Hematology

HEMATOLOGY
Physiology
Faculty of Medicine
Diponegoro University
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
Normal Values
Hematocrit
Females
35-47%
Males
40-52%
Hemoglobin
Females
12.0-16.0 gm/dl
Males
13.5-17.5 gm/dl
MCV
80-100 fl
Reticulocyte Count
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
Lymphocyte
Basophil
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
NORMAL
Leukemia
white blood cell cancer
Myelocytic leukemia
involves
myeloblasts
Lymphocytic
leukemia involves
lymphocytes
Acute leukemia primarily affects children
Chronic leukemia - more
prevalent in older people
AML
ALL
CML
www-sdc.med.nagasaki-u.ac.jp/. ../Leukemia-E.html
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
A and B
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
A GLANCE OF IMMUNOLOGY:
INNATE AND ADAPTIVE
IMMUNITY
(hanya sebagai tambahan materi)
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

Hematology

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HEMATOLOGY

Department of Physiology Diponegoro University Faculty of Medicine

Study of blood & its components

COMPONENTS OF FORMED ELEMENTS

Red Blood Cells Oxygen & CO2 transport

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

RED BLOOD CELLS

Normal - Anucleated, highly flexible biconcave

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

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

Young red blood cell; still have small amounts of

Before birth, blood cell formation takes place in the

Department of Physiology Diponegoro University Faculty of Medicine

Distinguished by reticulocyte count

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

RBC DESTRUCTION - EXTRAVASCULAR

Heme metabolized to bilirubin in macrophage; globin

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, the only blood components that are

Granulocytes neutrophils, eosinophils, and

Neutrophils have two types of granules that:

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:

Monocytes account for 48% of leukocytes

Department of Physiology Diponegoro University Faculty of Medicine

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

Leukopoiesis is hormonally stimulated by two

Macrophages and T cells are the most important

Department of Physiology Diponegoro University Faculty of Medicine

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

Acute leukemia involves blast-type cells and

Department of Physiology Diponegoro University Faculty of Medicine

Hemostasis: prevention of blood loss.

Department of Physiology Diponegoro University Faculty of Medicine

Platelet Plug Formation

Platelets do not stick to each other or to the endothelial

With the help of von Willebrand factor (VWF) adhere to collagen

The platelet plug is limited to the immediate area of injury

Department of Physiology Diponegoro University Faculty of Medicine

A set of reactions in which blood is transformed

Department of Physiology Diponegoro University Faculty of Medicine

Detailed Events of Coagulation

Factors Limiting Clot Growth or Formation

Two homeostatic mechanisms prevent clots

Inhibition of Clotting Factors