Hematology Dai Modul 22 2014

HEMATOLOGY
Darmawati A. Indraswari
Department of Physiology Diponegoro University Faculty of Medicine
HEMATOLOGY
Study of blood & its components Window of rest of body

BLOOD Delivery of nutrients
Oxygen, Food, Vitamins
Removal of wastes
Carbon dioxide, nitrogenous wastes, cellular toxins
Repair of vessels Protection versus invading microorganisms Multiple cellular & non-cellular elements
COMPONENTS OF FORMED ELEMENTS
Red Blood Cells Oxygen & CO2 transport White Blood Cells Protection versus microorganisms Platelets Coagulation: Maintenance of vascular integrity
HEMATOLOGY
Hematopoiesis
In humans, occurs in bone marrow exclusively All cellular elements derived from pluripotent stem cell (PPSC) PPSC retains ability to both replicate itself and differentiate Types of differentiation determined by the influence of various cytokines
RED BLOOD CELLS
Normal - Anucleated, highly flexible biconcave discs, 80-100 femtoliters in volume Flexibility essential for passage through capillaries Major roles - Carriers of oxygen to & carbon dioxide away from cells
ERYTHROPOIETIN
A hormone produced in the kidney (probably peritubular cells) A transmembrane protein; cytokine receptor superfamily Necessary for erythroid proliferation and differentiation Its absence results in apoptosis (programmed cell death) of erythroid committed cells Binds specifically to Erythropoietin Receptor Binding leads to dimerization of receptor dimerization activates tyrosine kinase activity multiple cytoplasmic & nuclear proteins phosphorylated Nuclear signal sent to activate production of proteins leading to proliferation and differentiation
ERYTHROPOIETIN
Regulation of Production
RBC Precursors
Pronormoblast Basophilic normoblast Polychromatophilic Normoblast Orthrochromatophilic Normoblast Reticulocyte
Mature Red Blood Cell

5-7 days from Pronormoblast to Reticulocyte
RBC Assessment
Number - Generally done by automated counters, using impedance measures Size - Large, normal size, or small; all same size versus variable sizes (anisocytosis). Mean volume by automated counter Shape - Normal biconcave disc, versus spherocytes, versus oddly shaped cells (poikilocytosis) Color - Generally an artifact of size of cell
Red Blood Cells
Normal Values
RBC Parameters Hematocrit Females Males Hemoglobin Females Males MCV Reticulocyte Count
Normal Values
35-47% 40-52%
12.0-16.0 gm/dl 13.5-17.5 gm/dl 80-100 fl 0.2-2.0%
RETICULOCYTE
Young red blood cell; still have small amounts of RNA present in them
Tend to stain somewhat bluer than mature RBCs on Wright stain (polychromatophilic)
Slightly larger than mature RBC Undergo removal of RNA on passing through spleen, in 1st day of life
Can be detected using supravital stain

Important marker of RBC production
Developmental Aspects
Before birth, blood cell formation takes place in the fetal yolk sac, liver, and spleen By the seventh month, red bone marrow is the primary hematopoietic area Blood cells develop from mesenchymal cells called blood islands The fetus forms HbF, which has a higher affinity for oxygen than adult hemoglobin
ANEMIA
Causes
Blood loss Decreased production of red blood cells (Marrow failure) Increased destruction of red blood cells
Hemolysis
Distinguished by reticulocyte count

Decreased in states of decreased production
Increased in destruction of red blood cells
RBC DESTRUCTION - EXTRAVASCULAR
Heme metabolized to bilirubin in macrophage; globin metabolized intracellularly
Unconjugated bilirubin excreted into plasma & carried to liver

Bilirubin conjugated in liver &excreted into bile & then into upper GI tract Conjugated bilirubin passes to lower GI tract & metabolized to urobilinogen, which is excreted into stool & urine
LEUKOCYTES AND IMMUNITY
Leukocytes (WBCs)
Leukocytes, the only blood components that are complete cells:

Are less numerous than RBCs Make up 1% of the total blood volume Can leave capillaries via diapedesis
Move through tissue spaces
Leukocytosis WBC count over 11,000 per cubic millimeter

Normal response to bacterial or viral invasion
Granulocytes
Neutrophils Eosinophils Basophils
granules stain pink, blue or purple (Wrights stain)
larger and usually shorter-lived than RBCs Have lobed nuclei

Are all phagocytic cells
Agranulocytes
lymphocytes and monocytes:

Lack visible cytoplasmic granules
Have spherical (lymphocytes) or kidney-shaped (monocytes) nuclei
Agranulocyte
Granulocyte
Granulocytes
Granulocytes neutrophils, eosinophils, and basophils

Contain cytoplasmic granules that stain specifically (acidic, basic, or both) with Wrights stain Are larger and usually shorter-lived than RBCs Have lobed nuclei Are all phagocytic cells
Neutrophils
Neutrophils have two types of granules that:

Take up both acidic and basic dyes
Give the cytoplasm a lilac color
Contain peroxidases, hydrolytic enzymes, and defensins (antibiotic-like proteins)
Neutrophils are our bodys bacteria slayers
Eosinophils
Eosinophils account for 14% of WBCs

Have red-staining, bilobed nuclei connected via a broad band of nuclear material Have red to crimson (acidophilic) large, coarse, lysosome-like granules Lead the bodys counterattack against parasitic worms Lessen the severity of allergies by phagocytizing immune complexes
Basophils
Account for 0.5% of WBCs and:

Have U- or S-shaped nuclei with two or three conspicuous constrictions Are functionally similar to mast cells
Have large, purplish-black (basophilic) granules that contain histamine Histamine inflammatory chemical that acts as a vasodilator and attracts other WBCs (antihistamines counter this effect)
Agranulocytes
Agranulocytes lymphocytes and monocytes:

Lack visible cytoplasmic granules
Are similar structurally, but are functionally distinct and unrelated cell types Have spherical (lymphocytes) or kidneyshaped (monocytes) nuclei
Lymphocytes
Account for 25% or more of WBCs and:

Have large, dark-purple, circular nuclei with a thin rim of blue cytoplasm Are found mostly enmeshed in lymphoid tissue (some circulate in the blood)
There are two types of lymphocytes: T cells and B cells

T cells function in the immune response
B cells give rise to plasma cells, which produce antibodies
Monocytes
Monocytes account for 48% of leukocytes

They are the largest leukocytes
They have abundant pale-blue cytoplasms
They have purple-staining, U- or kidneyshaped nuclei They leave the circulation, enter tissue, and differentiate into macrophages
Monocytes
Macrophages:
Are highly mobile and actively phagocytic Activate lymphocytes to mount an immune response
Leukocytes (WBCs)
Neutrophil
Eosinophil
Basophil
Lymphocyte
Monocyte
Summary of Formed Elements
Production of Leukocytes
Leukopoiesis is hormonally stimulated by two families of cytokines (hematopoietic factors) interleukins and colony-stimulating factors (CSFs)
Interleukins are numbered (e.g., IL-1, IL-2), whereas CSFs are named for the WBCs they stimulate (e.g., granulocyte-CSF stimulates granulocytes)
Macrophages and T cells are the most important sources of cytokines
Many hematopoietic hormones are used clinically to stimulate bone marrow

Formation of Leukocytes
All leukocytes originate from hemocytoblasts Hemocytoblasts differentiate into myeloid stem cells and lymphoid stem cells Myeloid stem cells become myeloblasts or monoblasts Lymphoid stem cells become lymphoblasts
Myeloblasts develop into eosinophils, neutrophils, and basophils

Monoblasts develop into monocytes
Lymphoblasts develop into lymphocytes

Formation of Leukocytes
Immune response
Leukocytes Disorders: Leukemias

Leukemia refers to cancerous conditions involving white blood cells
Leukemias are named according to the abnormal white blood cells involved
Myelocytic leukemia involves myeloblasts Lymphocytic leukemia involves lymphocytes
Acute leukemia involves blast-type cells and primarily affects children Chronic leukemia is more prevalent in older people
WBC disorder
Leukopenia WBC count less than normal Caused by viral or intracell bacteria infection, drugs Leukocytosis WBC count more than normal Caused by bacterial infection Leukemia WBC malignancy
Leukocytes Disorders
Leukemia
white blood cell cancer Myelocytic leukemia involves myeloblasts Lymphocytic leukemia involves lymphocytes
AML CML NORMAL ALL
Acute leukemia primarily affects children Chronic leukemia - more prevalent in older people
www-sdc.med.nagasaki-u.ac.jp/. ../Leukemia-E.html
A GLANCE OF IMMUNOLOGY: INNATE AND ADAPTIVE IMMUNITY
Components of Innate Immunity
Abbas & Lichtman,2005

Immunity: Two Intrinsic Defense Systems
Innate (nonspecific) system responds quickly and consists of:

First line of defense intact skin and mucosae prevent entry of microorganisms
Second line of defense antimicrobial proteins, phagocytes, and other cells Inhibit spread of invaders throughout the body Inflammation is its hallmark and most important mechanism
Immunity: Two Intrinsic Defense Systems
Adaptive (specific) defense system

Third line of defense mounts attack against particular foreign substances Takes longer to react than the innate system
Works in conjunction with the innate system
External Defenses: Surface Barriers
Skin, mucous membranes, and their secretions make up the first line of defense
Epithelial membranes produce protective chemicals that destroy microorganisms

Mucus-coated hairs in the nose trap inhaled particles Mucosae provide similar mechanical barriers
Internal Defenses: Cells and Chemicals
The body uses nonspecific cellular and chemical devices to protect itself
Phagocytes and natural killer (NK) cells
Antimicrobial proteins in blood and tissue fluid
Inflammatory response enlists macrophages, mast cells, WBCs, and chemicals
Harmful substances are identified by surface carbohydrates unique to infectious organisms

Mechanism of Phagocytosis
Figure 21.1a, b
Antimicrobial Proteins
Enhance the innate defenses by: Attacking microorganisms directly Hindering microorganisms ability to reproduce The most important antimicrobial proteins: 1. Interferon 2. Complement proteins 3. C-Reactive Protein (CRP): a clinical marker used to assess for: The presence of an acute infection An inflammatory condition and its response to treatment
Events in Inflammation
Figure 21.2
Adaptive (Specific) Defenses
The adaptive immune system is a functional system that: Recognizes specific foreign substances Acts to immobilize, neutralize, or destroy foreign substances Amplifies inflammatory response and activates complement The adaptive immune system is antigenspecific, systemic, and has memory It has two separate but overlapping arms Humoral, or antibody-mediated immunity Cellular, or cell-mediated immunity
Antigens The ultimate targets of all immune responses are mostly large, complex molecules not normally found in the body (nonself) Antigens are substances that can mobilize the immune system and provoke an immune response Only certain parts of an entire antigen are immunogenic. Antibodies and activated lymphocytes bind to these antigenic determinants
Cells of the Adaptive Immune System
Two types of lymphocytes

B lymphocytes oversee humoral immunity T lymphocytes non-antibody-producing cells that constitute the cell-mediated arm of immunity
Antigen-presenting cells (APCs):

Do not respond to specific antigens
Play essential auxiliary roles in immunity

Cells of the Adaptive Immune System
Adaptive Immunity: Summary
Two-fisted defensive system that uses lymphocytes, APCs, and specific molecules to identify and destroy nonself particles Its response depends upon the ability of its cells to:
Recognize foreign substances (antigens) by binding to them
Communicate with one another so that the whole system mounts a response specific to those antigens
Humoral Immunity Response
Antigen challenge first encounter between an antigen and a naive immunocompetent cell
Takes place in the spleen or other lymphoid organ If the lymphocyte is a B cell:
The challenging antigen provokes a humoral immune response
Antibodies are produced against the challenger
Antibodies
Also called immunoglobulins Constitute the gamma globulin portion of blood proteins Are soluble proteins secreted by activated B cells and plasma cells in response to an antigen Are capable of binding specifically with that antigen There are five classes of antibodies: IgD, IgM, IgG, IgA, and IgE
Mechanisms of Antibody Action
Figure 21.13
Primary and Secondary Humoral Responses
Figure 21.10
Types of Acquired Immunity
Figure 21.11
Cell-Mediated Immune Response

Since antibodies are useless against intracellular antigens, cell-mediated immunity is needed
Two major populations of T cells mediate cellular immunity
CD4 cells (T4 cells) are primarily helper T cells (TH) CD8 cells (T8 cells) are cytotoxic T cells (TC) that destroy cells harboring foreign antigens
Other types of T cells are:

Suppressor T cells (TS)
Memory T cells
Major Types of T Cells
Figure 21.14
MHC Proteins
Both types of MHC proteins are important to T cell activation Class I MHC proteins: Always recognized by CD8 T cells Display peptides from endogenous antigens Class II MHC proteins Found only on mature B cells, some T cells, and antigen-presenting cells Antigen recognition: Provides the key for the immune system to recognize the presence of intracellular microorganisms
Antigen Recognition
Provides the key for the immune system to recognize the presence of intracellular microorganisms MHC proteins are ignored by T cells if they are complexed with self protein fragments
T Cell Activation: Step One Antigen Binding
Figure 21.16
Cytokines
Mediators involved in cellular immunity, including hormone-like glycoproteins released by activated T cells and macrophages Some are co-stimulators of T cells and T cell proliferation Interleukin 1 (IL-1) released by macrophages co-stimulates bound T cells to: Release interleukin 2 (IL-2) Synthesize more IL-2 receptors IL-2 is a key growth factor, which sets up a positive feedback cycle that encourages activated T cells to divide It is used therapeutically to enhance the bodys defenses against cancer Other cytokines amplify and regulate immune and nonspecific responses Examples include: Perforin and lymphotoxin cell toxins Gamma interferon enhances the killing power of macrophages Inflammatory factors
Helper T Cells (TH)

Regulatory cells that play a central role in the immune response Once primed by APC presentation of antigen, they: Chemically or directly stimulate proliferation of other T cells Stimulate B cells that have already become bound to antigen Without TH, there is no immune response
TH cells interact directly with B cells that have antigen fragments on their surfaces bound to MHC II receptors TH cells stimulate B cells to divide more rapidly and begin antibody formation B cells may be activated without TH cells by binding to T cellindependent antigens Most antigens, however, require TH co-stimulation to activate B cells Cytokines released by TH amplify nonspecific defenses
Helper T Cells (TH)
Figure 21.17a
Cytotoxic T Cell (Tc)

TC cells, or killer T cells, are the only T cells that can directly attack and kill other cells
They circulate throughout the body in search of body cells that display the antigen to which they have been sensitized
Their targets include:
Virus-infected cells Cells with intracellular bacteria or parasites Cancer cells Foreign cells from blood transfusions or transplants
Mechanisms of Tc Action
Figure 21.18a, b
Importance of Humoral Response

Soluble antibodies The simplest ammunition of the immune response Interact in extracellular environments such as body secretions, tissue fluid, blood, and lymph
Importance of Cellular Response

T cells recognize and respond only to processed fragments of antigen displayed on the surface of body cells T cells are best suited for cellto-cell interactions, and target: Cells infected with viruses, bacteria, or intracellular parasites Abnormal or cancerous cells Cells of infused or transplanted foreign tissue
Summary of the Primary Immune Response
Figure 21.19
PLATELETS AND HEMOSTASIS
HEMOSTASIS
Hemostasis: prevention of blood loss.
Whenever a vessel is severed or ruptured, hemostasis is achieved by several mechanisms:

(1) vascular constriction, (2) formation of a platelet plug,
(3) formation of a blood clot as a result of blood coagulation, (4) eventual growth of fibrous tissue into the blood clot to close the hole in the vessel permanently.
Platelets
Platelets are fragments of megakaryocytes with a bluestaining outer region and a purple granular center Platelets are irregularly-shaped, colorless bodies that are present in blood. Their sticky surface lets them form clots to stop bleeding. Their granules contain serotonin, Ca2+, enzymes, ADP, and platelet-derived growth factor (PDGF) Platelets function in the clotting mechanism by forming a temporary plug that helps seal breaks in blood vessels
Platelets not involved in clotting are kept inactive by NO and prostaglandin I2

Genesis of Platelets
The stem cell for platelets is the hemocytoblast The sequential developmental pathway is hemocytoblast, megakaryoblast, promegakaryocyte, megakaryocyte, and platelets
Platelet Plug Formation
Platelets do not stick to each other or to the endothelial lining of blood vessels Upon damage to blood vessel endothelium (which exposes collagen) platelets:
With the help of von Willebrand factor (VWF) adhere to collagen Are stimulated by thromboxane A2 Stick to exposed collagen fibers and form a platelet plug Release serotonin and ADP, which attract still more platelets
The platelet plug is limited to the immediate area of injury by PGI2
Coagulation
A set of reactions in which blood is transformed from a liquid to a gel Coagulation follows intrinsic and extrinsic pathways
The final three steps of this series of reactions are:

Prothrombin activator is formed Prothrombin is converted into thrombin Thrombin catalyzes the joining of fibrinogen into a fibrin mesh
Coagulation
Detailed Events of Coagulation

Phase I: prothrombin activator Once factor X has been activated, it complexes with calcium ions, PF3, and factor V to form prothrombin activator
Phase II: thrombin formation Prothrombin activator catalyzes the transformation of prothrombin to the active enzyme thrombin
Phase III: fibrin mesh Thrombin catalyzes the polymerization of fibrinogen into fibrin Insoluble fibrin strands form the structural basis of a clot Fibrin causes plasma to become a gellike trap Fibrin in the presence of calcium ions activates factor XIII that: Cross-links fibrin Strengthens and stabilizes the clot
Factors Limiting Clot Growth or Formation
Two homeostatic mechanisms prevent clots from becoming large Swift removal of clotting factors Inhibition of activated clotting factors
Clot retraction stabilization of the clot by squeezing serum from the fibrin strands Repair
Platelet-derived growth factor (PDGF) stimulates rebuilding of blood vessel wall Fibroblasts form a connective tissue patch Stimulated by vascular endothelial growth factor (VEGF), endothelial cells multiply and restore the endothelial lining
Inhibition of Clotting Factors

Fibrin acts as an anticoagulant by binding thrombin and preventing its:
Positive feedback effects of coagulation
Ability to speed up the production of prothrombin activator via factor V
Acceleration of the intrinsic pathway by activating platelets
Thrombin not absorbed to fibrin is inactivated by antithrombin III Heparin, another anticoagulant, also inhibits thrombin activity
Factors Preventing Undesirable Clotting
Unnecessary clotting is prevented by the structural and molecular characteristics of endothelial cells lining the blood vessels Platelet adhesion is prevented by:
The smooth endothelial lining of blood vessels Heparin and PGI2 secreted by endothelial cells
Vitamin E quinone, a potent anticoagulant
Factors Preventing Undesirable Clotting #2

Substances used to prevent undesirable clots include:
Aspirin an antiprostaglandin that inhibits thromboxane A2 Heparin an anticoagulant used clinically for pre- and postoperative cardiac care Warfarin used for those prone to atrial fibrillation
Hemostasis Disorders: Thromboembolytic Conditions

Thrombus a clot that develops and persists in an unbroken blood vessel
Thrombi can block circulation, resulting in tissue death Coronary thrombosis thrombus in blood vessel of the heart
Embolus a thrombus freely floating in the blood stream

Pulmonary emboli can impair the ability of the body to obtain oxygen
Cerebral emboli can cause strokes
Hemostasis Disorders: Bleeding Disorders
Thrombocytopenia condition where the number of circulating platelets is deficient

Thrombus a clot that develops and persists in an unbroken blood vessel
Embolus a thrombus freely floating in the blood stream Disseminated Intravascular Coagulation (DIC): widespread clotting in intact blood vessels Hemophilia hereditary bleeding disorders caused by lack of clotting factors
BLOOD GROUP AND TRANSFUSION
Human Blood Groups

RBC membranes have glycoprotein antigens on their external surfaces
These antigens are:

Unique to the individual Recognized as foreign if transfused into another individual Promoters of agglutination and are referred to as agglutinogens
Presence or absence of these antigens is used to classify blood groups

ABO Blood Groups

The ABO blood groups consists of:
Two antigens (A and B) on the surface of the RBCs Two antibodies in the plasma (anti-A and anti-B)
An individual with ABO blood may have various types of antigens and spontaneously preformed antibodies Agglutinogens and their corresponding antibodies cannot be mixed without serious hemolytic reactions
Blood Typing
Positive reactions indicate agglutination Humans have 30 varieties of naturally occurring RBC antigens The antigens of the ABO and Rh blood groups cause vigorous transfusion reactions when they are improperly transfused Other blood groups (M, N, Dufy, Kell, and Lewis) are mainly used for legalities When serum containing anti-A or anti-B agglutinins is added to blood, agglutination will occur between the agglutinin and the corresponding agglutinogens
ABO Blood Groups
Table 17.4
Blood Typing
Blood type being tested
RBC agglutinogens
Serum Reaction
Anti-A Anti-B + +
AB B A O
A and B B A None
+ +
Rh Blood Groups
There are eight different Rh agglutinogens, three of which (C, D, and E) are common Presence of the Rh agglutinogens on RBCs is indicated as Rh+ Anti-Rh antibodies are not spontaneously formed in Rh individuals However, if an Rh individual receives Rh+ blood, anti-Rh antibodies form A second exposure to Rh+ blood will result in a typical transfusion reaction
Blood Products and Blood Typing (1 of 2)
Blood Types Antigens A, B, AB, O Universal donors Rh factor Whole blood transfusions are used: When blood loss is substantial In treating thrombocytopenia Packed red cells (cells with plasma removed) are used to treat anemia
Blood Products and Blood Typing (2 of 2)
Plasma Volume Expanders
When shock is imminent from low blood volume, volume must be replaced Plasma or plasma expanders can be administered Plasma expanders Have osmotic properties that directly increase fluid volume Are used when plasma is not available Examples: purified human serum albumin, plasminate, and dextran Isotonic saline can also be used to replace lost blood volume
Transfusion Reactions
Hemolytic Reactions Signs and Symptoms Facial flushing, hyperventilation, tachycardia, hives, chest pain, wheezing, fever, chills, and cyanosis. Treatment Stop transfusion, change all IV tubing, and initiate IV therapy with normal saline or lactated Ringers.Consider furosemide, dopamine, and diphenhydramine. Febrile Nonhemolytic Reactions Signs and Symptoms Headache, fever, and chills.
Hemolytic Disease of the Newborn

Hemolytic disease of the newborn Rh+ antibodies of a sensitized Rh mother cross the placenta and attack and destroy the RBCs of an Rh+ baby Rh mother becomes sensitized when Rh+ blood (from a previous pregnancy of an Rh+ baby or a Rh+ transfusion) causes her body to synthesis Rh+ antibodies Treatment of hemolytic disease of the newborn involves pre-birth transfusions and exchange transfusions after birth
Transfusion Reactions Transfusion reactions occur when mismatched blood is infused
Donors cells are attacked by the recipients plasma agglutinins causing:

Diminished oxygen-carrying capacity Clumped cells that impede blood flow
Ruptured RBCs that release free hemoglobin into the bloodstream
Circulating hemoglobin precipitates in the kidneys and causes renal failure

Diagnostic Blood Tests
Laboratory examination of blood can assess an individuals state of health Microscopic examination:
Variations in size and shape of RBCs predictions of anemias
Type and number of WBCs diagnostic of various diseases
Chemical analysis can provide a comprehensive picture of ones general health status in relation to normal values
THANK YOU
darmawatiayu@gmail.com

Hematology Dai Modul 22 2014

Hochgeladen von

Dokumentinformationen

Originalbeschreibung:

Copyright

Verfügbare Formate

Dieses Dokument teilen

Dokument teilen oder einbetten

Freigabeoptionen

Stufen Sie dieses Dokument als nützlich ein?

Sind diese Inhalte unangemessen?

Copyright:

Verfügbare Formate

Hematology Dai Modul 22 2014

Hochgeladen von

Copyright:

Verfügbare Formate

HEMATOLOGY

Department of Physiology Diponegoro University Faculty of Medicine

Study of blood & its components Window of rest of body

COMPONENTS OF FORMED ELEMENTS

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

RED BLOOD CELLS

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

Pronormoblast Basophilic normoblast Polychromatophilic Normoblast Orthrochromatophilic Normoblast Reticulocyte

Mature Red Blood Cell

Department of Physiology Diponegoro University Faculty of Medicine

Red Blood Cells

12.0-16.0 gm/dl 13.5-17.5 gm/dl 80-100 fl 0.2-2.0%

Can be detected using supravital stain

Department of Physiology Diponegoro University Faculty of Medicine

Distinguished by reticulocyte count

Department of Physiology Diponegoro University Faculty of Medicine

RBC DESTRUCTION - EXTRAVASCULAR

Heme metabolized to bilirubin in macrophage; globin metabolized intracellularly

Unconjugated bilirubin excreted into plasma & carried to liver

Department of Physiology Diponegoro University Faculty of Medicine

LEUKOCYTES AND IMMUNITY

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

Leukocytes, the only blood components that are complete cells:

Move through tissue spaces

Leukocytosis WBC count over 11,000 per cubic millimeter

larger and usually shorter-lived than RBCs Have lobed nuclei

lymphocytes and monocytes:

Granulocytes neutrophils, eosinophils, and basophils

Neutrophils have two types of granules that:

Contain peroxidases, hydrolytic enzymes, and defensins (antibiotic-like proteins)

Neutrophils are our bodys bacteria slayers

Department of Physiology Diponegoro University Faculty of Medicine

Eosinophils account for 14% of WBCs

Account for 0.5% of WBCs and:

Agranulocytes lymphocytes and monocytes:

Department of Physiology Diponegoro University Faculty of Medicine

Account for 25% or more of WBCs and:

There are two types of lymphocytes: T cells and B cells

Monocytes account for 48% of leukocytes

Department of Physiology Diponegoro University Faculty of Medicine

Summary of Formed Elements

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

Macrophages and T cells are the most important sources of cytokines

Many hematopoietic hormones are used clinically to stimulate bone marrow

Myeloblasts develop into eosinophils, neutrophils, and basophils

Lymphoblasts develop into lymphocytes

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

Leukocytes Disorders: Leukemias

A GLANCE OF IMMUNOLOGY: INNATE AND ADAPTIVE IMMUNITY

Department of Physiology Diponegoro University Faculty of Medicine

Components of Innate Immunity

Abbas & Lichtman,2005

Immunity: Two Intrinsic Defense Systems

Innate (nonspecific) system responds quickly and consists of:

Immunity: Two Intrinsic Defense Systems

Adaptive (specific) defense system