Hematologic diseases are more commonly known as  Leukocytes (leukocytosis or

blood disease. There are many different blood diseases that leukopenia)
are diagnosed and treated by hematologists. Some of these
are benign (non-cancerous) and others are types of blood  Platelets (thrombocytopenia or
cancer. They can involve one or more of the three main thrombocytosis)
types of blood cells (red blood cells, white blood cells, and
platelets). They can also involve blood proteins involved in 2. Defective hemostasis (hemorrhage or
clotting. It is important to note that not every blood disorder intravascular coagulation)
requires treatment and therefore an effective dental patient 3. Neoplasia of the lymphoreticular system
management is imperative which would start with a
(lymphomas, reticuloendothelioses or
comprehensive knowledge about the said disease.   
plasma cell dyscrasias)
.
Symptoms of bleeding disorders
Hematologic Disorders
 The symptoms can vary depending on the specific
Composition of Blood
type of bleeding disorder. However, the main signs
include:

 unexplained and easy bruising

 pallor

 heavy menstrual bleeding

 frequent nosebleeds

 excessive bleeding from small cuts or an

injury

 bleeding into joints

Extrinsic vs intrinsic pathway

 Extrinsic Pathway – needs a substance from outside

of the blood to make it work ; trigerred by tissue
trauma/injury

 Intrinsic Pathway – the substances that need to

make it work is already within the blood ; trigerred
by trauma to the blood cells and inside the vessel

Laboratory tests

1. Complete Blood Count includes Actual Platelet Count

2. Peripheral Blood Smear

3. Bone marrow aspiration and biopsy

4. Tests of the Vascular Platelet Phase of Hemostasis:

 Bleeding Time (BT)

Introduction to hematologic disorders 5. Tests of the Coagulation Cascade:

 The cardinal symptoms and signs associated with  Clotting Time ( CT) or Coagulation time
hematologic disease are those resulting from:  Activated Partial Thromboplastin Time
1. Underproduction or overproduction of : (APTT). – Intrinsic factor

 RBCs (anemia or erythrocytosis)  Prothrombin Time (PT). – Extrinsic factor

 6. Tests of Fibrinolysis and the Mechanisms That  When a patient is to undergo invasive
Control Hemostasis: medical/dental procedure such as surgery to
ensure normal clotting ability.
 Fibrin Degradation Products (FDP)

 An elevated PT may indicate:

PLATELET COUNT
 Vitamin K deficiency
 100,000-400,000 NORMAL
 Disseminated Intravascular Coagulation
 < 100,000 Thrombocytopenia
 Liver disease
 50,000 - 100,000 Mild
Thrombocytopenia  Deficiency in Factors I, II, V, VII, IX
 < 50,000 Severe  On anticoagulant (Warfarin) therapy
Thrombocytopenia

International normalized ratio (INR)

Coagulation Factors
 A PT test may also be called an INR test.

 INR (international normalized ratio) stands for a way

of standardizing the results of prothrombin time
tests, no matter the testing method.

 So your doctor can understand results in the same

way even when they come from different labs and
different test methods.

 Using the INR system, treatment with (anticoagulant

therapy) will be the same. In some labs, only the INR
is reported and the PT is not reported

 An INR of 1.0 means that the patient PT is normal.

Prothrombin time
 Measures the effectiveness of the Extrinsic Pathway
 Normal value : 10 – 15 secs
 The time required for the plasma to clot after an
excess of thromboplastin and an optimal
concentration of calcium have been added.
 Sensitive to Factors I, II, V, VII, X.
 The PT evaluates patients suspected of having an
inherited or acquired deficiency in these pathways.
Partial Thromboplastin Time
 An INR greater than 1.0 means the clotting time is
elevated.
 INR of greater than 5 or 5.5 = unacceptable high risk
of bleeding,whereas if the INR=0.5 then there is a
high chance of having a clot.
 Normal range for a healthy person is 0.9–1.3, and
for people on warfarin therapy, 2.0–3.0, although
the target INR may be higher in particular situations,
such as for those with a mechanical heart valve.

 Measures effectiveness of the Intrinsic Pathway

 When is it ordered?
 Used to monitor anticoagulant therapy
Warfarin(Coumadin)
 When a patient not taking anti-coagulants
has signs of bleeding disorder.
 Normal value : 25-40 secs
 The partial thromboplastin time (PTT) or activated
partial thromboplastin time (aPTT or APTT( is a
performance indicator measuring the efficacy of
both the "intrinsic" and the common coagulation
pathways.
  It is also used to monitor the treatment effects with
heparin a major anticoagulant.

 Normal PTT times require the presence of the

following coagulation factors:

I, II, III, IV, V, VI, VIII, IX, X, XI, & XII

 When is it ordered?

 When a patient presents with unexplained

bleeding or bruising,

 It may be ordered as part of a pre-surgical

evaluation for bleeding tendencies,

Disorders of red blood cell production and iron metabolism

 When a patient is on intravenous (IV) or
injection heparin therapy, the APTT is
ordered at regular intervals to monitor the Introduction to anemia and approach to patients with
degree of anticoagulation. anemia

 Prolonged PTT may indicate:  Anemia is defined as a significant decrease in red

corpuscles or hemoglobin.
 Use of heparin.
 Anemia is usually discovered accidentally, since this
 antiphospholipid antibody:especially lupus clinical condition has vague, nonspecific symptoms
anticoagulant, which paradoxically increases and commonly occurs in such a slow, chronic fashion
propensity to thrombosis that the patient may not realize that he or she is
 coagulation factor deficiency , unwell.

 Once the anemia is discovered the health

e.g hemophilia
professional should determine the underlying
 Disseminated Intravascular Coagulation disease process.
 Liver disease  The lab measurements that are generally used to
determine the presence or the absence of anemia
are the packed red blood cell (RBC) volume or the
hematocrit and the hemoglobin concentration of
the peripheral blood.

 Hemoglobin :

 Male : 140-180 g/L ; Female : 120-160 g/L

 Hematocrit :

 Male : 0.40-0.54 ; Female : 0.37-0.47

Normal RBC production and pathology


Iron deficiency anemia
Acute posthemorrhagic anemia
 Results from the rapid loss of whole blood.
 It may occur from trauma (including surgery),
rupture or erosion of blood vessels, or defects in
hemostasis.
 Clinical manifestations vary with the amount, rate
and location of the hemorrhage, as well as the
patient’s general state of health and the presence
of disease in critical organ systems.
 In the healthy young adult the rapid loss of 500 to
1000ml of blood (10% to 20% of blood volume) is
usually tolerated without symptoms. Some have
weakness, sweating, nausea, bradycardia,
hypotension and syncope.
 The rapid loss of 1000 to 1500ml of blood (20% to
30% of blood volume) may cause symptoms only in
the upright position or with exertion.
 The rapid loss of 1500 to 2000ml (30% to 40% of
blood volume) usually results in hypovolemic shock,
Megaloblastic anemia
which may be irreversible if the blood loss extends
2000 to 2500ml (40% to 50% of blood volume)
 It is the most common cause of anemia
encountered in epidemiologic studies and clinical
practice.
 The most important cause of iron deficiency anemia
in adults is blood loss.
 In women menstrual blood loss accounts for most
instances of iron deficiency anemia.
 Dietary lack of iron is an important cause of iron
deficiency anemia only in children under 3 years of
age.
 IDA results, ultimately, from an inadequate supply of
iron for normal hemoglobin synthesis in developing
erythroid cells in the bone marrow.
 Most symptoms of iron deficiency are due to
anemia. Such symptoms include fatigue, loss of
stamina, shortness of breath, weakness, dizziness,
and pallor.
 Fatigue also may result from dysfunction of iron-
containing cellular enzymes.
 In addition to the usual manifestations of anemia,
some uncommon symptoms occur in severe iron
deficiency.
 Patients may have pica, an abnormal craving to eat
substances (eg, ice, dirt, paint).
 Other symptoms of severe deficiency include
glossitis, cheilosis, concave nails (koilonychia), and,
rarely, dysphagia caused by a postcricoid esophageal
web (Plummer-Vinson syndrome).
 Diagnosis
 CBC, serum iron, iron-binding capacity, and
serum ferritin
 Rarely bone marrow examination
 Treatment
 Oral supplemental iron
 Rarely parenteral iron
  Results most often from deficiencies of vitamin
B 12 and folate.
 Ineffective hematopoiesis affects all cell lines but
particularly RBCs.
 Anemia develops insidiously and may not cause
symptoms until it is severe.
 Deficiencies of vitamin B 12 may cause neurologic
manifestations, including peripheral neuropathy,
dementia, and subacute combined degeneration.
 Folate deficiency may also cause diarrhea and
glossitis.
 Many patients with folate deficiency appear wasted,
particularly with temporal wasting.
 Diagnosis
 CBC, RBC indices, reticulocyte count, and
peripheral smear
 Sometimes bone marrow examination
 Treatment is directed at the underlying disorder.
Aplastic anemia
 Aplastic anaemia is a rare disease in which the bone
marrow and the hematopoietic stem cells that reside
there are damaged.
 This causes a deficiency of all three blood cell types
(pancytopenia): red blood cells (anemia), white
blood cells (leukopenia), and platelets
(thrombocytopenia).
 Aplastic refers to the inability of stem cells to
generate mature blood cells.
 It is more frequent in people in their teens and
twenties, but is also common among the elderly.
 It can be caused by heredity, immune disease, or
exposure to chemicals, drugs, or radiation.
 However, in about half the cases, the cause is
unknown.
 Symptoms include fatigue, weakness, dizziness, and
shortness of breath. It can cause heart problems
such as an irregular heartbeat, an enlarged heart,
and heart failure. You may also have frequent
infections and bleeding.
 The definitive diagnosis is by bone marrow biopsy;
normal bone marrow has 30–70% blood stem cells,
but in aplastic anaemia, these cells are mostly gone
and replaced by fat.
 First line treatment for aplastic anaemia consists of
immunosuppressive drugs, typically either anti-
lymphocyte globulin or anti-thymocyte globulin,
combined with corticosteroids and ciclosporin.
Hematopoietic stem cell transplantation is also used,
especially for patients under 30 years of age with a
related matched marrow donor.[
Hemolytic anemias
 At the end of their normal life span (about 120
days), RBCs are removed from the circulation.
Hemolysis involves premature destruction and
hence a shortened RBC life span (< 120 days).
 Anemia results when bone marrow production can
no longer compensate for the shortened RBC
survival; this condition is termed hemolytic anemia.
 If the marrow can compensate, the condition is
termed compensated hemolytic anemia.
Hereditary spherocytosis
 Hereditary SPHEROcytosis (chronic familial icterus;
congenital hemolytic jaundice; familial
spherocytosis; spherocytic anemia) is an autosomal
dominant disease with variable gene penetrance.
 It is characterized by hemolysis of spheroidal RBCs
and anemia.
 Alterations in membrane proteins cause the RBC
abnormalities.
 The cell membrane surface area is decreased
disproportionately to the intracellular content. The
decreased surface area of the cell impairs the
flexibility needed for the cell to traverse the spleen’s
microcirculation, causing intrasplenic hemolysis. 
 Symptoms and signs of hereditary spherocytosis are
usually mild, and the anemia may be so well
compensated that it is not recognized until an
intercurrent viral illness transiently decreases RBC
production, simulating an aplastic crisis.
 However, these episodes are self-limited, resolving
with resolution of the infection.
  Moderate jaundice and symptoms of anemia are
present in severe cases.
 Splenomegaly is almost invariable but only rarely
causes abdominal discomfort.
 Hepatomegaly may be present.
 Cholelithiasis (pigment stones) is common and may
be the presenting symptom.
 Congenital skeletal abnormalities (eg, tower-shaped
skull, polydactylism) occasionally occur.
 Diagnosis
 RBC fragility assay, RBC autohemolysis assay,
and direct antiglobulin (Coombs) test
 Splenectomy (review function of spleen) is the only
specific treatment for the disorder but is rarely
needed.
Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency
 This enzyme, which is active in virtually all types of
cells, is involved in the normal processing of
carbohydrates. It plays a critical role in red blood
cells, which carry oxygen from the lungs to tissues
throughout the body. This enzyme helps protect red
blood cells from damage and premature
destruction.
 G6PD deficiency reduces energy available to
maintain the integrity of the red cell membrane,
which shortens RBC survival.
 Hemolysis occurs commonly after fever, acute viral
or bacterial infections, and diabetic acidosis.
 Less commonly, hemolysis occurs after exposure to
drugs or to other substances that produce peroxide
and cause oxidation of Hb and RBC membranes.
 These drugs and substances include primaquine,
salicylates, sulfonamides, nitrofurans, phenacetin,
naphthalene, some vitamin K
derivatives, dapsone, phenazopyridine, nalidixic acid,
methylene blue
 Diagnosis:
 G6PD assay (Newborn screening)
 During acute hemolysis, treatment is supportive;
transfusions are rarely needed. Patients are advised
to avoid drugs or substances that initiate hemolysis.
Sickle cell disease
 Sickle cell anemia is an inherited form of anemia.
 Normally, your red blood cells are flexible and round,
moving easily through your blood vessels.
 In sickle cell anemia, the red blood cells become rigid
and sticky and are shaped like sickles or crescent
moons.
 These irregularly shaped cells can get stuck in small
blood vessels, which can slow or block blood flow
and oxygen to parts of the body.
 Anemia. Sickle cells are fragile. They break apart
easily and die, leaving you without a good supply of
red blood cells.
 Episodes of pain. Periodic episodes of pain, called
crises, are a major symptom of sickle cell anemia.
Pain develops when sickle-shaped red blood cells
block blood flow through tiny blood vessels to your
chest, abdomen and joints. Pain can also occur in
your bones
 Hand-foot syndrome. Swollen hands and feet may
be the first signs of sickle cell anemia in babies. The
swelling is caused by sickle-shaped red blood cells
blocking blood flow out of their hands and feet.
 Frequent infections. Sickle cells can damage your
spleen, an organ that fights infection. This may make
you more vulnerable to infections
 Delayed growth. Red blood cells provide your body
with the oxygen and nutrients you need for growth.
A shortage of healthy red blood cells can slow
growth in infants and children and delay puberty in
teenagers.
 Vision problems. Some people with sickle cell
anemia experience vision problems. Tiny blood
vessels that supply your eyes may become plugged
with sickle cells. This can damage the retina — the
portion of the eye that processes visual images.
 Diagnosis
 DNA testing (prenatal diagnosis)
 Peripheral smear
 Solubility testing
 Hb electrophoresis (or thin-layer isoelectric
focusing)
 Treatment
  Broad-spectrum antibiotics (for infection) Chronic granulomatous disease

 Analgesics and IV hydration (for vaso-
occlusive pain crisis)
 Sometimes transfusions
 Immunizations, folate supplementation,
and hydroxyurea (for health maintenance)
Thalassemia
 These are groups of inherited microcytic, hemolytic
anemias characterized by defective hemoglobin
synthesis.
 It results from unbalanced Hb synthesis caused by
decreased production of at least one globin
polypeptide chain.
 In Beta thalassemia, decreased production of the
Beta chain is observed; autosomal inheritance
 Alpha thalassemia which results from decreased
production of alpha chains.
 Clinical features of thalassemias are similar but vary
in severity.
 Chronic granulomatous disease (CGD) is a primary
immunodeficiency that affects phagocytes of the
innate immune system and leads to recurrent or
persistent intracellular bacterial and fungal
infections and to granuloma formation.
 The disease becomes apparent during the first 2
years of life in most patients, but the onset is
occasionally delayed into the second decade of life.
 The earliest manifestations often involve the
skin. Recurrent pyodermas are common, and
they often appear as perianal, axillary, or
scalp abscesses.
 Systemic findings include osteomyelitis,
pulmonary abscesses and granulomas,
spleen and/or liver abscesses, and
hepatosplenomegaly.
 Pyrexia may be noted.
 Diarrhea may occur.

 Beta thalassemia major presents by age 1 to 2 with

symptoms of severe anemia and transfusional and
absorptive iron overload.

 Patients are jaundiced and leg ulcers and

cholelithiasis occurs.

 Splenomegaly probably due to splenic sequestration

may develop, accelerating destruction of transfused
normal RBCs.

 Bone marrow hyperactivity causes thickening of the  Diagnosis

cranial bones and malar eminences.
 Flow cytometric oxidative (respiratory) burst
 Long bone involvement predisposes to pathologic assay
fractures and impairs growth possibly delaying or
 Treatment
preventing puberty.
 Prophylactic antibiotics and usually
 Iron deposits in heart muscle may cause heart
antifungals
failure.
 Usually interferon gamma
 Diagnosis is based on quantitative Hb analysis.
 For severe infections, granulocyte
 Treatment for severe forms may include transfusion,
transfusions
splenectomy, chelation and stem cell
transplantation.  Bone marrow transplantation
White blood cell disorders
Hemostatic disorders  Infection, particularly with gram-negative
organisms: Gram-negative endotoxin causes
The Three Stages of Hemostasis
generation or exposure of tissue factor
 In the primary hemostasis a platelet plug is formed activity in phagocytic, endothelial, and tissue
within 5 minutes to seal the site of injury. cells.

 In the secondary hemostasis fibrin is formed  Cancer, particularly mucin-secreting

(coagulation) and a fibrin mesh reinforces the frail adenocarcinomas of the pancreas and
platelet plug (timescale hours). prostate and acute promyelocytic leukemia:
Tumor cells express or release tissue factor.
 The third part is (secondary) fibrinolysis which
dissolves the clot but takes place first after tissue  Shock due to any condition that causes
repair (timescale days). ischemic tissue injury and release of tissue
factor.
Coagulation disorders
 If DIC is suspected, platelet count, PT, PTT, plasma
Disseminated intravascular coagulation (DIC)
fibrinogen level, and plasma d-dimer level (an
 Disseminated intravascular coagulation (DIC), also indication of in vivo fibrin deposition and
known as disseminated intravascular degradation) are obtained.
coagulopathy or less commonly as consumptive  Treatment
coagulopathy, is a pathological process
characterized by the widespread activation of the  Treatment of cause
clotting cascade that results in the formation of
 Possibly replacement therapy (eg, platelets,
blood clots in the small blood vessels throughout
cryoprecipitate, fresh frozen plasma, natural
the body.
anticoagulants)
 This leads to compromise of tissue blood flow and
 Sometimes heparin
can ultimately lead to multiple organ damage. In
addition, as the coagulation process consumes
clotting factors and platelets, normal clotting is
disrupted and severe bleeding can occur from
various sites.

 DIC does not occur by itself but only as a

complicating factor from another underlying
condition, usually in those with a critical illness.

 The combination of widespread loss of tissue blood

flow and simultaneous bleeding leads to an Hemophilia
increased risk of death in addition to that posed by
the underlying disease.

 DIC usually results from exposure of tissue factor to

blood, initiating the coagulation cascade.

 DIC occurs most often in the following clinical

circumstances:

 Complications of obstetrics (eg, abruptio

placentae, saline-induced therapeutic
abortion, retained dead fetus or products of
conception, amniotic fluid embolism):
Placental tissue with tissue factor activity
enters or is exposed to the maternal
circulation.  Hemophilia A (factor VIII deficiency), which affects
about 80% of patients with hemophilia, and
 Hemophilia B (factor IX deficiency) have identical
clinical manifestations and screening test
abnormalities.
 Hemophilia is an inherited disorder that results from
mutations, deletions, or inversions affecting a factor
VIII or factor IX gene. Because these genes are
located on the X chromosome, hemophilia affects
males almost exclusively.
 Normal hemostasis requires > 30% of normal factor
VIII and IX levels. Most patients with hemophilia
have levels < 5%; some have extremely low levels (<
1%). The functional level (activity) of factor VIII or IX
in hemophilia A and B, and thus bleeding severity,
varies depending on the specific mutation in the
factor VIII or IX gene.
normal), excessive bleeding may occur after surgery
or dental extraction.
 Hemophilia is suspected in patients with recurrent
bleeding, unexplained hemarthroses, or a
prolongation of the PTT.
 If hemophilia is suspected, PTT, PT, platelet count,
and factor VIII and IX assays are obtained.
 In hemophilia, the PTT is prolonged, but the PT and
platelet count are normal. Factor VIII and IX assays
determine the type and severity of the hemophilia. 
 Patients with bleeding or in whom bleeding is
anticipated (eg, before surgery or dental extraction)
are given replacement factor, preferably using a
recombinant product; dose depends on the
circumstances.

 Replacement of the deficient factor is the primary

treatment. In hemophilia A, the factor VIII level
should be raised transiently to

 About 30% of normal to prevent bleeding

after dental extraction or to abort an
incipient joint hemorrhage

 50% of normal if severe joint or IM bleeding

is already evident
 Patients with hemophilia bleed into tissues (eg,
hemarthroses, muscle hematomas, retroperitoneal  100% of normal before major surgery or if
hemorrhage). The bleeding may be immediate or bleeding is intracranial, intracardiac, or
occur slowly, depending on the extent of trauma and otherwise life threatening
plasma level of factor VIII or IX.
 An antifibrinolytic agent (ε-aminocaproic acid 2.5 to
 Pain often occurs as bleeding commences, 4 g po qid for 1 wk or tranexamic acid 1.0 to 1.5 g po
sometimes before other signs of bleeding develop. tid or qid for 1 wk) should be given to prevent late
bleeding after dental extraction or other
 Chronic or recurrent hemarthroses can lead to
oropharyngeal mucosal trauma (eg, tongue
synovitis and arthropathy.
laceration).
 Even a trivial blow to the head can cause intracranial
bleeding.

 Bleeding into the base of the tongue can cause life-

threatening airway compression.

 Severe hemophilia (factor VIII or IX level < 1% of

normal) causes severe bleeding throughout life,
usually beginning soon after birth (eg, scalp
hematoma after delivery or excessive bleeding after
circumcision).

 Moderate hemophilia (factor levels 1 to 5% of

normal) usually causes bleeding after minimal
trauma. In mild hemophilia (factor levels 5 to 25% of

Platelet disorders
Von willebrand disease
Idiopathic thrombocytopenic purpura
 Idiopathic (immunologic) thrombocytopenic purpura
is a bleeding disorder caused by thrombocytopenia
not associated with a systemic disease.
 ITP usually results from development of an
autoantibody directed against a structural platelet
antigen.
 In childhood ITP, the autoantibody may be triggered
by viral antigens.
 The trigger in adults is unknown.
 ITP tends to worsen during pregnancy and increases
the risk of maternal morbidity.
 The symptoms and signs are petechiae, purpura, and
mucosal bleeding.
 Gross GI bleeding and hematuria are less common.
 The spleen is of normal size unless it is enlarged by a
coexisting viral infection or autoimmune hemolytic
anemia.
 Like the other disorders of increased platelet
destruction, ITP is also associated with an increased
risk of thrombosis.
 Diagnosis
 CBC with platelets, peripheral blood smear
 Rarely bone marrow aspiration
 Exclusion of other thrombocytopenic
disorders
 Treatment
 Oral corticosteroids
 IV immunoglobulin (IVIG)
 IV anti-D immune globulin
 Splenectomy
 Thrombopoietin receptor agonist drugs
 Rituximab
 Other immunosuppressants
 For severe bleeding, IVIG, IV anti-D immune
globulin, IV corticosteroids, and/or platelet
transfusions
 Von Willebrand Factor (VWF) is synthesized and
secreted by vascular endothelium to form part of the
perivascular matrix.
 VWF promotes the platelet adhesion phase of
hemostasis by binding with a receptor on the
platelet surface membrane (glycoprotein Ib/IX), thus
connecting the platelets to the vessel wall.
 VWF is also required to maintain normal plasma
factor VIII levels. Levels of VWF can temporarily
increase in response to stress, exercise, pregnancy,
inflammation, or infection.
 Von Willebrand disease (VWD) is a hereditary
deficiency of von Willebrand factor (VWF), which
causes platelet dysfunction. 
 Bleeding manifestations are mild to moderate and
include easy bruising, mucosal bleeding, bleeding
from small skin cuts that may stop and start over
hours, sometimes increased menstrual bleeding, and
abnormal bleeding after surgical procedures (eg,
tooth extraction, tonsillectomy).
 Platelets function well enough that petechiae and
purpura do not occur.
 Diagnosis requires measuring total plasma VWF
antigen, VWF function as determined by the ability
of plasma to support agglutination of normal
platelets by ristocetin (ristocetin cofactor activity),
and plasma factor VIII level.
 Patients are treated only if they are actively bleeding
or are undergoing an invasive procedure (eg,
surgery, dental extraction).
 Desmopressin is an analog
of vasopressin (antidiuretic hormone) that stimulates
 release of VWF into the plasma and may increase
levels of factor VIII.
Malignancies
Leukemias
Lymphocytic leukemia
 Leukemias are cancers of the hematopoietic tissues
characterized by infiltration of the peripheral blood,
bone marrow and other tissues by cells of a
particular line,usually lymphoid or myeloid.
 The involved cells may be immature in appearance,
in which case the process is called “acute”, or they
may be mature looking, in which case the process is
“chronic”.
Myeloid leukemia
 Characterized by a rapid increase in the number of
immature blood cells called blasts or leukemia cells.
 Crowding due to such cells makes the bone marrow
unable to produce healthy blood cells.
 Immediate treatment is required in acute leukemia
due to the rapid progression and accumulation of
Acute lymphocytic leukemia
the malignant cells, which then spill over into the
bloodstream and spread to other organs of the body.
 Acute forms of leukemia are the most common
forms of leukemia in children.
Chronic leukemias
 Characterized by the excessive buildup of relatively
mature, but still abnormal, white blood cells.
 Typically taking months or years to progress, the
cells are produced at a much higher rate than
normal, resulting in many abnormal white blood
cells.
 Whereas acute leukemia must be treated
immediately, chronic forms are sometimes
monitored for some time before treatment to
ensure maximum effectiveness of therapy.
 Chronic leukemia mostly occurs in older people, but
can theoretically occur in any age group.
  The cancerous change takes place to a type of
marrow cell that normally goes on to
form lymphocytes, which are infection-fighting
immune system cells.
 Most lymphocytic leukemias involve a specific
subtype of lymphocyte, the B cell.
 The cancerous change takes place in a  group of
white blood cells called the myeloid cells, which
normally develop into the various types of mature
blood cells, such as red blood cells, white blood cells
and platelets.
 Acute lymphocytic leukemia (ALL) is the most
common pediatric cancer; it also strikes adults of all
ages.
 Develops when abnormal white blood cells
accumulate in the bone marrow. These cells divide
rapidly, replacing healthy cells and, in some cases,
invade healthy organs. Also known as acute
lymphoblastic leukemia and acute lymphoid
leukemia
 (AML) occurs in both adults and children. This type
of leukemia is sometimes called acute
nonlymphocytic leukemia (ANLL).
 The most common type of acute leukemia in adults,
occurs when the bone marrow makes immature
blood cells called myeloblasts.

Chronic lymphocytic leukemia
 (CLL) most often affects adults over the age of 55. It
sometimes occurs in younger adults, but it almost
never affects children.
 It is a slow-growing cancer that begins in immune
cells called lymphocytes.
 These cells develop in bone marrow, but eventually
travel into the blood.
 CLL develops when too many abnormal lymphocytes
grow, crowding out normal blood cells.
 (CML) occurs mainly in adults. A very small number
of children also develop this disease.
 Chronic myelogenous (or myeloid or myelocytic)
leukemia (CML), also known as chronic granulocytic
leukemia (CGL), is a cancer of the white blood cells.
 It is a form of leukemia characterized by the
increased and unregulated growth of predominantly
myeloid cells in the bone marrow and the
accumulation of these cells in the blood.
Treatment
 Some of the common treatment options for ALL
include:
 Chemotherapy
 Radiation therapy
 Stem cell transplant
 Targeted therapy - does its work by using
drugs that are designed to seek out features
unique to specific cancer cells or ones that
influence their behavior.  sometimes with fever, night sweats, unintentional
Multiple myeloma
 Also known as plasma cell myeloma, myelomatosis,
or Kahler's disease (after Otto Kahler), is
a cancer of plasma cells, a type of white blood
cell normally responsible for producing antibodies.  consists of chemotherapy with or without radiation
 In multiple myeloma, collections of abnormal
plasma cells accumulate in the bone marrow,
where they interfere with the production of normal
blood cells.
 Most cases of multiple myeloma also feature the
production of a paraprotein—an abnormal antibody
which can cause kidney problems.
 Bone lesions and hypercalcemia(high blood calcium
levels) are also often encountered.
 Persistent bone pain (especially in the back or
thorax), renal failure, and recurring bacterial
infections are the most common problems on
presentation, but many patients are identified when
routine laboratory tests show an elevated total
protein level in the blood or show proteinuria.
 Pathologic fractures are common, and vertebral
collapse may lead to spinal cord compression and
paraplegia.
 Symptoms of anemia predominate or may be the
sole reason for evaluation in some patients, and a
few patients have manifestations of hyperviscosity
syndrome .
 Peripheral neuropathy, carpal tunnel syndrome,
abnormal bleeding, and symptoms of hypercalcemia
(eg, polydipsia, dehydration) are common.
 Patients may also present with renal failure.
 Lymphadenopathy and hepatosplenomegaly are
unusual.
hodgkin lymphoma & Non-hodgkin lymphoma
Hodgkin lymphoma
 Hodgkin lymphoma is a localized or disseminated
malignant proliferation of cells of the
lymphoreticular system, primarily involving lymph
node tissue, spleen, liver, and bone marrow.
 Hodgkin lymphoma results from the clonal
transformation of cells of B-cell origin, giving rise to
pathognomic binucleated Reed-Sternberg cells. 
 Symptoms include painless lymphadenopathy,
weight loss, pruritus, splenomegaly, and
hepatomegaly.
 Diagnosis is based on lymph node biopsy.
 Treatment is curative in about 75% of cases and
therapy.
Non-hodgkin lymphoma
 Non-Hodgkin lymphomas (NHL) are a heterogeneous
group of disorders involving malignant monoclonal
proliferation of lymphoid cells in lymphoreticular
 sites, including lymph nodes, bone marrow, the
spleen, the liver, and the GI tract.

 Presenting symptoms usually include peripheral

lymphadenopathy. However, some patients present
without lymphadenopathy but with abnormal
lymphocytes in circulation.

 Diagnosis is usually based on lymph node or bone

marrow biopsy or both.

 Treatment involves radiation therapy,

chemotherapy, or both.

 Stem cell transplantation is usually reserved for

salvage therapy after incomplete remission or
relapse.