface of activated platelets when clotting is initiated which converts prothrombin to thrombin. The submembrane area - It plays a vital role in transmitting signals from the surface to organelles in the cytoplasm regulating signal processes of platelet activation. Sol-gel zone - This is the matrix that is made of microtubules and microfilament, which plays a vital role in platelet structure and its support. This zone is responsible for various shape changes on activation during hemostasis and during ex vivo storage. Organelles are embedded within this matrix. Organelle zone Alpha-granules which stores fibrinogen fibronectin FV vWF, PDGF cytokines, chemokines, TG-beta-1, and VEGF Dense- granules stores calcium ATP, ADP, serotonin, and pyrophosphate Mitochondria- Are the powerhouse of platelets Glycogen Lysosome and peroxisome When a platelet is activated, secretions from the α and dense granules are involved in further platelet activation and aggregation. Secretions also have immune-mediated effects.[rx] Platelets Overviews Platelets, also called thrombocytes, are membrane-bound cell fragments that are essential for clot formation during wound healing. Key Points Platelets, also called thrombocytes, are derived from megakaryocytes, which are derived from stem cells in the bone marrow. Platelets circulate in the blood and are involved in hemostasis, leading to the formation of blood clots and blood coagulation. Platelets lack a nucleus but do contain some organelles, such as mitochondria and endoplasmic reticulum fragments. If the number of platelets in the blood is too low, excessive bleeding can occur. However, if the number of platelets is too high, blood clots can form ( thrombosis ), which may obstruct blood vessels. Platelets are a natural source of growth factors involved in wound healing, coagulants, and inflammatory mediators. Key Terms extracellular matrix: All the connective tissues and fibers that are not part of a cell, but rather provide support. platelet: A small, colorless, disc-shaped particle found in the blood of mammals. It plays an important role in the formation of blood clots. Platelets, also called thrombocytes, are membrane-bound cell fragments derived from the fragmentation of larger precursor cells called megakaryocytes, which are derived from stem cells in the bone marrow. Platelets are important for the blood clotting process, making them essential for wound healing. Platelet Structure and Distribution Platelets are irregularly shaped, have no nucleus, and typically measure only 2–3 micrometers in diameter. Platelets are not true cells but are instead classified as cell fragments produced by megakaryocytes. Because they lack a nucleus, they do not contain nuclear DNA. However, they do contain mitochondria and mitochondrial DNA, as well as endoplasmic reticulum fragments and granules from the megakaryocyte parent cells. Platelets also contain adhesive proteins that allow them to adhere to fibrin mesh and the vascular endothelium, as well as to a microtubule and microfilament skeleton that extends into filaments during platelet activation. Less than 1% of whole blood consists of platelets. They are about 1/10th to 1/20th as abundant as white blood cells. Platelet: Image from a light microscope (40×) from a peripheral blood smear surrounded by red blood cells. One platelet can be seen in the upper left side of the image (purple) and is significantly smaller in size than the red blood cells (stained pink) and the two large neutrophils (stained purple). Functions of Platelets Platelets circulate in blood plasma and are primarily involved in hemostasis (stopping the flow of blood during injury), by causing the formation of blood clots, also known as coagulation. The adhesive surface proteins of platelets allow them to accumulate on the fibrin mesh at an injury site to form a platelet plug that clots the blood. The complex process of wound repair can only begin once the clot has stopped bleeding. Platelets secrete many factors involved in coagulation and wound healing. During coagulation, they release factors that increase local platelet aggregation (thromboxane A), mediate inflammation (serotonin), and promote blood coagulation through increasing thrombin and fibrin (thromboplastin). They also release wound healing-associated growth factors including platelet-derived growth factor (PDGF), which directs cell movement; TGF beta, which stimulates the deposition of extracellular matrix tissue into a wound during healing; and vascular endothelial growth factor (VEGF), which stimulates angiogenesis, or the regrowth of blood vessels. These growth factors play a significant role in the repair and regeneration of connective tissues. Local application of these platelet-produced healing-associated factors in increased concentrations has been used as an adjunct to wound healing for several decades. or Platelets have a crucial role in thrombus formation and hemostasis. Platelets circulate in the blood in a quiescent discoid form but may become activated by contact with damaged blood vessel walls. Following blood vessel damage, substances in the exposed subendothelial extracellular matrix such as collagen and von Willebrand factor may bind to platelet surface receptors.[rx] Platelets will adhere to sites of injury, and receptor binding will lead to platelet activation. As described above, platelets undergo a structural transformation at this point and begin to secrete granule contents to promote platelet aggregation and platelet plug formation. Activated platelets release factors such as ADP, thromboxane A2, and thrombin, which can promote activation of other nearby platelets in a positive feedback mechanism.[rx] Activation also leads to the surface expression of glycoprotein IIb-IIIa. This protein binds to fibrinogen, allowing cross-linking of platelets and mediating platelet aggregation.[rx] A final change during activation is the expression of phosphatidylserine, which generates a negative charge on platelet surfaces. This negative charge allows clotting factor complexes to assemble on the surface, as part of the secondary hemostasis response.[rx] The above processes ultimately lead to the production of a thrombus: a structure formed of aggregated, activated platelets, combined with a mesh of cross-linked fibrin and entrapped erythrocytes and leukocytes. This thrombus restores the structural integrity of the damaged vessel wall and prevents blood loss while the vessel heals. There is additional growing evidence of the role of platelets in inflammatory and immune responses. Leukocytes are recruited to thrombi via interactions with platelet P-selectin, and platelet α-granules contain a range of pro-inflammatory cytokines. Antiplatelet medications have been found to affect immunity and may even reduce mortality related to infection and sepsis.[rx] Platelets: A blood slide of platelets aggregating, or, clumping together. The platelets are the small, bright purple fragments. If the number of platelets is too low, excessive bleeding can occur and wound healing will be impaired. However, if the number of platelets is too high, blood clots can form (thrombosis), which may obstruct blood vessels and result in ischemic tissue damage caused by a stroke, myocardial infarction, pulmonary embolism, or the blockage of blood vessels to other parts of the body. Thrombosis also occurs when blood is allowed to pool, which causes clotting factors and platelets to form a blood clot even in the absence of an injury. Platelet Formation Platelets are membrane-bound cell fragments derived from megakaryocytes, which are produced during thrombopoiesis. Key Points Megakaryocytes are produced from stem cells in the bone marrow by a process called thrombopoiesis. Megaryocytes create platelets by releasing protoplatelets that break up into numerous smaller, functional platelets. Thrombopoiesis is stimulated and regulated by the hormone thrombopoietin. Platelets have an average life span of five to ten days. Old platelets are destroyed by phagocytosis. The spleen holds a reservoir of additional platelets. Abnormal numbers of platelets result from problems in thrombopoiesis. This is associated with various disorders and potential pathological complications. Key Terms megakaryocyte: A large cell found in bone marrow that is responsible for the production of platelets. Thrombopoietin: A hormone produced by the liver or kidneys that stimulates megakaryocyte differentiation and platelet release. bone marrow: The fatty vascular tissue that fills the cavities of bones; the place where new blood cells are produced. Platelets are small, clear, irregularly-shaped cell fragments produced by larger precursor cells called megakaryocytes. Platelets are also called thrombocytes because they are involved in the blood clotting process, which is necessary for wound healing. Platelets are continuously produced as a component product of hematopoiesis (blood cell formation). Thrombopoiesis Platelets are produced during hematopoiesis in a sub-process called thrombopoiesis, or the production of thrombocytes. Thrombopoiesis occurs from common myeloid progenitor cells in the bone marrow, which differentiate into promegakaryocytes and then into megakaryocytes. Megakaryocytes stay in the bone marrow and are thought to produce protoplatelets within their cytoplasm, which are released in cytoplasmic extensions upon cytokine stimulus. The protoplatelets then break up into hundreds of platelets that circulate throughout the bloodstream, while the remaining nucleus of the ruptured megakaryocyte is consumed by macrophages. Megakaryocyte and platelet production is regulated by thrombopoietin, a hormone produced by the liver and kidneys. Thrombopoietin stimulates the differentiation of myeloid progenitor cells into megakaryocytes and causes the release of platelets. Thrombopoietin is regulated by a negative feedback mechanism based on platelet levels in the body so that high levels of platelets result in lower levels of thrombopoietin, while low levels of platelets result in higher levels of thrombopoietin. Each megakaryocyte produces between 5,000 and 10,000 platelets before its cellular components are fully depleted. Altogether, around 10^11 platelets are produced each day in a healthy adult. The average lifespan of a platelet is just 5 to 10 days. Old platelets are destroyed by macrophage phagocytosis in the spleen and by Kupffer cells in the liver. Up to 40% of platelets are stored in the spleen as a reserve, released when needed by sympathetically-induced splenic muscle contractions during severe injury. Hematopoiesis: Myeloid progenitor cells differentiate into promegakaryocytes, and megakaryocytes, which release platelets. Implications of Platelet Formation Balanced thrombopoiesis is important because it directly influences the amount of platelets in the body and their associated complications. If the number of platelets is too low, excessive bleeding can occur, even from minor or superficial injuries. If the number of platelets is too high, blood clots can form (thrombosis) and travel through the bloodstream, which may obstruct blood vessels and result in ischemic events. These include stroke, myocardial infarction, pulmonary embolism, or infarction of other tissues. An abnormality or disease of the platelets is called a thrombocytopathy, which could be either a low number of platelets (thrombocytopenia), a decrease in function of platelets (thrombasthenia), or an increase in the number of platelets (thrombocytosis). In any case, issues with the number of circulating platelets is often due to issues in thrombopoietin feedback regulation, but may also be associated with genetic characteristics and certain medications and diseases. For example, thrombocytopenia often occurs in leukemia patients. Cancerous myeloid cells crowd out healthy ones in the bone marrow, causing impaired thrombopoiesis. Disorders of Platelets The three broad categories of platelet disorders are "not enough"; "dysfunctional"; and "too many".[rx]:vii Thrombocytopenia Immune thrombocytopenias (ITP) – formerly known as immune thrombocytopenic purpura and idiopathic thrombocytopenic purpura Splenomegaly Gaucher's disease Familial thrombocytopenia[rx] Chemotherapy Babesiosis Dengue fever Onyalai Thrombotic thrombocytopenic purpura HELLP syndrome Hemolytic–uremic syndrome Drug-induced thrombocytopenic purpura (five known drugs – most problematic is heparin-induced thrombocytopenia (HIT) Pregnancy-associated Neonatal alloimmune associated Aplastic anemia Transfusion-associated Pseudothrombocytopenia idiopathic thrombocytopenic purpura Gilbert's syndrome[rx] Altered platelet function Congenital Disorders of adhesion Bernard–Soulier syndrome Disorders of activation Disorders of granule amount or release Hermansky–Pudlak syndrome Gray platelet syndrome ADP receptor defect Decreased cyclooxygenase activity Storage pool defects, acquired or congenital Disorders of aggregation Glanzmann's thrombasthenia Wiskott–Aldrich syndrome Acquired Disorders of adhesion Paroxysmal nocturnal hemoglobinuria Asthma Samter's triad (aspirin-exacerbated respiratory disease/AERD)[58] Cancer Malaria Decreased cyclooxygenase activity Thrombocytosis and thrombocythemia Reactive Chronic infection Chronic inflammation Malignancy Hyposplenism (post-splenectomy) Iron deficiency Acute blood loss Myeloproliferative neoplasms – platelets are both elevated and activated Essential thrombocytosis Polycythemia vera Associated with other myeloid neoplasms Congenital What Causes Low Platelets?

A low platelet count occurs when: A person’s bone marrow is damaged and unable to make enough of its own platelets. This can be caused by certain cancers, such as Leukemia – and it can also be caused by cancer treatments. Platelets have been lost due to severe bleeding, such as following a traumatic injury or during surgery. Platelets have been destroyed by autoimmune diseases, certain medicines, infections, or other conditions. The patient’s spleen, which filters the bloodstream, removes too…

Bone marrow problems Your bone marrow is the spongy tissue inside the bone. It’s where all the components of blood, including platelets, are produced. If your bone marrow isn’t producing enough platelets, you’ll have a low platelet count. The causes of low platelet production include: aplastic anemia vitamin B-12 deficiency folate deficiency iron deficiency viral infections, including HIV, Epstein-Barr, and chickenpox exposure to chemotherapy, radiation, or toxic chemicals consuming too much alcohol cirrhosis leukemia myelodysplasia Platelet destruction Each platelet lives about 10 days in a healthy body. A low platelet count can also be a result of the body destroying too many platelets. This can be due to the side effects of certain medications, include diuretics and anti-seizure medications. It can also be a symptom of: hypersplenism, or an enlarged spleen an autoimmune disorder pregnancy a bacterial infection in the blood idiopathic thrombocytopenic purpura thrombotic thrombocytopenic purpura hemolytic uremic syndrome disseminated intravascular coagulation Causes of High Platelet Count If the body has too many platelets in circulation, you may develop a condition called thrombocytosis. The following factors may contribute to high platelet count:3 Primary bone marrow disorder - Essential thrombocytosis is a condition in which the megakaryocytes in the bone marrow produce too many platelets, increasing the risk of blood clots. Chronic inflammation in the body - Inflammatory conditions such as rheumatoid arthritis (RA) and inflammatory bowel disease (IBD) may result in elevated platelet counts as high levels of inflammation may cause the bone marrow to produce more white blood cells and platelets to combat cellular damage. Infection - Bone marrow cells increase the production of white blood cells and platelets to help fight infection, causing an elevation in platelet count. Iron deficiency anemia - Reactive or secondary thrombocytosis may result when the body is undergoing a breakdown of red blood cells and the bone marrow cells go into overproduction to meet needs. Spleen removal - Up to one-third of platelets are stored in the spleen at any time, and so removal of this organ will cause an increase in platelet concentration in the bloodstream. This is generally a temporary condition, however. Cancer - High platelet counts can also be seen in cancer, especially with gastrointestinal cancer, as well as lymphoma, lung, ovarian, and breast cancer. This is thought to be due to the inflammation associated with the malignancy stimulating the production of platelets in the bone marrow. In addition, a temporary increase in the platelet count can happen after major surgery or trauma. What are the symptoms of a low platelet count?

Whether or not you experience symptoms depends on your platelet count. Mild cases, such as when a low platelet count is caused by pregnancy, usually don’t cause any symptoms. More severe cases may cause uncontrollable bleeding, which requires immediate medical attention. If you have a low platelet count, you may experience: red, purple, or brown bruises, which are called purpura a rash with small red or purple dots called petechiae nosebleeds bleeding gums bleeding from wounds that lasts for a prolonged period or…

How is a low platelet count diagnosed?

If your doctor suspects a low platelet count, they’ll first perform a physical examination. During the exam, your doctor will check your body for any unusual bruising or evidence of petechiae, which is a sign of capillary bleeding that often accompanies a low platelet count. Your doctor may also feel your abdomen to check for an enlarged spleen, which can cause a low platelet count. You may also be asked if you have any family history of bleeding disorders since…

What is the treatment for a low platelet count?

The treatment for a low platelet count depends on the cause and severity of your condition. If your condition is mild, your doctor may wish to hold off on treatment and simply monitor you. Your doctor may recommend that you take measures to prevent your condition from worsening. This could include: avoiding contact sports avoiding activities with a high risk of bleeding or bruising limiting alcohol consumption stopping or switching medications that affect platelets, including aspirin and ibuprofen

Medicines You may need one or more medicines to treat a low or high platelet count. Medicines to treat high platelet count Anagrelide: This medicine can lower platelet counts in people who have a high risk of complications such as serious blood clots. This medicine may cause anemia and scarring of your bone marrow. Aspirin: This medicine helps prevent blood clots. Aspirin can raise your risk of bleeding. Hydroxyurea: This is used to reduce platelet counts. Possible side effects include making fewer blood cells, skin wounds, problems with your digestive system, and fever. Interferon-a and pegylated interferon: These medicines help reduce platelet counts. Side effects include extreme tiredness, flu-like symptoms, and confusion. Medicine to treat low platelet count Anti-D immunoglobulin: This medicine is used to increase platelet counts in some people who have immune thrombocytopenia. Possible side effects include flu-like symptoms, low hemoglobin  levels, and a breakdown of your red blood cells. Corticosteroids: These medicines help increase platelet counts. Corticosteroids include prednisone, prednisolone, and dexamethasone. This may be the first treatment your provider recommends for a low platelet count. Possible side effects include diabetes, insomnia, high blood pressure, digestive problems, mood changes, and slow growth in children. Fondaparinux: This is used to treat heparin-induced thrombocytopenia (HIT). This medicine may cause bleeding, anemia, insomnia, dizziness, low blood pressure, and confusion. Immunosuppressors: These medicines stop your immune system from destroying your platelets. They are used to treat immune thrombocytopenia when corticosteroids do not work. Examples of this type of medicine include azathioprine, cyclophosphamide, cyclosporine, danazol, and dapsone. These medicines may increase your risk for infection. Other, less serious side effects can include loss of appetite, nausea, vomiting, increased hair growth, and hand trembling. These effects get better and may go away as the body adjusts to the medicine. Intravenous immunoglobulin (IVIG): This is used to increase your platelet count and treat major bleeding in immune thrombocytopenia. IVIG is also used to treat HIT. Complications may include serious allergic reactions and damage to your kidneys or lungs. Rituximab: This is an antibody treatment that may be used to treat immune thrombocytopenia or thrombotic thrombocytopenic purpura. This medicine may raise your risk of infections. Thrombopoetin receptor agonist (TPO-RA) such as romiplostim and eltrombopag: These increase platelets in immune thrombocytopenia. They are used most often after other treatments have not worked. Possible side effects include low platelets, damage to the liver, venous thromboembolism, cataracts, bruising, and nosebleeds. Procedures You may need one or more of the following procedures to treat your platelet disorder. Plasma exchange: This is used to treat thrombotic thrombocytopenic purpura. In this procedure, the liquid part of your blood (plasma) is replaced with donor plasmas using a machine that collects the cells in your blood. Plasma infusion: This is used to treat thrombotic thrombocytopenic purpura that is caused by your body not making enough of a protein called ADAMTS13. A plasma infusion helps replace the missing protein. Platelet transfusion: This procedure is used to quickly increase your platelet count when you are having serious bleeding. Possible complications include risk of infectious disease, allergic reaction, and difficulty with future transfusions. If you have HIT, a platelet transfusion can raise your risk of forming blood clots. Plateletpheresis: This is used to treat life-threatening clotting in people who have high platelet counts. This procedure removes platelets from your blood and returns the liquid part of your blood (plasma) to your bloodstream. Bone marrow transplant: This procedure can help treat life-threatening types of platelet disorders. It is used to treat conditions that occur when the stem cells in your bone marrow do not make enough platelets. Surgery to remove your spleen (splenectomy): Your spleen is an organ in your upper left abdomen that stores platelets. Removing your spleen helps raise your platelet count. This helps treat a low platelet count. Possible complications include bleeding, infection, and blood clots. What health problems can platelet disorders cause?

Platelet disorders can cause the following complications: Bleeding from your nose and gums Menstrual bleeding lasting more than 7 days, called menorrhagia Bleeding in your brain or your digestive system Blood clots, which can block blood flow to your limbs and organs, such as your lungs and brain Blood or bone marrow cancer Bone marrow failure Heart attack or decreased blood flow to your heart Pregnancy complications If you think that you are or someone else is having symptoms of serious…

References

Add references, clinical guidelines, textbooks, journal articles, or trusted medical sources here. You can edit this area from the RX Article Professional Blocks panel.

More from this topic
  1. Congenital Epstein–Barr Virus Infection

    DefinitionCongenital? Epstein–Barr virus infection? means a baby is thought to get Epstein–Barr virus, or EBV, before birth while still inside the mother’s womb. EBV is also...

    April 4, 2026 • Rx Blood, Metabolism, and Infectious Diseases (A - Z)
  2. Mother-to-Child Transmission of Enterovirus Infection

    DefinitionMother-to-child transmission of enterovirus infection? means an enterovirus infection? passes from a pregnant mother to her baby before birth, during labor, at the time of delivery,...

    April 4, 2026 • Rx Blood, Metabolism, and Infectious Diseases (A - Z)
  3. Congenital Enterovirus Infectious Disease

    DefinitionCongenital? enterovirus infectious disease means an enterovirus infection? that is already present in the baby before birth or becomes apparent at birth or in the first...

    April 4, 2026 • Rx Blood, Metabolism, and Infectious Diseases (A - Z)
  4. Congenital Enterovirus Infection

    DefinitionCongenital? enterovirus infection? means a baby is infected with an enterovirus before birth or around the time of birth from the mother. In very simple words,...

    April 3, 2026 • Rx Blood, Metabolism, and Infectious Diseases (A - Z)
  5. Congenital Enterocyte Heparan Sulfate Deficiency

    DefinitionCongenital? enterocyte heparan sulfate deficiency is a real but ultra-rare genetic intestinal disease. It causes the small-intestine lining cells, called enterocytes, to lack heparan sulfate on...

    April 3, 2026 • Rx Blood, Metabolism, and Infectious Diseases (A - Z)
  6. Congenital Dyserythropoietic Anemia Type 4

    DefinitionCongenital? dyserythropoietic anemia? type 4, often called CDA type IV, is a very rare inherited red blood cell disorder linked to KLF1 dysfunction. In this disease,...

    April 1, 2026 • Rx Blood, Metabolism, and Infectious Diseases (A - Z)
  7. Congenital Dyserythropoietic Anemia

    DefinitionCongenital? dyserythropoietic anemia?, or CDA, is a rare inherited blood disease. In this disease, the bone marrow makes red blood cells in an abnormal way. Many...

    April 1, 2026 • Rx Blood, Metabolism, and Infectious Diseases (A - Z)
  8. Congenital Dyshaematopoietic Anemia

    DefinitionCongenital? dyshaematopoietic anemia? is more commonly called congenital? dyserythropoietic anemia?, or CDA. It is a rare inherited blood disorder. In this disease, the bone marrow makes...

    April 1, 2026 • Rx Blood, Metabolism, and Infectious Diseases (A - Z)
  9. Congenital Dyserythropoietic Anemia

    DefinitionCongenital? dyserythropoietic anemia?, often called CDA, is a rare inherited blood disorder. In this disease, the bone marrow makes red blood cells in an abnormal way....

    April 1, 2026 • Rx Blood, Metabolism, and Infectious Diseases (A - Z)
  10. Carbohydrate-Deficient Glycoprotein Syndrome Type IE

    DefinitionCarbohydrate-deficient glycoprotein syndrome type Ie is an old name for DPM1-congenital? disorder of glycosylation, often written as DPM1-CDG. It is a very rare inherited metabolic disease....

    April 1, 2026 • Rx Blood, Metabolism, and Infectious Diseases (A - Z)