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CARDIOVASCULAR SYSTEM;

BLOOD

Miss Nurul
At the end of this lecture, the student will
be able to;
 Describe the general function of blood.
 State the composition of blood.
 Explain the formation of blood
(haemopoeisis/ hemopoeisis).
 Describe the ABO and RH blood group.
 Explain the mechanism of blood clotting.
 The CARDIOVASCULAR system consists of 3
interrelated components;
1. Blood
2. Heart
3. Blood vessels
* cardio= heart, vascular= blood & blood
vessels
 Hematology is the study about blood.
3 general function of blood
1. Transportation
 Oxygen from lungs to cells
 Carbon dioxide from cells to lungs
 Carries nutrient from GIT to cells
 Eliminate heat & waste product from cells
 Hormones from endocrine gland to other body
cells
2. Regulation
 pH of body fluids
 Heat absorbing & coolant properties of the
water in blood plasma
 Help skin to adjust temperature
 Blood osmotic pressure
3. Protection
 Blood clot when injury  blood loss
 WBCs protect against disease.
 Phagocytes, antibodies
 Additional protein help to against disease
 Interferon, complement
 Composed of 2 portion;
1. Plasma
2. Formed elements
A liquid extracellular matrix that contains dissolved
substance.
3 elements that formed blood
1. Red blood cells (RBCs)
2. White blood cells (WBCs)
a. Granular leukocytes
 Neutrophils
 Eosinophils
 basophils
b. Agranular leukocytes
 T & B lymphocytes, natural killer cells
 monocytes
3. Platelets
 Isknown as haemopoeisis/ hemopoeisis.
 Occurs throughout life
 In response to specific hormones, stem cells
undergo a series of changes to form blood cells
 Pluripotent(several) stem cells in red bone
marrow can develop;
 Lymphoid stem cells  lymphocytes (in
lymphatic tissues)
 Myeloid stem cells  all other WBCs, all RBCs,
and platelets (in red bone marrow)
 Also known as erythrocytes
 Structure
 Biconcave disc  concave both side
 Provides for maximal gas exchange
 8µm in diameter
 Mature RBCs
 no nucleus & other organelles
 Lack of nucleus causes biconcave disc shape
 flexible for passing through capillaries
 HEMOGLOBIN
 oxygen-carrying protein
 Carries 98.5% of O2 and 23% of CO2
 pigment that give whole blood red colour
 Live only ~ 120 days due to
 Wear & tear on their plasma membrane as they
squeeze through blood capillaries

 DamagedRBCs will be cleared by


macrophages
 In the spleen, liver & red bone marrow.
 Globin amino acids recycled to form proteins
 Heme broken down into:
 Fe
 Carried in blood by transferrin (“protein escort” of Fe)
 Recycled in bone marrow for forming synthesis of new hemoglobin;
proteins and vitamin B12
 Non-Fe portion of heme biliverdin  bilirubin
 Bilirubin to liver  bile  helps absorb fats
 Intestinal bacteria convert bilirubin into other chemicals that exit in
feces (stercobilin) or urine (urobilin)
Circulation for about
120 days

3 7

Amino Reused for


protein synthesis Fe3+ Transferrin
acids
Globin

4 6
5
Fe3+
2 Heme Ferritin Fe3+

Transferrin +
Bilirubin Globin
9 +
Biliverdin Liver Vitamin B12
Bilirubin 11
1 Red blood cell +
death and 10
Small Erythopoietin
phagocytosis
intestine
Kidney
Bilirubin
8 Erythropoiesis in
13 red bone marrow
12
Urobilin
Macrophage in Urobilinogen Bacteria Key:
spleen, liver, or
red bone marrow in blood
Stercobilin
Large 14
intestine in bile

Urine Feces
 Get a rest, take 5!!
 The process of RBC synthesis

 Develop from myeloid stem cells in red bone marrow

 Other substances that help in this process


 Vitamin B12
 Erytropoietin
 Cells
lose their nucleus near the end of
erythropoiesis

 Known as reticulocytes
 34% Hb, some organelles
 Will develop into erythrocytes after 1-2 days in
bloodstream.
 Production and destruction normally
balanced
 Stimulus for erythropoiesis
1. low O2 delivery (hypoxia) in blood passing to
kidneys  erythropoietin (EPO) release
2. EPO circulate to red bone marrow 
increased O2 delivery in blood
 Signsof lower than normal RBC count 
changes in skin, mucous membranes, and
finger nail beds

 Cyanosis: bluish colour


 Anemia: pale colour
 To be continued..
 Also known as leukocytes
 Structure
 Have nuclei
 Do not contain Hb.
 Classification
 Granular  contain conspicuous granules that visible under
microscope
 Agranular  no granules visible under microscope
 Appear to be white because lack of Hb

 Normal WBC count : 5000-10000/µL


 WBC count usually increase in infection

 Major Fx  defense against  phagocytosis


 Infection
 Inflammation
 Antigen-antibody reaction (allergic)
 Lifespan only a few hours to a few days
 Leukocytes develop in red bone marrow
 Monocytes & granular leukocytes develop from a
myeloid stem cells.
 Leukocytosis
 An increase in number of WBCs in response to infection,
exercise, surgery
 Leukopenia
 Low WBCs count
Neutrophils
 first responders to infection
 Phagocytosis
 Release bacteria-destroying enzyme lysozyme

Microbes enter the body  phagocytosis


(neutrophils)  lysozyme (enzyme) 
destroy the microbes.
Monocytes
 Take longer to reach the site of infection
 macrophages (“big eaters”)
 come in large numbers
 Known as wandering macrophages
 migrate into the infected tissue
 Can phagocytize many more microbes than
neutrophils
Eosinophils
 Leave the capillaries & enter interstitial fluid
 Release enyzme to combat inflammation in
allergic reaction
 Phagocytize antibody-antigen complexes
 Respond to parasitic infections
Basophils
 Intensify inflammatory responses and allergic reactions
 Release chemicals that dilate blood vessels: histamine
and serotonin; also heparin (anticoagulant)

Leave capillary  enter tissue  release chemicals 


dilation of blood vessels
Lymphocytes

 Play major roles in


immune responses

 Three types of lymphocytes


1. T cells
2. B cells
3. Natural killer (NK) cells
1. T cells
 directly attack virus, fungi, transplanted cells, cancer
cells, some bacteria.
2. B cells
 Destroy bacteria
 respond to foreign substances called antigens and
differentiate into plasma cells that produce antibodies.
Antibodies attach to antigens and inactivate the antigens.
3. Natural killer (NK) cells
 Attack wide variety of microbes infection & certain
spontaneously arising tumor cells.
 Myeloid stem cells  megakaryocytes  2000–3000
fragments  platelets
 Disc shape; diameter 2-4 µm
 No nucleus
 Normal count: 150,000-400,000/µL blood
 Functions
 Plug damaged blood vessels
 Promote blood clotting
 Life span 5–9 days
 RBCs have antigens on their surfaces
 Known as agglutinogens
 Eachblood group consists of two or more different
blood types
 Two examples:
 ABO group has types A, B, AB, O
 Rh group has type Rh positive(Rh+), Rh negative(Rh–)
 Blood types in each person are determined by genetics
ABO blood group is based on 2 antigens;
1. A
2. B

 Type A has only A antigen


 Type B has only B antigen
 Type AB has both A and B antigen
 Type O has neither A nor B antigen
 Typically blood has antibodies/ agglutinins in plasma
 These can react with antigens
 Two types
1. anti-A antibody
2. anti-B antibody

 Blood lacks antibodies against own antigens


 Type A blood has anti-B antibodies (not anti-A)
 Type AB blood has neither anti-A nor anti-B antibodies
 Rh= Rhesus
 Also known as Rh factor
 Rh blood type
 If RBCs have Rh antigen:Rh+
 If RBCs lack Rh antigen:Rh–
 Normally an individual have neither Rh+ nor Rh-
has anti-Rh antibodies.
 Antibodies develop in Rh- persons after first
exposure to Rh+ blood in transfusion
 Type AB  universal recipient
 Have no anti-A and anti-B antibodies
 So can receive any ABO blood type
 Type O  universal donor
 Have neither A nor B antigen on RBCs
 So can donate to any ABO blood type
 Isa sequence of responses that stop
bleeding/ hemorrahage

 The response must be


 Quick
 Localized to the region of damage
 Carefully controlled
3 mechanism of hemostasis

1. Vascular spasm

2. Platelet plug formation

3. Blood clotting (coagulation)


Blood vessel damage

Smooth muscle wall contract immediately

Reduce blood loss (for several minutes to


hours)
Platelet contact and stick to part of damage blood
vessels (collagen fibers)

Interact with each other to liberate the chemicals

Chemical activate nearby platelet make it sticky

Platelet plug

Stop blood loss completely (for small blood vessel)


 Coagulation
 The process of clot formation
 Series of chemical reaction involving clotting factors
 Calcium ions (Ca² )
 Enzyme made by liver cells

3 stages of clotting process


1. Formation of prothrombinase enzyme
2. Prothrombin prothrombinase
thrombin
3. Thrombin  fibrinogen (soluble)  fibrin (insoluble)  clot
 Prothrombinase can be formed in 2 ways

1. Extrinsic pathway

2. Intrinsic pathway
 Blood clotting occur rapidly
 So-named due to damaged tissue cells
release a tissue protein  tissue factor
(TF) into the blood from outside the blood
vessels.
 With helped of Ca² and several factor

Damage tissue prothrombinase


TF + Calcium ions + clotting
factors
 More slow than extrinsic pathway, require
several minutes
 So-named due to its activators are either in
direct contact with blood or contained within
the blood.
tissue damage  blood come in contact with
collagen factor in the adjacent connective
tissue  activate clotting factor + Ca² 
prothrombinase
 The clot will plug the ruptures area
 Clot retraction
 The consolidation or tightening of the fibrin clot.
 Gradually contract (retraction)
 Pulls sides of wound together  decrease the risk of
further damage
 Repair
Fibroblast replace connective tissue  new
endothelial cells repair lining
 Fibrinolysis
 breakdown of clots by plasmin
 Clot  Inactivated plasminogen  Activated (by
tPA)  plasmin
 Substance to activate plasminogen
 Thrombin
 Tissue plasminogen acticator (tPA)
 Inappropriate (unneeded) clots
 Clots can be triggered by roughness on vessel
wall = thrombosis
 Loose (on-the-move) clot = embolism

 Anticoagulants drugs: decrease clot


formation
 Heparin
 Warfarin (Coumadin)