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- MONOCYTES enlarge and mature to become macrophage or

histiocytes; they perform phagocytosis.

- LYMPHOCYTES (T- lymphocytes and B-lymphocytes) are

responsible for specific immune responses. T-cells are involved in

cell-mediated immunity, while B-cells are involved in humoralimmunity.

THROMBOCYTES (PLATELETS)  – along with the coagulation factors in

plasma, are essential to normal blood clotting.

-  They help constrict damaged blood vessels.

-  They form hemostatic plugs in injuryed blood vessels by

becoming swollen, spiky, sticky, and secretory.

-  They provide substances that accelerate blood clotting such as

factors III and XIII and platelets factor 3.

LEUKEMIA

Are cancers of the blood-forming tissues. White blood cells may be produced in excessive

amounts and are unable to work properly which weakens the immune system.

Normally, blood cells are produced in an orderly, controlled way, as the body needs them.

This process helps keep us healthy. When leukemia develops, the body produces large numbers of 

abnormal blood cells. In most types of leukemia, the abnormal cells are white blood cells. The

leukemia cells usually look different from normal blood cells, and they do not function properly.

POSSIBLE RISK FACTORS

• ionizing radiation

• exposure to chemicals and drugs

• bone marrow hypoplasia (reduced production of blood cells)

• genetic factors

• immunologic factors

• Environmental factors and the interaction of theses factors.

PATHOPHYSIOLOGY

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PHYSICAL MANISFESTATION

Integumantary Manifestations:

Ecchymoses

Petechiae

Open infected lesions

Pallor of the conjunctiva, nail beds, palmar creases, and around the mouth.

Gastrointestinal Manifestations:

Bleeding gums

Anorexia

Weight loss Enlarged liver and spleen

Renal Manifestations:

Hematuria

Cardiovascular Manifestations:

Tachycardia at basal activity levels.

Orthostatic hypotension

Palpitations

Respiratory Manifestations:

Dyspnea on exertion.

Neurologic Manifestations:

Fatigue

Headache

Fever 

Musculoskeletal Manifestations:

Bone pain

Joint swelling and pain.

Diagnostic Evaluation

1. CBC and blood smear – peripheral WBC count varies widely from 1,000 to 100,000/mm3

and may include significant numbers of abnormal immature (blast) cells, anemia may be

profound; platelet count may be abnormal and coagulopathies may exist.

2. Bone marrow aspiration and biopsy – cells also studied for chromosomal abnormalities

(cytogenetics) and immunologic markers to classify type of leukemia further.

3. Lymph node biopsy – to detect the spread.

4. Lumbar puncture and examination of cerebrospinal fluid for leukemic cells (especially ALL).

Treatment

To eradicate leukemic cells and allow restoration of normal hematopoiesis.

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1. High-dose chemotherapy given as an induction course to obtain a remission (disappearance

of abnormal cells in bone marrow and blood) and then in cycles as consolidation or maintenance

therapy to prevent recurrence of disease.

2. Leukapheresis (or exchange transfusion to infants) may be used when abnormally high

numbers of white cells are present to reduce the risk of leukostasis and tumor burden before

chemotherapy.

3. Radiation particularly of central nervous system (CNS) in ALL.

4. Autologous or allogeneic bone marrow or stem cell transplantation.

Complications

1. Leukostasis; in setting of high numbers (greater than 50,000/mm3) of circulating leukemic

cells (blasts), blood vessel walls are infiltrated and weakened, with high risk of rupture and

bleeding, including intracranial hemorrhage.

2. Disseminated intravascular coagulation(DIC).

3. Tumor lysis syndrome: rapid destruction of large numbers of malignant cells leads to

alteration in electrolytes (hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia).4. May lead to renal failure and other complications.

5. Infection, bleeding, and organ damage.

Pharmacologic Interventions

Acute leukemia

 Different types of leukemia are best treated with different kinds of medicine.

Acute lymphoblastic leukemia (ALL) drugs include prednisone, vincristine, daunorubicin, L-

asparaginase or pegaspargase, methotrexate, and cyclophosphamide. Imatinib (Gleevec) is

sometimes used to treat ALL. Dasatinib (Sprycel) is a newer drug for treating some ALL that has

not improved with other drugs. Acute myelogenous leukemia (AML) drugs include daunorubicin, idarubicin, cytosine

arabinoside, and mitoxantrone.10 Gemtuzumab (Mylotarg) may be given to people whose AML

has relapsed. It helps your body destroy cancer cells.

Acute promyelocytic leukemia (APL) drugs include all-trans-retinoic acid (ATRA) and

chemotherapy with arsenic trioxide, idarubicin, or daunorubicin. ATRA helps control the risk of 

life-threatening bleeding from disseminated intravascular coagulation (DIC). Later treatment can

include ATRA with or without methotrexate and 6-mercaptopurine. Or if a first round of ATRA

and chemotherapy does not work, arsenic trioxide may be used.10

To treat leukemia in the brain or prevent it from spreading to the brain and central nervous

system, methotrexate and cytarabine/cytosine arabinoside are injected into the spinal canal. This

is called intrathecal chemotherapy.

Supportive treatments during cancer treatment include:

Antibiotics and immunoglobulins help to prevent or fight infections. This is important when

you do not have enough normal white blood cells to fight infections on your own.

Transfusions of red blood cells and platelets.

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Epoetin and hematopoietic stimulants help your body make new blood cells.

Allopurinol  to prevent kidney problems and gout.

Saline or steroid eyedrops for relief during treatment with cytarabine/cytosine arabinoside.

Chronic leukemia

Chemotherapy for chronic leukemia can involve a single drug or a combination of drugs. For 

example, you may be given a combination of cyclophosphamide, vincristine, and prednisone.

Other drug choices include fludarabine, chlorambucil, hydroxyurea

(hydroxycarbamide),cytarabine, busulfan, rituximab, and alemtuzumab.

Allopurinol  may be given to prevent kidney problems and gout.

Dasatinib (Sprycel) blocks the growth of cancer cells. It can be used for CML that has not

been helped by imatinib or other drugs.

Imatinib (Gleevec) blocks the growth of cancer cells. It is often given to people who

havechronic myelogenous leukemia (CML).

Immune globulin (IG) helps prevent infections. It is sometimes used for people with chronic

lymphocytic leukemia (CLL), because CLL weakens the immune system.

Interferon alfa helps your immune system fight disease and may keep cancer cells from

growing. It is often given to people who have CML.

Medication for nausea and vomiting

 Nausea and vomiting are common side effects of chemotherapy. These side effects usually are

temporary and go away when treatment is stopped. Your doctor will prescribe drugs to help

relieve nausea. These may include:

Aprepitant  (Emend), which is used in combination with ondansetron and dexamethasone as

part of a 3-day program. Dimenhydrinate, such as Dramamine.

Metoclopramide, such as Reglan and Octamide.

Phenothiazines, such as Compazine and Phenergan.

Serotonin antagonists, such as ondansetron (Zofran), granisetron (Kytril), or dolasetron

(Anzemet). These drugs work best when they are combined with corticosteroids such as

dexamethasone (Hexadrol).

Nursing Interventions

Preventing infection:

Frequently monitor the client for pneumonia, pharyngitis, esophagitis, perianal cellulitis,

urinary tract infection, and cellulitis, which are common in leukemia and which carry significantmorbidity and mortality.

Monitor for fever, flushed appearance, chills, tachycardia; appearance of white patches in

the mouth; redness, swelling, heat or pain in the eyes, ears, throat, skin, joints, abdomen, rectal

and perineal areas; cough, changes in sputum; skin rash.

Check results of granulocyte counts. Concentrations less than 500/mm3 put the patient at

serious risk for infection.

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RBC’s are produced by the bone marrow a process known as erythropoiesis. Before a red blood cell

is formed, the hematopoietic stem cell first produces an uncommitted stem cell to be formed to

committed progenitor cell. Progenitor cells are not only the precursor of RBC, but also of 

lymphocytes and megakaryocytes (antecedent of platelets). Before an erythrocyte is formed the

progenitor cells develop an erythroblast, then a reticulocyte, and finally erythrocyte (RBC). A

hormone, erythropoietin, which is secreted by the kidney, also controls RBC production by

stimulating the bone marrow.

Types of anemia

Hypoproliferative Anemias

This type of anemia covers all condition where the bone marrow incapable of producing enough cells

to develop to erythrocyte. Lack of erythropoietin may also be a contributing factor of the

abnormality. The following types of anemia are under this classification:

 Aplastic anemia –In this condition, the precursor cells (stem or progenital cells, which is

responsible in forming components of blood) are extremely deficient, thereby, production of all

formed elements (including RBC, lymphocyte, megakaryocytes) are reduced. Because of thedepressed bone marrow function, it is replaced by fat cells leading to anemia, excessive

bleeding (thrombocytopenia) and infections (depressed WBC count). This type of anemia is also

a common example of a pancytopenic disorder.

Iron-deficiency anemia – It is also called microcytic, hypochromic anemia. This is type of 

anemia is the most common form among all ages, and is characterized by a low iron

concentration in the body.

Megaloblastic anemia – A macrocytic, normochromic anemia results as the essential

factors (vitamin B12 and folic acid) for normal DNA synthesis are missing causing suppression of 

mitosis in the bone marrow and allowing the RNA or protein synthesis to take place for the

progression of cell growth without cell division. The resulting cells remain enlarged (becausemitosis is absent).

1. 1. Vitamin B12 deficiency – Vitamin B12 or cobalamin is required for normal DNA synthesis.

It is not synthesized in the tissues of but solely depends on the dietary intake of meat, liver, dairy

products and sea foods.

2. 2. Folic Acid Deficiency – folic acid is also important for the DNA synthesis of cells. The

dietary sources of folate are meats, eggs, leafy vegetables which are easily available.

Hemolytic Anemias

This type of anemia refers to the state where hemolysis (erythrocyte destruction) causes symptoms

of anemia. Classification of this condition is further narrowed into intrinsic (inherited) or extrinsic

(damage in erythrocyte is caused by environmental factors).

Intrinsic Hemolytic Anemia

1. Sickle Cell anemia – an inherited disorder on the beta chain of the hemoglobin resulting to

abnormally shaped red blood cells. In this condition an abnormal hemoglobin S (HbS) is

contained in the RBC’s causing distortions or sickling of the red blood cells.

2. Thalassemia – group of genetic disorders that involve a defective hemoglobin- chain

synthesis. Thalassemia major is threatening disease characterized by severe anemia,

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hemolysis and ineffective erythropoiesis. Thalassemia minor is a mild form of anemia. The

affected individual has only one defective gene and is asymptomatic.

Extrinsic Hemolytic Anemia

1. Immune hemolytic anemia – a person’s own antibodies destroy his own red blood cells

(hemolysis).

2. Mechanical hemolytic anemia – hemolysis is caused by trauma or physical injuries that

disrupt red blood cells altering and tearing them through the small vessels.

Erythrocyte Disorders

If the number of erythrocytes is excessive or inadequate, erythrocytes problems would arise.

Excessive numbers of erythrocytes result to a condition called polycythemia. When erythrocytes

numbers is decreased or hemoglobin levels drop, the condition of compromised oxygen transport

occurs resulting to anemia.

Anemia

Whatever the reason is, when a decrease in the oxygen-carrying capacity of the blood takes placethe resulting condition is anemia. This is usually indicated by a hemoglobin levels that falls below the

lower limit of its normal range (listed above). Anemia may be the result of the following:

1. Decreased number of Red Blood Cells

2. Abnormal or deficient Hemoglobin content in the RBCs

 

As a result, a decline in the blood’s oxygen transport capacity would trigger the various physiologic

compensations. The following physiologic compensatory events follow when hemoglobin or red

blood cells levels drop:

1. Arteriolar dilatation to provide increased blood flow.

2. Increased blood flow would result to an elevation of cardiac output.3. Shift to anaerobic metabolism to reduce oxygen compensation and indirectly promote the

dissociation of oxygen from hemoglobin.

4. Increased renal secretion of erythropoietin to stimulate the marrow to

increase erythropoiesisand speed RBC production.

Inability of the body to facilitate the listed compensatory mechanisms would result to a drop in

hemoglobin levels to 7-8 g/dl. Thus, signs and symptoms of hypoxia emerge such as the following:

1. Paleness or pallor 

2. Weakness

3. Lethargy

4. Excessive intolerance

 

Polycythemia

Increased red blood cell concentration in the blood leads to a condition cally polycythemia.

Polycythemia may be due to:

1. An increase in red cell numbers with a normal plasma volume

2. Absolute polycythemia

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3. Normal red blood cell numbers suspended in a reduced plasma volume a condition called

relative polycythemia

These conditions would result to an elevated packed cell volume (PCV), hematocrit and the

hemoglobin level.

Absolute Polycythemia versus Secondary Polycythemia

In primary absolute polycythemia, an overproduction of erythrocytes by the marrow takes place.

Secondary polycythemia occurs when the renal output of eryhthropoiesis is elevated hence,

resulting to an increased activity of the marrow. The latter condition is a result of physiologic

compensatory mechanism of the tissue to hypoxia. In cases where erythropoietin (EPO) production

is increased but no physiologic requirement is present, possible renal tumor is present. Aside from

that, smokers may also suffer from secondary polycythemia. Significant levels of carbon monoxide

are delivered to the blood when products of combustion are inhaled. Carbon monoxide binds with

hemoglobin 200 times than that of oxygen. Thus, presence of this chemical in a smoker’s blood

would result to a compromised oxygen delivery and increased erythropoietin secretion in the renal

system.In primary absolute polycythemia, there is no elevated erythropoietin stimulus even when the

marrow stem cells are proliferating. This condition is an effect of the presence of a benign tumor.

The red cells are proliferating resulting to a dominant amount of eryhthrocytes in the blood over 

other components. In such cases, the normal or elevated tissue supply of oxygen suppresses EPO

secretion.

Polycythemia Vera

Sometimes called polycythemia rubra vera, polycythemia vera is another myeloproliferative condition

which is characterized by an increased viscosity of the blood. The thickened blood sluggishly flows

through the small vessels. Coagulation within these vessels is predisposed by this event especially

in the kidneys, spleen and liver. Blockage of the vessels results to nutrient deprivation and tissuedestruction.

Relative Polycythemia

With relative polycythemia, hematocrit levels are increased (information about hematocrit discussed

below), however, the total number of red blood cells is just normal. The plasma deficiency that

produces this state may be the result of the following conditions:

Generalized dehydration

Extensive skin burns

Pronounced diarrhea or vomiting

Diuresis

Heavy smoking – smoker’s polycythemia.

Stress – stress polycythemia. Typically, hard-driving male sufferers are also at high risk for 

heart and brain vascular diseases.

Points to Remember 

The major problem in cases of polycythemia or excessive red blood cells is the increased

viscosity of the blood, which causes it to flow sluggishly in the body and worst impairing the

circulation.

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The major problem in cases of anemia or decreased red blood cell count or hemoglobin

levels is the decreased in blood viscosity, which results to thinning of the blood and its flowing

rapidly into the vessels.

Megaloblastic Anemias

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Definition

Megalosblastic anemias are characterized by the presence of enlarged red cells (megaloblasts) due

to the impaired cell division. Because the erythrocytes that reach the circulation are enlarged, a

macrocytic and normochromic anemia results.

Pathophysiology

Causes

Vitamin B12 deficiency

Folic acid deficiency

Vitamin B12 and Folic acid are essential for normal DNA synthesis of erythrocyte formation. When

these vitamins are deficient erythrocyte’s DNA synthesis is affected. Mitosis in the progenitor lines issuppressed and abnormal increase in the number of normal cells or hyperplasia occurs. Since there

is no impairment of the RNA or protein synthesis cell growth still proceeds. However, because

mitosis or cell division can’t occur (because of the absence of Vitamin B12 and Folic Acid) the

marrow precursors (erythroid and myeloid cells) remain enlarged which are termed

asMEGALOBLASTS. Many of these cells die within the marrow so the mature cells that leave the

marrow is decreased in number. As a result, pancytopenia (deficiency of all cellular elements of the

blood) develops.

Types of megaloblastic anemia

Vitamin B12 deficiency 

Vitamin B12, also known as cobalamin, is not synthesized in the tissues. Thus, the body relies onthe dietary intake of meat, liver, seafood and dairy products to supply our needs. The body stores

more than a 3-year supply of vitamin B12 in the liver.

Causes:

1. Inadequate dietary intake

2. Impaired gastrointestinal absorption (absence of intrinsic factor, pernicious anemia,

gastrectomy, chronic gastritis)

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Clinical Manifestations:

1. Weakness

2. Listless

3. Pale

4. Smooth sore red tongue and diarrhea (those with pernicious anemia)

5. Neurologic manifestations (confusion, paresthesia, paralysis, severe neuropathy)

Diagnostic evaluation:

Schilling test (to determine the cause of Vitamin B12 deficiency)

Management:

Vitamin B12 replacement

Oral supplementation if the cause is inadequate cobalamin intake.

In cases of defective absorption or absence of intrinsic factor, replacement is by

intramuscular (IM) injection of Vitamin B12.

Folic Acid Deficiency 

Folic Acid is another vitamin that is necessary for normal red blood cell production. It is stored in thebody as folates. The dietary sources of folate are meats, eggs and leafy vegetables. Body stores of 

folic acid provide a five-month period of tolerance from proven deficient folic acid in the diet.

Causes:

1. Inadequate folate in the diet

2. Alcoholism (alcohol increases folic acid requirements in the body)

Clinical Manifestations:

Symptoms of folic acid and Vitamin B12 deficiency are the same however, neurologic manifestations

of Vitamin B12 deficiency do not occur when folic acid is deficient.

Management:

1. Nutritious diet2. Administration of 1 mg folic acid a day (oral)

3. For patients with malabsorption, folic acid is administered intramuscularly (IM)

Iron-deficiency Anemia

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Definition: Iron deficiency anemia (IDA)is an

ailment when there is not enough hemoglobin produced by the body to meet its requirement.

The benchmark for its diagnosis is marked by below-normal total body iron

Etiology:

It is caused by inadequate intake of iron-rich foods or inadequate absorption of iron.

Some of the known could be due to:

a.) chronic diarrhea

b.) malabsorption syndromes

c.) high cereal intake with low animal protein ingestion partial or complete gastrectomy

Prevalence: It is more common in developing countries and tropical zones. According to the Food

and Nutrition Research Institute (FNRI) as of 2003, in the Philippines iron deficiency anemia is

common among children 6 months to one year old, pregnant and lactating women. Government

efforts are still being implemented since it poses a public concern. Women between 15 – 45 years

old are the ones being mostly affected.

Pathophysiology: In IDA, when iron levels in the body decreases, transferrin which binds with andtransport iron is also depleted. As a result, red blood cells (RBCs) the oxygen carrying component of 

the blood is likewise depleted leading to decreased levels of hemoglobin in the body.

Physical Findings:

Asymptomatic if in mild cases

palpitations, dizziness and cold sensitivity

brittleness of hair, nails and pallor 

dysphagia, stomatis, atrophic glossitis

dyspnea and weakness

Diagnosttic Examinations:

Complete Blood count – first test to check the levels of the parts of the blood (red blood cells,white blood cells, platelets)

Reticulocyte count - The test shows whether your bone marrow is making red blood cells at

the correct rate.

Peripheral smear – To check whether the red blood cells look (microcytic) smaller and

(hypochromic) paler than normal

Serum iron markedly decreased

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Serum ferritin decreased

*Ferritin – a protein that binds with iron in the body making it easier to be transported.

Medical Management:

1. Oral supplements of iron (Ferrous Sulphate)

2. Parenteral Iron – for children with iron malabsorption or chronic hemoglobinuria

3. Transfusion – indicated for severe anemia cases of severe infection, cardiac dysfunction

Nursing Management:

1. Asses for fatigue, activity intolerance, and other sings of impaired tissue oxygenation

2. Promote an adequate intake of iron-rich foods (iron fortified formula and cereals, liver, egg

yolk, and organ meats

3. Emphasize to family members or care givers proper administration of oral iron supplements.

Give supplements in two or three divided doses in small amount of Vitamin C-containing liquid.

(This enhances absorption)

4. Explain the potential adverse effects of iron which includes nausea and vomiting, diarrhea or 

constipation or black stools and tooth discoloration.5. Instruct care givers to keep iron supplements out of reach of children since it is toxic when

overdosed.

Idiopathic Thrombocytopenic Purpura

(Also Called 'ITP (Immune Thrombocytopenic Purpura)')

What is Idiopathic Thrombocytopenic Purpura?Idiopathic thrombocytopenic purpura (ITP) is a bleeding condition in which the blood

doesn't clot as it should. This is due to a low number of blood cell fragments called

platelets (PLATE-lets).

Platelets also are called thrombocytes. They're made in your bone marrow along with

other kinds of blood cells. Platelets stick together (clot) to seal small cuts or breaks on

blood vessel walls and stop bleeding.

"Idiopathic" means that the cause of the condition isn't known. "Thrombocytopenic"

means there's a lower than normal number of platelets in the blood. "Purpura" refers to

purple bruises caused by bleeding under the skin.

OverviewPeople who have ITP often have purple bruises that appear on the skin or on the

mucous membranes (for example, in the mouth). The bruises mean that bleeding has

occurred in small blood vessels under the skin.

A person who has ITP also may have bleeding that results in tiny red or purple dots on

the skin. These pinpoint-sized dots are called petechiae. Petechiae may look like a rash.

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petechiae (red/purple dots) and purpura (bruises) in the skin. Bleeding under the skin

causes the purple, brown, and red color of the petechiae and purpura.

People who have ITP also may have nosebleeds, bleeding from the gums when they

have dental work done, or other bleeding that's hard to stop. Women who have ITP may

have menstrual bleeding that's heavier than usual.

More extensive bleeding can cause hematomas. A hematoma is a collection of clotted

or partially clotted blood under the skin. It looks or feels like a lump.

Bleeding in the brain as a result of ITP is very rare, but can be life threatening if it

occurs.

In most cases, an autoimmune response is believed to cause ITP. Normally your immune

system helps your body fight off infections and diseases. But if you have ITP, your

immune system attacks and destroys its own platelets. The reason why this happens

isn’t known.

ITP can't be passed from one person to another.

Types of Idiopathic Thrombocytopenic Purpura There are two types of ITP: acute (temporary or short-term) and chronic (long-lasting).

Acute ITP generally lasts less than 6 months. It mainly occurs in children, both boys and

girls, and is the most common type of ITP. Acute ITP often occurs after an infection

caused by a virus.

Chronic ITP is long-lasting (6 months or longer) and mostly affects adults. However,

some teenagers and children can get this type of ITP. Chronic ITP affects women 2 to 3

times more often than men.

 Treatment depends on how severe the bleeding symptoms are and the platelet count.

In mild cases, treatment may not be needed.

Outlook For most children and adults, ITP isn't a serious or life-threatening condition.

Acute ITP in children often goes away on its own within a few weeks or months and

doesn't return. In 80 percent of children who have ITP, the platelet count returns to

normal within 6 to 12 months. Treatment may not be needed.

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A small number of children, about 5 percent, whose ITP doesn't go away on its own may

need to have further medical or surgical treatment.

Chronic ITP will vary with each individual and can last for many years. Even people who

have severe forms of chronic ITP can live for decades. Most people who have chronic ITP

are able at some point to stop treatment and keep a safe platelet count.

Other names for Idiopathic Thrombocytopenic Purpura

• Immune thrombocytopenic purpura

• Autoimmune thrombocytopenic purpura

What causes Idiopathic Thrombocytopenic Purpura?In most cases, it's believed that an autoimmune response causes idiopathic

thrombocytopenic purpura (ITP).

Normally, the immune system makes antibodies (proteins) to fight off germs or other

harmful things that enter the body. In ITP, however, the immune system attacks and

destroys the body's platelets by mistake. Why this happens isn't known.

Children who get acute (short-term) ITP often have had recent viral infections. It's

possible that the infection somehow "triggers" or sets off the immune reaction that

leads to ITP in these children. ITP in adults, on the other hand, doesn't seem to be linked

to infections.

Who is at risk for Idiopathic Thrombocytopenic Purpura?Both children and adults can develop idiopathic thrombocytopenic purpura (ITP).

Children usually get the acute (short-term) type of ITP. Acute ITP often develops after an

infection caused by a virus. Adults tend to get the chronic (long-lasting) type of ITP.

Women are 2 to 3 times more likely than men to get chronic ITP.

ITP is a fairly common blood disorder, with 50 to 150 new cases per every 1 million

people each year; about half of these cases are children. However, the number of cases

of ITP is rising because routine blood tests that can detect a low platelet count are being

done more often.

ITP can't be passed from one person to another.

What are the signs and symptoms of IdiopathicThrombocytopenic Purpura?

Having a low platelet count doesn’t cause symptoms. However, the bleeding that a low

platelet count can cause may have the following signs and symptoms:

• Pinpoint red spots on the skin that often are found in groups and may look like a

rash. The spots, called petechiae, are due to bleeding under the skin.

• Bruising or purplish areas on the skin or mucous membranes (such as in the

mouth) due to bleeding under the skin. The bruises may occur for no known

reason. This type of bruising is called purpura. More extensive bleeding can

cause hematomas. A hematoma is a collection of clotted or partially clotted blood

under the skin. It looks or feels like a lump.

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• Nosebleeds or bleeding from the gums (for example, when dental work is done).

• Blood in the urine or stool (bowel movement).

Any kind of bleeding that's hard to stop could be a sign of ITP. This includes menstrual

bleeding in women that’s heavier than usual.

Bleeding in the brain is rare, and the symptoms of bleeding in the brain may vary in

severity.

A low number of platelets doesn't cause pain, fatigue (tiredness), problems

concentrating, or any other symptoms.

How is Idiopathic Thrombocytopenic Purpura Diagnosed? Your doctor will diagnose idiopathic thrombocytopenic purpura (ITP) based on your

medical history, a physical exam, and test results.

 Your doctor will want to make sure that your low platelet count isn't due to another

condition (such as an infection) or a side effect of medicines you're taking (such as

chemotherapy medicines or aspirin).

Medical history 

 Your doctor may ask about:

•  Your signs and symptoms of bleeding and any other signs or symptoms you're

having

• Whether you have illnesses that could lower your platelet count or cause

bleeding

• Medicines or any other over-the-counter supplements or remedies you take that

could cause bleeding or lower your platelet count

Physical exam

 Your doctor will give you a physical exam and look for signs of bleeding and infection.For example, your doctor may look for pinpoint red spots on the skin and bruising or

purplish areas on the skin or mucous membranes. These are signs of bleeding under the

skin.

Diagnostic tests

 You'll likely have blood tests to check your platelets. These tests usually include:

• A complete blood count. This test shows the numbers of different kinds of blood

cells, including platelets, in a small sample of your blood. In ITP, the red and

white blood cell counts are normal.

• A blood smear. During this test, some of your blood is put on a slide. A

microscope is then used to look at your platelets and other blood cells. In ITP, the

number of platelets is lower than normal.

 You also may have a blood test to check for the antibodies that attack platelets.

If blood tests show that you have a low number of platelets, your doctor may

recommend more tests to confirm a diagnosis of ITP. For example, bone marrow tests,

may be used to see whether your bone marrow is making platelets.

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Some people who have mild ITP have few or no signs of bleeding. These people may be

diagnosed only after a blood test done for another reason shows that they have a low

platelet count.

How is Idiopathic Thrombocytopenic Purpura treated? Treatment for idiopathic thrombocytopenic purpura (ITP) is based on how much and

how often you’re bleeding and your platelet count. In some cases, treatment may not

be needed.

Medicines often are used as the first course of treatment. Treatments used for children

and adults are similar.

Adults with ITP who have very low platelet counts or problems with bleeding often are

treated. Adults who have milder cases of ITP may not need any treatment, other than

watching their symptoms and platelet counts.

 The acute (short-term) type of ITP that occurs in children often goes away within a few

weeks or months. Children who have bleeding symptoms, other than merely bruising

(purpura), usually are treated.

Children who have milder cases of ITP may not need treatment other than monitoring

and follow-up to make sure platelet counts return to normal.

Medicines

If adults or children who have ITP need treatment, medicines often are tried first.

Corticosteroids, such as prednisone, are commonly used to treat ITP.

 These medicines, called steroids for short, help increase your platelet count by lowering

the activity of your immune system. However, steroids have a number of side effects,

and some people relapse (get worse) when treatment ends.

 The steroids used to treat ITP are different from illegal steroids taken by some athletes

to enhance performance. Corticosteroids aren't habit-forming, even if you take them for

many years.

Some medicines used to help raise the platelet count are given through a needle

inserted into a vein. These medicines include immune globulin and anti-Rh (D)

immunoglobulin.

Medicines also may be used along with a procedure to remove the spleen, called

splenectomy.

If steroids, immunoglobulins, or splenectomy don’t help, two newer medicines—eltrombopag and romiplostim—can be used to treat ITP.

Removal of the spleen (splenectomy)

If necessary, the spleen will be removed surgically. This organ is located in the upper

left abdomen. The spleen is about the size of a golf ball in children and a baseball in

adults.

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 The spleen makes antibodies (proteins) that help fight infection. In ITP, these antibodies

destroy platelets.

If ITP hasn't responded to steroids, removing the spleen will reduce the destruction of 

platelets. However, it also may make you more likely to get certain infections. Before

you have the surgery, your doctor may give you vaccines to help prevent these

infections.

If your spleen is removed, your doctor will explain what steps you can take to help avoid

infections and what symptoms to watch for.

Other Treatments 

Platelet transfusions

Some people with ITP who have severe bleeding may need to have platelet transfusions

and be hospitalized. Some people will need a platelet transfusion before having surgery.

For a platelet transfusion, donor platelets from a blood bank are injected into therecipient's bloodstream. This increases the platelet count for a short time.

Treating infections

Some infections can briefly lower a person's platelet count. If a person who has ITP has

an infection that can lower his or her platelet count, treating the infection may help

increase the platelet count and reduce bleeding problems.

Stopping medicines

If a person who has ITP is taking medicine that can lower his or her platelet count or

cause bleeding, stopping the medicine can sometimes help increase the platelet count

or prevent bleeding.

For example, aspirin and ibuprofen are common medicines that increase the chance of 

bleeding. If you have ITP, your doctor may suggest that you avoid these medicines.

How can Idiopathic Thrombocytopenic Purpura be prevented?

 You can't prevent idiopathic thrombocytopenic purpura (ITP), but you can prevent its

complications.

•  Talk to your doctor about which medicines you can take. Your doctor may advise

you to avoid medicines such as aspirin or ibuprofen that can affect your platelets

and increase your risk of bleeding.

• Protect yourself from injuries that can cause bruising or bleeding.• Seek treatment right away if you develop any infections. Report any symptoms

of infection, such as a fever, to your doctor. This is very important for people with

ITP who have had their spleens removed.

Living with Idiopathic Thrombocytopenic PurpuraIf you have idiopathic thrombocytopenic purpura (ITP), you can take steps to prevent

complications. Lifestyle changes and ongoing care can help you manage the condition.

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Lifestyle changes

If you have ITP, try to avoid injuries, especially head injuries, that can cause bleeding in

the brain. For example, don’t participate in contact sports such as boxing, football, or

karate. Other sports, such as skiing or horseback riding, also put you at risk for injuries

that can cause bleeding.

Some safe activities are swimming, biking, and walking. Ask your doctor about physical

activities that are safe for you.

 Take precautions such as regular use of seatbelts and wearing gloves when working

with knives and other tools.

If your child has ITP, ask his or her doctor whether you need to restrict your child's

activities.

Ongoing care

Find a doctor, preferably a hematologist, who is familiar with treating people who have

ITP. Hematologists are doctors who specialize in diagnosing and treating blood diseases

and disorders. Discuss with your doctor how to manage ITP and when to seek medical

care.

 Talk to your doctor before taking prescription and over-the-counter medicines and

nutritional supplements. Some medicines and supplements can affect platelets and

increase your chance of bleeding. Common examples are aspirin or ibuprofen.

 Tell your doctor about all of the over-the-counter medicines you take, including

vitamins, supplements, and herbal remedies. These products may contain substances

that increase your risk of bleeding.

Watch for symptoms of infection, such as a fever, and report them to your doctor

promptly. If you've had your spleen removed, you may be more likely to become ill from

certain types of infection.

Idiopathic Thrombocytopenic Purpura in pregnancyIn women who are pregnant and have ITP, the ITP usually doesn't affect the baby.

However, some babies born to mothers who have ITP are born with or develop low

numbers of platelets soon after birth.

 Their platelet counts almost always return to normal without any treatment. Treatment

can speed the recovery in the few babies whose platelet counts are very low.

 Treatment for ITP during pregnancy depends on a woman's platelet count. If treatment

is needed, the doctor will take a close look at the possible effects of the treatment on

the unborn baby.

Women who have milder cases of ITP usually can go through pregnancy without

treatment. Pregnant women who have very low platelet counts or a lot of bleeding are

more likely to have serious heavy bleeding during delivery or afterward. To prevent

serious bleeding, these women usually are treated.

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Key PointsIdiopathic thrombocytopenic purpura (ITP) is a bleeding condition in which the blood

doesn't clot as it should. This is due to a low number of blood cell fragments called

platelets.

Platelets stick together (clot) to seal small cuts or breaks on blood vessel walls and stop

bleeding.

 There are two types of ITP. Acute ITP is a short-term illness that mainly affects children

and often occurs after a viral infection. Most children get well quickly without any

treatment. Adults who have ITP most often have chronic (long-lasting) ITP. Symptoms

can vary a great deal, and some adults who have mild ITP don't need treatment.

In most cases, an autoimmune response is believed to cause ITP. Normally your immune

system helps your body fight off infections and diseases. But if you have ITP, your

immune system attacks and destroys its own platelets. The reason why this happens

isn't known.

ITP can't be passed from one person to another.

ITP can affect children and adults of all ages. Women are 2 to 3 times more likely than

men to get chronic ITP.

People who have ITP may have signs of bleeding, such as bruises (purpura) that appear

for no reason or tiny red dots (petechiae) that are visible on the skin.

Bleeding in ITP also occurs in the form of nosebleeds, bleeding gums, menstrual

bleeding that’s heavier than usual, or other bleeding that's hard to stop. Bleeding in the

brain as a result of ITP is very rare, but it can be life threatening when it occurs.

ITP is diagnosed based on your medical history, a physical exam, and results from bloodtests.

 Treatment for ITP is based on how much and how often you’re bleeding and your

platelet count. Medicines often are used as the first course of treatment. Treatments

used for children and adults are similar.

 The spleen is sometimes removed if treatment with medicine fails to keep the platelet

level high enough to prevent bleeding.

 You can't prevent ITP, but you can prevent its complications. Talk to your doctor about

what medicines are safe for you, protect yourself from injuries that can cause bruising

or bleeding, and seek treatment if any signs of infection develop.

For most children and adults, ITP isn't a serious or life-threatening condition. Even

people who have severe forms of chronic ITP can live for decade