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Hematologic System and
its pathology
Dr. Shivani Ravichinayan, MDS
19/04/2011 1
Hematology
 Study of blood and blood forming tissues
 Key components of hematologic system
are:
 Blood
 Blood forming tissues
 Bone marrow
 Spleen
 Lymph system
19/04/2011 2
What Does Blood Do?
 Transportation
 Oxygen
 Nutrients
 Hormones
 Waste Products
 Regulation
 Fluid, electrolyte
 Acid-Base balance
 Protection
 Coagulation
 Fight Infections
19/04/2011 3
Components of Blood
 Plasma
 55%
 Blood Cells
 45%
 Three types
 Erythrocytes/RBCs
 Leukocytes/WBCs
 Thrombocytes/Platelets
19/04/2011 4
Erythrocytes/Red Blood Cells
 Composed of hemoglobin
 Erythropoiesis
 = RBC production
 Stimulated by hypoxia
 Controlled by erythropoietin
 Hormone synthesized in kidney
 Hemolysis
 = destruction of RBCs
 Releases bilirubin into blood stream
 Normal lifespan of RBC = 120 days
19/04/2011 5
Leukocytes/White Blood Cells
 5 types
 Basophils
 Eosinophils
 Neutrophils
 Monocytes
 Lymphocytes
19/04/2011 6
Types and Functions of Leukocytes
Granulocytes
Neutrophil
Eosinophil
Basophil
Phagocytosis, early phase of
inflammation
Phagocytosis, parasitic infections
Inflammatory response, allergic
response
Agranulocytes
Lymphocyte
Monocyte
Cellular, humoral immune response
Phagocytosis; cellular immune
response
TYPE CELL FUNCTION
19/04/2011 7
Thrombocytes/Platelets
 Must be present for clotting to occur
 Involved in hemostasis
19/04/2011 8
Normal Clotting Mechanisms
 Hemostasis
 Goal: Minimizing blood loss when injured
1. Vascular Response
 vasoconstriction
1. Platelet response
 Activated during injury
 Form clumps (agglutination)
1. Plasma Clotting Factors
 Factors I – XIII
 Intrinsic pathway
 Extrinsic pathway
19/04/2011 9
Anticoagulation
 Elements that interfere with blood
clotting
 Countermechanism to blood clotting—
keeps blood liquid and able to flow
19/04/2011 10
Structures of the Hematologic System
 Bone Marrow
 Liver
 Lymph System
19/04/2011 11
Bone Marrow
 Bone Marrow
 Soft substance in core of bones
 Blood cell production (Hematopoiesis):The
production of all types of blood cells
generated by a remarkable self-regulated
system that is responsive to the demands
put upon it.
 RBCs
 WBCs
 Platelets
19/04/2011 12
Liver
Receives 24% of the cardiac output
(1500 ml of blood each minute)
 Liver has many functions
 Hematologic functions:
 Liver synthesis plasma proteins
including clotting factors and
albumin
 Liver clears damaged and non-
functioning RBCs/erythrocytes from
circulation
19/04/2011 13
Spleen
 Located in upper L quadrant of
abdomen
 Functions
 Hematopoietic function
 Produces fetal RBCs
 Filter function
 Filter and reuse certain cells
 Immune function
 Lymphocytes, monocytes
 Storage function
 30% platelets stored in spleen
19/04/2011 14
Pluripotential Stem Cell
Myeloid Stem Cells Lymphoid stem cells
Granulocyte;
Macrophage
Stem Cells
Granulocyte
Stem Cells
Neutrophils
Eosinophils
& Basophils
Monocytic
Stem Cells
Monocytes &
Macrophages
Megakaryocytic
Stem Cells
Megacaryocytes
& Platelets
Erythropoietic
Stem Cells
Erythrocytes Lymphocytes:
(T cells, B cells,
plasma cells)
HEMATOPOIESIS
Effects of Aging on the Hematologic
System
 CBC Studies
 ↓ Hemoglobin (Hb or Hgb)
 ↓ response to infection (WBC)
 Platelets=no change
 Clotting Studies
 ↓ PTT
19/04/2011 16
Diagnostic Studies of the Hematologic
System: Complete Blood Count (CBC)
 WBCs
 Normal 4,000 -11,000 µ/ℓ
 Associated with infection, inflammation, tissue injury or
death
 Leukopenia-- ↓ WBC
 Neutropenia -- ↓ neutrophil count
 RBC
 ♂ 4.5 – 5.5 x 106
/ℓ
 ♀ 4.0 – 5.0 x 106
/ℓ
 Hematocrit (Hct)
 The hematocrit is the percent of whole blood that is
composed of red blood cells. The hematocrit is a measure
of both the number of red blood cells and the size of red
blood cells.
19/04/2011 20
Diagnostic Studies of the Hematologic System:
Complete Blood Count (CBC) Cont’d
 Platelet count
 Normal 150,000- 400,000
 Thrombocytopenia-↓ platelet count
 Spontaneous hemorrhage likely when count is
below 20,000
 Pancytopenia
 Decrease in number of RBCs, WBCs, and
platelets
19/04/2011 21
Diagnostic Studies
of the Hematologic System
 Radiologic Studies
 CT/MRI of lymph tissues
 Biopsies
 Bone Marrow examination
 Lymph node biopsies
19/04/2011 22
BLOOD
DISORDERS
19/04/2011 28
RBC disorders
WBC disorders
Platelets
disorders
19/04/2011 29
RBC DISORDERS
19/04/2011 30
Anemia
 Anemia is a reduction in the number of
RBCs, the quantity of hemoglobin, or
the volume of RBCs
 Because the main function of RBCs is
oxygenation, anemia results in varying
degrees of hypoxia
19/04/2011 31
Anemia
 Prevalent conditions
 Blood loss
 Decreased production of erythrocytes
 Increased destruction of erythrocytes
19/04/2011 32
Anemia (cont’d)
 Clinical Manifestations:
1. Pallor.
2. Fatigue, weakness.
3. Dyspnea.
4. Palpitations, tachycardia.
5. Headache, dizziness, and restlessness.
6. Slowing of thought.
7. Paresthesia.
19/04/2011 33
Anemia Caused By Blood Loss
 Acute Blood Loss
 Chronic Blood Loss
19/04/2011 36
Acute Blood Loss
 Result of sudden hemorrhage
 Trauma, surgery, vascular disruption
 Collaborative Care
1. Replacing blood volume
2. Identifying source of hemorrhage
3. Stopping blood loss
19/04/2011 37
Chronic Blood Loss
 Symptoms
 Pallor, glossitis, chelitis, weakness
 GI bleeding, hemorrhoids, menstrual blood loss
 Diagnostic Studies
 Identifying source
 Stopping bleeding
 Collaborative Care
 Supplemental iron administration
19/04/2011 38
Anemia Caused by Decreased Erythrocyte
Production
 Iron Deficiency Anemia
 Thalassemia
 Megablastic Anemia
19/04/2011 39
Iron-Deficiency Anemia
Etiology
1. Inadequate dietary intake
 Found in 30% of the
world’s population
1. Malabsorption
 Absorbed in duodenum
 GI surgery
1. Blood loss
 2 ml of blood contain 1mg iron
 GI, GU losses
1. Hemolysis
19/04/2011 40
Iron-Deficiency Anemia
 Clinical Manifestations
 Most common: pallor
 Second most common: inflammation of the tongue
(glossistis)
 Cheilitis=inflammation/fissures of lips
 Sensitivity to cold
 Weakness and fatigue
 Diagnostic Studies
 CBC
 Iron studies Diagnostics:
 Iron levels: Total iron-binding capacity (TIBC), Serum
Ferritin.
 Endoscopy/Colonscopy
19/04/2011 41
Iron-Deficiency Anemia
 Collaborative Care
 Treatment of underlying disease/problem
 Replacing iron
 Diet
 Drug Therapy
 Iron replacement
 Oral iron
 Feosol, DexFerrum, etc
 Absorbed best in acidic environemtn
 GI effects
 Parenteral iron
 IM or IV
19/04/2011 42
Thalassemia
 Etiology
 Autosomal recessive genetic disorder of
inadequate production of normal hemoglobin
 Found in Mediterranean ethnic groups
 Clinical Manifestations
 Asymptomatic  major retardation  life
threatening
 Splenomegaly, hepatomegaly
19/04/2011 44
Thalassemia
Collaborative Care
 No specific drug or diet are effective in
treating thalassemia
 Thalassemia minor
 Body adapts to Hgb↓
 Thalassemia major
 Blood transfusions with IV deferoxamine
(used to remove excess iron from the body)
19/04/2011 45
Megaloblastic Anemias
 Characterized by large
RBCs which are fragile
and easily destroyed
 Common forms of
megaloblastic anemia
1. Cobalamin deficiency
2. Folic acid deficiency
This picture shows large, dense,
oversized, red blood cells (RBCs)
that are seen in megaloblastic
anemia.
19/04/2011 46
Cobalamin (Vitamin B12) Deficiency
 Cobalamin Deficiency--formerly known as
pernicious anemia
 Vitamin B12 (cobalamin) is an important water-
soluble vitamin.
 Intrinsic factor (IF) is required for cobalamin
absorption
 Causes of cobalamin deficiency
 Gastric mucosa not secreting IF
 GI surgery →loss of IF-secreting gastric mucosal cells
 Long-term use of H2-histamine receptor blockers cause
atrophy or loss of gastric mucosa.
 Nutritional deficiency
 Hereditary defects of cobalamine utilization19/04/2011 47
Cobalamin (Vitamin B12) Deficiency
 Clinical manifestations
 General symptoms of anemia
 Sore tongue
 Anorexia
 Weakness
 Parathesias of the feet and hands
 Altered thought processes
 Confusion → dementia
19/04/2011 48
Cobalamin Deficiency
Diagnostic Studies
 RBCs appear large
 Abnormal shapes
 Structure contributes to erythrocyte
destruction
 Schilling Test: a medical investigation used
for patients with vitamin B12 deficiency. The
purpose of the test is to determine if the
patient has pernicious anemia.
19/04/2011 49
Cobalamin Deficiency
 Collaborative Care
 Parenteral administration of cobalamin
 ↑ Dietary cobalamin does not correct the anemia
 Still important to emphasize adequate dietary intake
 Intranasal form of cyanocobalamin (Nascobal) is
available
 High dose oral cobalamin and SL cobalamin can
use be used
19/04/2011 50
Folic Acid Deficiency
 Folic Acid Deficiency also causes
megablastic anemia (RBCs that are large
and fewer in number)
 Folic Acid required for RBC formation and
maturation
 Causes
 Poor dietary intake
 Malabsorption syndromes
 Drugs that inhibit absorption
 Alcohol abuse
 Hemodialysis
19/04/2011 52
Folic Acid Deficiency
 Clinical manifestations are similar to those of
cobalamin deficiency
 Insidious onset: progress slowly
 Absence of neurologic problems
 Treated by folate replacement therapy
 Encourage patient to eat foods with large amounts
of folic acid
 Leafy green vegetables
 Liver
 Mushrooms
 Oatmeal
 Peanut butter
 Red beans
19/04/2011 53
Anemia of Chronic Disease
 Underproduction of RBCs, shortening of RBC
survival
 2nd
most common cause of anemia (after iron
deficiency anemia)
 Generally develops after 1-2 months of sustained
disease
 Causes
 Impaired renal function
 Chronic, inflammatory, infectious or malignant disease
 Chronic liver disease
 Folic acid deficiencies
 Splenomegaly
 Hepatitis19/04/2011 54
Aplastic Anemia
 Characterized by Pancytopenia
 ↓ of all blood cell types
 RBCs
 White blood cells (WBCs)
 Platelets
 Hypocellular bone marrow
19/04/2011 55
Aplastic Anemia
 Etiology
 Congenital
 Chromosomal alterations
 Acquired
 Results from exposure to ionizing radiation, chemical
agents, viral and bacterial infections
Low incidence
Affecting 4 of every 1 million persons
Manageable with erythropoietin or blood transfusion
Can be a critical condition
Hemorrhage
Sepsis
19/04/2011 56
Aplastic Anemia
 Clinical Manifestations
 Gradual development
 Symptoms caused by suppression of any or all bone
marrow elements
 General manifestations of anemia
 Fatigue
 Dyspnea
 Pale skin
 Frequent or prolonged infections
 Unexplained or easy bruising
 Nosebleed and bleeding gums
 Prolonged bleeding from cuts
 Dizziness
 headache19/04/2011 57
Aplastic Anemia
 Diagnosis
 Blood tests
 CBC
 Bone marrow biopsy
19/04/2011 58
Aplastic Anemia
 Treatment
 Identifying cause
 Blood transfusions
 Antibiotics
 Immunosuppressants (neoral, sandimmune)
 Corticosteroids (Medrol, solu-medrol)
 Bone marrow stimulants
 Filgrastim (Neupogen)
 Epoetin alfa (Epogen, Procrit)
 Bone marrow transplantation
 Preventing complications from infection and hemorrhage
 Prognosis is poor if untreated
 75% fatal
19/04/2011 59
Anemia caused by Increased Erythrocyte
Destruction
 Hemolytic Anemia
 Sickle Cell disease (peds)
 Acquired Hemolytic Anemia
 Hemochromatosis
 Polycythemia
19/04/2011 60
Hemolytic Anemia
 Destruction or hemolysis of RBCs at a rate that
exceeds production
 Third major cause of anemia
 Intrinsic hemolytic anemia
 Abnormal hemoglobin
 Enzyme deficiencies
 RBC membrane abnormalities
 Extrinsic hemolytic anemia
 Normal RBCs
 Damaged by external factors
 Liver
 Spleen
 Toxins
 Mechanical injury (heart valves)19/04/2011 61
Sequence of Events in Hemolysis
Fig. 30-1
19/04/2011 62
Acquired Hemolytic Anemia
 Causes
 Medications
 Infections
 Manifestations
 S/S of anemia
 Complications
 Accumulation of hemoglobin molecules can
obstruct renal tubules → Tubular necrosis
 Treatment
 Eliminating the causative agent
19/04/2011 63
Hemochromatosis
 Iron overload disease
 Over absorption and
storage of iron causing
damage especially to
liver, heart and
pancreas
19/04/2011 65
Polycythemia
 Polycythemia is a condition in which
there is a net increase in the total number
of red blood cells
 Overproduction of red blood cells may
be due to
 a primary process in the bone marrow (a so-
called myeloproliferative syndrome)
 or it may be a reaction to chronically low
oxygen levels or
 malignancy
19/04/2011 66
Polycythemia
 Complications
 ↑d viscosity of blood
 → hemorrhage and thrombosis
 Treatment
 Phlebotomy
 Myelosupressive agents: A number of new
therapeutic agents such as, interferon alfa-2b (Intron A)
therapy, agents that target platelet number (e.g.,
anagrelide [Agrylin]), and platelet function (e.g., aspirin).
19/04/2011 67
WBC DISORDERS
19/04/2011 68
Neutropenia
 Neutropenia refers specifically to a decrease in neutrophils. It
commonly is defined as a circulating neutrophil count of less
than 1500 cells/ L.μ
 Agranulocytosis, which denotes a severe neutropenia, is
characterized by a circulating neutrophil count of less than 200
cells/ L.μ
 Neutropenia can be:
 Acquired
 Congenital
 Kostmann’s syndrome
 It occurs sporadically as an autosomal recessive disorder,
causes severe neutropenia while preserving the erythroid
and megakaryocyte cell lineages that result in red blood cell
and platelet production.
 The total white blood cell count may be within normal
limits, but the neutrophil count is less than 200/ L.μ
Monocyte and eosinophil levels may be elevated
(compensatory).
Acquired neutropenia
 Accelerated removal - removal of neutrophils from the circulation exceeds
production
 Inflammation
 Infection, viral or bacterial
 Increased destruction:
 Drug-induced granulocytopenia
 Treatment of cancer – chemotherapy (e.g., alkylating agents,
antimetabolites)
 Irradiation
 Autoimmune disorders or drug reactions
 May cause increased and premature destruction of neutrophils
 Splenomegaly
 Neutrophils may be trapped in the spleen along with other blood
cells
 Felty’s syndrome
 A variant of rheumatoid arthritis, there is increased destruction of
neutrophils in the spleen
 Neoplasms involving bone marrow (e.g., leukemias and lymphomas,
myeloma)
Acquired neutropenia
 Alcoholism
 Carentiale states:
 Folic acid
 Vitamin B12
 Iron
 Cooper
 Aplastic anemia
 All of the myeloid stem cells are affected, resulting in
anemia, thrombocytopenia, and agranulocytosis;
 Idiopathic neutropenia that occurs in the absence of other
disease or provoking influence.
Infectious Mononucleosis
 Self-limiting lymphoproliferative disorder
 Caused by Epstein-Barr virus (EBV)
 Most prevalent in adolescence/young adults
 Main mode of transmission → EBV-contaminated
saliva
 Pathogenesis: atypical lymphocytes proliferate
 Onset: insidious; incubation 4-8 weeks
Mono: Sore throat with erythema & white exudate
Infectious mononucleosis
 Clinical manifestations:
lymphadenopathy, hepatomegaly,
splenomegaly
 Labs:

WBC  (~ 12-18,000); 95% lymphocytes
(viral infection)
 Acute phase: 2-3 weeks
 Treatment: symptomatic & supportive
Leukemias
 Chronic
 CLL (chronic lymphocytic leukemia)
 CML (chronic myelocytic leukemia)
 Acute
 ALL (acute lymphocytic leukemia)
 AML (acute myelocytic leukemia)
DEFINED BY:
1.SITE OF ORIGIN
a. myeloid stem cell
b. lymphoid stem cell
2.ACUTE VS CHRONIC
a. acute
b. chronic
Leukemias
 Malignant neoplasms of cells originally derived from a
single hematopoietic cell line
 Leukemic cells:
 Are immature & unregulated
 Proliferate in bone marrow
 Circulate in blood
 Infiltrate spleen, lymph nodes & other tissues
 Disease of children & adults
Common feature of all leukemias:
Uncontrolled proliferation of immature leukocytes
results in crowding out of mature blood cells
including leuckocytes, red blood cells, and platelets
Pancytopenia = decrease in all functioning blood cells:
anemia, thrombocytopenia, neutropenia
Leukemia: Classifications
 Classified according to their PREDOMINANT CELL
type
 LYMPHOCYTIC or MYELOCYTIC AND
 whether dx is ACUTE or CHRONIC
1. Acute lymphocytic (lymphoblastic) leukemia (ALL)*
2. Chronic lymphocytic leukemia (CLL)**
3. Acute myelocytic leukemia (AML)
4. Chronic myelocytic leukemia (CML)
* Most common childhood leukemia
**Most common leukemia of older adults
Leukemia: Pathogenesis
 Causes:
 Unknown;  exposure to radiation
 Pathogenesis – Leukemic cells:
 Are an immature type of WBC
 Capable of  rate of proliferation/have prolonged
life span
 Cannot perform function of mature leukocytes →
are ineffective as phagocytes
 Interfere with maturation of normal bone marrow
cells (including RBC & platelets)
Leukemia: Acute vs Chronic
 Acute:
 Sudden, stormy onset
 S/S related to  (mature) WBC,  RBC,  platelets
 ALL 80% childhood acute leukemias→
 AML chiefly an adult disease→
 Diagnosis based on:
 Blood/bone marrow tissue presence of↔ immature WBC’s
(blasts) – may constitute 60-100% of cells
Leukemias: Acute vs Chronic
 Chronic
 More insidious onset
 May be discovered during a routine medical exam by a
blood count
 CLL older adults→
 Relatively mature lymphocytes that are immunologically
incompetent
 CML adults & children→
 Leukocytosis with immature cell types
 Hodgkin’s
disease
 Characterized by
PAINLESS, progressive,
rubbery enlargement of
a single node or group
of nodes – usually in
neck area
 Reed-Sternberg cell –
distinctive tumor cell
found with lymph biopsy
 Non-hodgkin’s
disease
 Also neoplastic disorder of
lymphoid tissue
 However, SPREADS EARLY
→ liver, spleen & bone
marrow
 Also characterized by
painless, superficial
lymphadenopathy; also
extranodal symptoms
 POORER PROGNOSIS
than Hodgkin’s
Malignant Lymphomas:
Neoplasms Of Cells Derived From
Lymphoid Tissue
Disorders of platelets
19/04/2011 84
Thrombocytopenia
 Disorder of decreased platelets
 platelet count below 150,000
 Causes
 Low production of platelets
 Increased breakdown of platelets
 Symptoms
 Bruising
 Nosebleeds
 Petechiae (pinpoint microhemorrhages)
19/04/2011 85
Thrombocytopenia
 Types of Thrombocytopenia
 Immune Thrombocytopenic Purpura
 Abnormal destruction of circulating platelets
 Autoimmune disorder
 Destroyed in hosts’ spleen by macrophages
 Thrombotic Thrombocytopenic Purpura
 ↑d agglutination of platelets that from microthrombi
19/04/2011 86
Heparin-Induced Thrombocytopenia
(HIT)
 HIT
 Associated with administration of heparin
 Develops when the body develops an antibody, or allergy
to heparin
 Heparin (paradoxically) causes thrombosis
 Immune mediated response that casues intense platelet
activation and relaese of procoaggulation particles.
 Clinical features
 Thrombocytopenia
 Possible thrombosis after heparin therapy
 Can be triggered by any type, route or amount of heparin
19/04/2011 87
Thrombocytopenia
Diagnostic Studies
 Platelet count
 Prothrombin Time (PT)
 Activated Partial Thromboplastin Time (aPTT)
 Hgb/Hct
 Treatment
 Based on cause
 Corticosteroids
 Plasmaphoresis
 Splenectomy
 Platelet transfusion
19/04/2011 88
Conclusion
 Oral manifestations of many of the blood
disorders mimics the oral lesions caused
by local etiologies such as irritations and
infections.
 Many of the dental treatments are
invasive so dental professionals must be
very careful while treating such patients.
19/04/2011 89
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Blood disorders

  • 1. Hematologic System and its pathology Dr. Shivani Ravichinayan, MDS 19/04/2011 1
  • 2. Hematology  Study of blood and blood forming tissues  Key components of hematologic system are:  Blood  Blood forming tissues  Bone marrow  Spleen  Lymph system 19/04/2011 2
  • 3. What Does Blood Do?  Transportation  Oxygen  Nutrients  Hormones  Waste Products  Regulation  Fluid, electrolyte  Acid-Base balance  Protection  Coagulation  Fight Infections 19/04/2011 3
  • 4. Components of Blood  Plasma  55%  Blood Cells  45%  Three types  Erythrocytes/RBCs  Leukocytes/WBCs  Thrombocytes/Platelets 19/04/2011 4
  • 5. Erythrocytes/Red Blood Cells  Composed of hemoglobin  Erythropoiesis  = RBC production  Stimulated by hypoxia  Controlled by erythropoietin  Hormone synthesized in kidney  Hemolysis  = destruction of RBCs  Releases bilirubin into blood stream  Normal lifespan of RBC = 120 days 19/04/2011 5
  • 6. Leukocytes/White Blood Cells  5 types  Basophils  Eosinophils  Neutrophils  Monocytes  Lymphocytes 19/04/2011 6
  • 7. Types and Functions of Leukocytes Granulocytes Neutrophil Eosinophil Basophil Phagocytosis, early phase of inflammation Phagocytosis, parasitic infections Inflammatory response, allergic response Agranulocytes Lymphocyte Monocyte Cellular, humoral immune response Phagocytosis; cellular immune response TYPE CELL FUNCTION 19/04/2011 7
  • 8. Thrombocytes/Platelets  Must be present for clotting to occur  Involved in hemostasis 19/04/2011 8
  • 9. Normal Clotting Mechanisms  Hemostasis  Goal: Minimizing blood loss when injured 1. Vascular Response  vasoconstriction 1. Platelet response  Activated during injury  Form clumps (agglutination) 1. Plasma Clotting Factors  Factors I – XIII  Intrinsic pathway  Extrinsic pathway 19/04/2011 9
  • 10. Anticoagulation  Elements that interfere with blood clotting  Countermechanism to blood clotting— keeps blood liquid and able to flow 19/04/2011 10
  • 11. Structures of the Hematologic System  Bone Marrow  Liver  Lymph System 19/04/2011 11
  • 12. Bone Marrow  Bone Marrow  Soft substance in core of bones  Blood cell production (Hematopoiesis):The production of all types of blood cells generated by a remarkable self-regulated system that is responsive to the demands put upon it.  RBCs  WBCs  Platelets 19/04/2011 12
  • 13. Liver Receives 24% of the cardiac output (1500 ml of blood each minute)  Liver has many functions  Hematologic functions:  Liver synthesis plasma proteins including clotting factors and albumin  Liver clears damaged and non- functioning RBCs/erythrocytes from circulation 19/04/2011 13
  • 14. Spleen  Located in upper L quadrant of abdomen  Functions  Hematopoietic function  Produces fetal RBCs  Filter function  Filter and reuse certain cells  Immune function  Lymphocytes, monocytes  Storage function  30% platelets stored in spleen 19/04/2011 14
  • 15. Pluripotential Stem Cell Myeloid Stem Cells Lymphoid stem cells Granulocyte; Macrophage Stem Cells Granulocyte Stem Cells Neutrophils Eosinophils & Basophils Monocytic Stem Cells Monocytes & Macrophages Megakaryocytic Stem Cells Megacaryocytes & Platelets Erythropoietic Stem Cells Erythrocytes Lymphocytes: (T cells, B cells, plasma cells) HEMATOPOIESIS
  • 16. Effects of Aging on the Hematologic System  CBC Studies  ↓ Hemoglobin (Hb or Hgb)  ↓ response to infection (WBC)  Platelets=no change  Clotting Studies  ↓ PTT 19/04/2011 16
  • 17. Diagnostic Studies of the Hematologic System: Complete Blood Count (CBC)  WBCs  Normal 4,000 -11,000 µ/ℓ  Associated with infection, inflammation, tissue injury or death  Leukopenia-- ↓ WBC  Neutropenia -- ↓ neutrophil count  RBC  ♂ 4.5 – 5.5 x 106 /ℓ  ♀ 4.0 – 5.0 x 106 /ℓ  Hematocrit (Hct)  The hematocrit is the percent of whole blood that is composed of red blood cells. The hematocrit is a measure of both the number of red blood cells and the size of red blood cells. 19/04/2011 20
  • 18. Diagnostic Studies of the Hematologic System: Complete Blood Count (CBC) Cont’d  Platelet count  Normal 150,000- 400,000  Thrombocytopenia-↓ platelet count  Spontaneous hemorrhage likely when count is below 20,000  Pancytopenia  Decrease in number of RBCs, WBCs, and platelets 19/04/2011 21
  • 19. Diagnostic Studies of the Hematologic System  Radiologic Studies  CT/MRI of lymph tissues  Biopsies  Bone Marrow examination  Lymph node biopsies 19/04/2011 22
  • 23. Anemia  Anemia is a reduction in the number of RBCs, the quantity of hemoglobin, or the volume of RBCs  Because the main function of RBCs is oxygenation, anemia results in varying degrees of hypoxia 19/04/2011 31
  • 24. Anemia  Prevalent conditions  Blood loss  Decreased production of erythrocytes  Increased destruction of erythrocytes 19/04/2011 32
  • 25. Anemia (cont’d)  Clinical Manifestations: 1. Pallor. 2. Fatigue, weakness. 3. Dyspnea. 4. Palpitations, tachycardia. 5. Headache, dizziness, and restlessness. 6. Slowing of thought. 7. Paresthesia. 19/04/2011 33
  • 26. Anemia Caused By Blood Loss  Acute Blood Loss  Chronic Blood Loss 19/04/2011 36
  • 27. Acute Blood Loss  Result of sudden hemorrhage  Trauma, surgery, vascular disruption  Collaborative Care 1. Replacing blood volume 2. Identifying source of hemorrhage 3. Stopping blood loss 19/04/2011 37
  • 28. Chronic Blood Loss  Symptoms  Pallor, glossitis, chelitis, weakness  GI bleeding, hemorrhoids, menstrual blood loss  Diagnostic Studies  Identifying source  Stopping bleeding  Collaborative Care  Supplemental iron administration 19/04/2011 38
  • 29. Anemia Caused by Decreased Erythrocyte Production  Iron Deficiency Anemia  Thalassemia  Megablastic Anemia 19/04/2011 39
  • 30. Iron-Deficiency Anemia Etiology 1. Inadequate dietary intake  Found in 30% of the world’s population 1. Malabsorption  Absorbed in duodenum  GI surgery 1. Blood loss  2 ml of blood contain 1mg iron  GI, GU losses 1. Hemolysis 19/04/2011 40
  • 31. Iron-Deficiency Anemia  Clinical Manifestations  Most common: pallor  Second most common: inflammation of the tongue (glossistis)  Cheilitis=inflammation/fissures of lips  Sensitivity to cold  Weakness and fatigue  Diagnostic Studies  CBC  Iron studies Diagnostics:  Iron levels: Total iron-binding capacity (TIBC), Serum Ferritin.  Endoscopy/Colonscopy 19/04/2011 41
  • 32. Iron-Deficiency Anemia  Collaborative Care  Treatment of underlying disease/problem  Replacing iron  Diet  Drug Therapy  Iron replacement  Oral iron  Feosol, DexFerrum, etc  Absorbed best in acidic environemtn  GI effects  Parenteral iron  IM or IV 19/04/2011 42
  • 33. Thalassemia  Etiology  Autosomal recessive genetic disorder of inadequate production of normal hemoglobin  Found in Mediterranean ethnic groups  Clinical Manifestations  Asymptomatic  major retardation  life threatening  Splenomegaly, hepatomegaly 19/04/2011 44
  • 34. Thalassemia Collaborative Care  No specific drug or diet are effective in treating thalassemia  Thalassemia minor  Body adapts to Hgb↓  Thalassemia major  Blood transfusions with IV deferoxamine (used to remove excess iron from the body) 19/04/2011 45
  • 35. Megaloblastic Anemias  Characterized by large RBCs which are fragile and easily destroyed  Common forms of megaloblastic anemia 1. Cobalamin deficiency 2. Folic acid deficiency This picture shows large, dense, oversized, red blood cells (RBCs) that are seen in megaloblastic anemia. 19/04/2011 46
  • 36. Cobalamin (Vitamin B12) Deficiency  Cobalamin Deficiency--formerly known as pernicious anemia  Vitamin B12 (cobalamin) is an important water- soluble vitamin.  Intrinsic factor (IF) is required for cobalamin absorption  Causes of cobalamin deficiency  Gastric mucosa not secreting IF  GI surgery →loss of IF-secreting gastric mucosal cells  Long-term use of H2-histamine receptor blockers cause atrophy or loss of gastric mucosa.  Nutritional deficiency  Hereditary defects of cobalamine utilization19/04/2011 47
  • 37. Cobalamin (Vitamin B12) Deficiency  Clinical manifestations  General symptoms of anemia  Sore tongue  Anorexia  Weakness  Parathesias of the feet and hands  Altered thought processes  Confusion → dementia 19/04/2011 48
  • 38. Cobalamin Deficiency Diagnostic Studies  RBCs appear large  Abnormal shapes  Structure contributes to erythrocyte destruction  Schilling Test: a medical investigation used for patients with vitamin B12 deficiency. The purpose of the test is to determine if the patient has pernicious anemia. 19/04/2011 49
  • 39. Cobalamin Deficiency  Collaborative Care  Parenteral administration of cobalamin  ↑ Dietary cobalamin does not correct the anemia  Still important to emphasize adequate dietary intake  Intranasal form of cyanocobalamin (Nascobal) is available  High dose oral cobalamin and SL cobalamin can use be used 19/04/2011 50
  • 40. Folic Acid Deficiency  Folic Acid Deficiency also causes megablastic anemia (RBCs that are large and fewer in number)  Folic Acid required for RBC formation and maturation  Causes  Poor dietary intake  Malabsorption syndromes  Drugs that inhibit absorption  Alcohol abuse  Hemodialysis 19/04/2011 52
  • 41. Folic Acid Deficiency  Clinical manifestations are similar to those of cobalamin deficiency  Insidious onset: progress slowly  Absence of neurologic problems  Treated by folate replacement therapy  Encourage patient to eat foods with large amounts of folic acid  Leafy green vegetables  Liver  Mushrooms  Oatmeal  Peanut butter  Red beans 19/04/2011 53
  • 42. Anemia of Chronic Disease  Underproduction of RBCs, shortening of RBC survival  2nd most common cause of anemia (after iron deficiency anemia)  Generally develops after 1-2 months of sustained disease  Causes  Impaired renal function  Chronic, inflammatory, infectious or malignant disease  Chronic liver disease  Folic acid deficiencies  Splenomegaly  Hepatitis19/04/2011 54
  • 43. Aplastic Anemia  Characterized by Pancytopenia  ↓ of all blood cell types  RBCs  White blood cells (WBCs)  Platelets  Hypocellular bone marrow 19/04/2011 55
  • 44. Aplastic Anemia  Etiology  Congenital  Chromosomal alterations  Acquired  Results from exposure to ionizing radiation, chemical agents, viral and bacterial infections Low incidence Affecting 4 of every 1 million persons Manageable with erythropoietin or blood transfusion Can be a critical condition Hemorrhage Sepsis 19/04/2011 56
  • 45. Aplastic Anemia  Clinical Manifestations  Gradual development  Symptoms caused by suppression of any or all bone marrow elements  General manifestations of anemia  Fatigue  Dyspnea  Pale skin  Frequent or prolonged infections  Unexplained or easy bruising  Nosebleed and bleeding gums  Prolonged bleeding from cuts  Dizziness  headache19/04/2011 57
  • 46. Aplastic Anemia  Diagnosis  Blood tests  CBC  Bone marrow biopsy 19/04/2011 58
  • 47. Aplastic Anemia  Treatment  Identifying cause  Blood transfusions  Antibiotics  Immunosuppressants (neoral, sandimmune)  Corticosteroids (Medrol, solu-medrol)  Bone marrow stimulants  Filgrastim (Neupogen)  Epoetin alfa (Epogen, Procrit)  Bone marrow transplantation  Preventing complications from infection and hemorrhage  Prognosis is poor if untreated  75% fatal 19/04/2011 59
  • 48. Anemia caused by Increased Erythrocyte Destruction  Hemolytic Anemia  Sickle Cell disease (peds)  Acquired Hemolytic Anemia  Hemochromatosis  Polycythemia 19/04/2011 60
  • 49. Hemolytic Anemia  Destruction or hemolysis of RBCs at a rate that exceeds production  Third major cause of anemia  Intrinsic hemolytic anemia  Abnormal hemoglobin  Enzyme deficiencies  RBC membrane abnormalities  Extrinsic hemolytic anemia  Normal RBCs  Damaged by external factors  Liver  Spleen  Toxins  Mechanical injury (heart valves)19/04/2011 61
  • 50. Sequence of Events in Hemolysis Fig. 30-1 19/04/2011 62
  • 51. Acquired Hemolytic Anemia  Causes  Medications  Infections  Manifestations  S/S of anemia  Complications  Accumulation of hemoglobin molecules can obstruct renal tubules → Tubular necrosis  Treatment  Eliminating the causative agent 19/04/2011 63
  • 52. Hemochromatosis  Iron overload disease  Over absorption and storage of iron causing damage especially to liver, heart and pancreas 19/04/2011 65
  • 53. Polycythemia  Polycythemia is a condition in which there is a net increase in the total number of red blood cells  Overproduction of red blood cells may be due to  a primary process in the bone marrow (a so- called myeloproliferative syndrome)  or it may be a reaction to chronically low oxygen levels or  malignancy 19/04/2011 66
  • 54. Polycythemia  Complications  ↑d viscosity of blood  → hemorrhage and thrombosis  Treatment  Phlebotomy  Myelosupressive agents: A number of new therapeutic agents such as, interferon alfa-2b (Intron A) therapy, agents that target platelet number (e.g., anagrelide [Agrylin]), and platelet function (e.g., aspirin). 19/04/2011 67
  • 56. Neutropenia  Neutropenia refers specifically to a decrease in neutrophils. It commonly is defined as a circulating neutrophil count of less than 1500 cells/ L.μ  Agranulocytosis, which denotes a severe neutropenia, is characterized by a circulating neutrophil count of less than 200 cells/ L.μ  Neutropenia can be:  Acquired  Congenital  Kostmann’s syndrome  It occurs sporadically as an autosomal recessive disorder, causes severe neutropenia while preserving the erythroid and megakaryocyte cell lineages that result in red blood cell and platelet production.  The total white blood cell count may be within normal limits, but the neutrophil count is less than 200/ L.μ Monocyte and eosinophil levels may be elevated (compensatory).
  • 57. Acquired neutropenia  Accelerated removal - removal of neutrophils from the circulation exceeds production  Inflammation  Infection, viral or bacterial  Increased destruction:  Drug-induced granulocytopenia  Treatment of cancer – chemotherapy (e.g., alkylating agents, antimetabolites)  Irradiation  Autoimmune disorders or drug reactions  May cause increased and premature destruction of neutrophils  Splenomegaly  Neutrophils may be trapped in the spleen along with other blood cells  Felty’s syndrome  A variant of rheumatoid arthritis, there is increased destruction of neutrophils in the spleen  Neoplasms involving bone marrow (e.g., leukemias and lymphomas, myeloma)
  • 58. Acquired neutropenia  Alcoholism  Carentiale states:  Folic acid  Vitamin B12  Iron  Cooper  Aplastic anemia  All of the myeloid stem cells are affected, resulting in anemia, thrombocytopenia, and agranulocytosis;  Idiopathic neutropenia that occurs in the absence of other disease or provoking influence.
  • 59. Infectious Mononucleosis  Self-limiting lymphoproliferative disorder  Caused by Epstein-Barr virus (EBV)  Most prevalent in adolescence/young adults  Main mode of transmission → EBV-contaminated saliva  Pathogenesis: atypical lymphocytes proliferate  Onset: insidious; incubation 4-8 weeks
  • 60.
  • 61. Mono: Sore throat with erythema & white exudate
  • 62. Infectious mononucleosis  Clinical manifestations: lymphadenopathy, hepatomegaly, splenomegaly  Labs:  WBC  (~ 12-18,000); 95% lymphocytes (viral infection)  Acute phase: 2-3 weeks  Treatment: symptomatic & supportive
  • 63. Leukemias  Chronic  CLL (chronic lymphocytic leukemia)  CML (chronic myelocytic leukemia)  Acute  ALL (acute lymphocytic leukemia)  AML (acute myelocytic leukemia) DEFINED BY: 1.SITE OF ORIGIN a. myeloid stem cell b. lymphoid stem cell 2.ACUTE VS CHRONIC a. acute b. chronic
  • 64. Leukemias  Malignant neoplasms of cells originally derived from a single hematopoietic cell line  Leukemic cells:  Are immature & unregulated  Proliferate in bone marrow  Circulate in blood  Infiltrate spleen, lymph nodes & other tissues  Disease of children & adults
  • 65. Common feature of all leukemias: Uncontrolled proliferation of immature leukocytes results in crowding out of mature blood cells including leuckocytes, red blood cells, and platelets Pancytopenia = decrease in all functioning blood cells: anemia, thrombocytopenia, neutropenia
  • 66. Leukemia: Classifications  Classified according to their PREDOMINANT CELL type  LYMPHOCYTIC or MYELOCYTIC AND  whether dx is ACUTE or CHRONIC 1. Acute lymphocytic (lymphoblastic) leukemia (ALL)* 2. Chronic lymphocytic leukemia (CLL)** 3. Acute myelocytic leukemia (AML) 4. Chronic myelocytic leukemia (CML) * Most common childhood leukemia **Most common leukemia of older adults
  • 67. Leukemia: Pathogenesis  Causes:  Unknown;  exposure to radiation  Pathogenesis – Leukemic cells:  Are an immature type of WBC  Capable of  rate of proliferation/have prolonged life span  Cannot perform function of mature leukocytes → are ineffective as phagocytes  Interfere with maturation of normal bone marrow cells (including RBC & platelets)
  • 68. Leukemia: Acute vs Chronic  Acute:  Sudden, stormy onset  S/S related to  (mature) WBC,  RBC,  platelets  ALL 80% childhood acute leukemias→  AML chiefly an adult disease→  Diagnosis based on:  Blood/bone marrow tissue presence of↔ immature WBC’s (blasts) – may constitute 60-100% of cells
  • 69. Leukemias: Acute vs Chronic  Chronic  More insidious onset  May be discovered during a routine medical exam by a blood count  CLL older adults→  Relatively mature lymphocytes that are immunologically incompetent  CML adults & children→  Leukocytosis with immature cell types
  • 70.  Hodgkin’s disease  Characterized by PAINLESS, progressive, rubbery enlargement of a single node or group of nodes – usually in neck area  Reed-Sternberg cell – distinctive tumor cell found with lymph biopsy  Non-hodgkin’s disease  Also neoplastic disorder of lymphoid tissue  However, SPREADS EARLY → liver, spleen & bone marrow  Also characterized by painless, superficial lymphadenopathy; also extranodal symptoms  POORER PROGNOSIS than Hodgkin’s Malignant Lymphomas: Neoplasms Of Cells Derived From Lymphoid Tissue
  • 72. Thrombocytopenia  Disorder of decreased platelets  platelet count below 150,000  Causes  Low production of platelets  Increased breakdown of platelets  Symptoms  Bruising  Nosebleeds  Petechiae (pinpoint microhemorrhages) 19/04/2011 85
  • 73. Thrombocytopenia  Types of Thrombocytopenia  Immune Thrombocytopenic Purpura  Abnormal destruction of circulating platelets  Autoimmune disorder  Destroyed in hosts’ spleen by macrophages  Thrombotic Thrombocytopenic Purpura  ↑d agglutination of platelets that from microthrombi 19/04/2011 86
  • 74. Heparin-Induced Thrombocytopenia (HIT)  HIT  Associated with administration of heparin  Develops when the body develops an antibody, or allergy to heparin  Heparin (paradoxically) causes thrombosis  Immune mediated response that casues intense platelet activation and relaese of procoaggulation particles.  Clinical features  Thrombocytopenia  Possible thrombosis after heparin therapy  Can be triggered by any type, route or amount of heparin 19/04/2011 87
  • 75. Thrombocytopenia Diagnostic Studies  Platelet count  Prothrombin Time (PT)  Activated Partial Thromboplastin Time (aPTT)  Hgb/Hct  Treatment  Based on cause  Corticosteroids  Plasmaphoresis  Splenectomy  Platelet transfusion 19/04/2011 88
  • 76. Conclusion  Oral manifestations of many of the blood disorders mimics the oral lesions caused by local etiologies such as irritations and infections.  Many of the dental treatments are invasive so dental professionals must be very careful while treating such patients. 19/04/2011 89

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