cardiovascular system; blood miss nurul
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CARDIOVASCULAR SYSTEM;BLOOD
Miss Nurul
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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.
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The CARDIOVASCULAR system consists of 3
interrelated components;
1. Blood
2. Heart3. Blood vessels
* cardio= heart, vascular= blood & blood
vessels
Hematology is the study about blood.
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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
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2. Regulation
pH of body fluids
Heat absorbing & coolant properties of thewater in blood plasma
Help skin to adjust temperature
Blood osmotic pressure
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3. Protection
Blood clot when injury blood loss
WBCs protect against disease. Phagocytes, antibodies
Additional protein help to against disease
Interferon, complement
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Composed of 2 portion;
1. Plasma
2. Formed elements
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A liquid extracellular matrix that contains dissolved
substance.
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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
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Is known 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 bonemarrow can develop; Lymphoid stem cells lymphocytes (in
lymphatic tissues) Myeloid stem cells all other WBCs, all RBCs,
and platelets (in red bone marrow)
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Also known as erythrocytes
Structure
Biconcave disc concave both side Provides for maximal gas exchange
8m in diameter
Mature RBCs
no nucleus & other organelles Lack of nucleus causes biconcave disc shape
flexible for passing through capillaries
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HEMOGLOBIN
oxygen-carrying protein
Carries 98.5% of O2 and 23% of CO2
pigment that give whole blood red colour
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Live only ~ 120 days due to
Wear & tear on their plasma membrane as they
squeeze through blood capillaries
Damaged RBCs will be cleared by
macrophages
In the spleen, liver & red bone marrow.
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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 hemebiliverdin bilirubin Bilirubin to liver bile helps absorb fats
Intestinal bacteria convert bilirubin into other chemicals that exit in
feces (stercobilin) or urine (urobilin)
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Amino
acids
Reused for
protein synthesisGlobin
Urine
Stercobilin
Bilirubin
Urobilinogen
Feces
Large
intestine
Small
intestine
Circulation for about
120 days
Bacteria
Bilirubin
Red blood cell
death and
phagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+
Globin
+
Vitamin B12
+
Erythopoietin
Key:
in blood
in bile
Erythropoiesis in
red bone marrow
Kidney
Macrophage in
spleen, liver, or
red bone marrow
Ferritin
Urobilin
Heme
BiliverdinBilirubin
Fe3+
14
13 12
1110
9
8
7
65
4
3
2
1
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Get a rest, take 5!!
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The process of RBC synthesis
Develop from myeloid stem cells in red bone marrow
Other substances that help in this process
Vitamin B12
Erytropoietin
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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.
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Production and destruction normally
balanced
Stimulus for erythropoiesis1. low O2 delivery (hypoxia) in blood passing to
kidneys erythropoietin (EPO) release
2. EPO circulate to red bone marrow
increased O2 delivery in blood
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Signs of lower than normal RBC count
changes in skin, mucous membranes, and
finger nail beds
Cyanosis: bluish colour
Anemia: pale colour
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To be continued..
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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
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Appear to be white because lack of Hb
Normal WBC count : 5000-10000/L WBC count usually increase in infection
Major Fx defense against phagocytosis Infection
Inflammation
Antigen-antibody reaction (allergic)
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Life span 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
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Neutrophils
first responders to infection
Phagocytosis
Release bacteria-destroying enzyme lysozyme
Microbes enter the bodyphagocytosis(neutrophils) lysozyme (enzyme) destroy the microbes.
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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 thanneutrophils
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Eosinophils
Leave the capillaries & enter interstitial fluid
Release enyzme to combat inflammation inallergic reaction
Phagocytize antibody-antigen complexes
Respond to parasitic infections
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Basophils
Intensify inflammatory responses and allergic reactions
Release chemicals that dilate blood vessels: histamineand serotonin; also heparin (anticoagulant)
Leave capillaryenter tissue release chemicals dilation of blood vessels
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Lymphocytes
Play major roles in
immune responses
Three types of lymphocytes1. T cells
2. B cells3. Natural killer (NK) cells
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1. T cells directly attack virus, fungi, transplanted cells, cancer
cells, some bacteria.
2. B cells Destroy bacteria
respond to foreign substances called antigens anddifferentiate 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.
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Myeloid stem cells megakaryocytes 20003000
fragments platelets
Disc shape; diameter 2-4 m
No nucleusNormal count: 150,000-400,000/L blood
Functions
Plug damaged blood vessels
Promote blood clotting
Life span 59 days
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RBCs have antigens on their surfaces
Known as agglutinogens
Each blood 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
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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
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Typically blood has antibodies/ agglutinins in plasma These can react with antigens
Two types1. 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
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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 firstexposure to Rh+ blood in transfusion
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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
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Is a sequence of responses that stop
bleeding/ hemorrahage
The response must be
Quick
Localized to the region of damage
Carefully controlled
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3 mechanism of hemostasis
1. Vascular spasm
2. Platelet plug formation
3. Blood clotting (coagulation)
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Blood vessel damage
Smooth muscle wall contract immediately
Reduce blood loss (for several minutes to
hours)
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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)
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Coagulation
The process of clot formation
Series of chemical reaction involving clotting factors
Calcium ions (Ca) Enzyme made by liver cells
3 stages of clotting process
1.Formation of prothrombinase enzyme
2.Prothrombin thrombin
3.Thrombin fibrinogen (soluble) fibrin (insoluble) clot
prothrombinase
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Prothrombinase can be formed in 2 ways
1. Extrinsic pathway
2. Intrinsic pathway
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Blood clotting occur rapidly
So-named due to damaged tissue cells
release a tissue protein tissue factor
(TF) into the blood from outside the bloodvessels.
With helped of Ca and several factor
Damage tissue prothrombinase
TF + Calcium ions + clotting
factors
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More slow than extrinsic pathway, require
several minutes
So-named due to its activators are either in
direct contact with blood or contained withinthe blood.
tissue damage blood come in contact with
collagen factor in the adjacent connective
tissue
activate clotting factor + Ca
prothrombinase
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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
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Fibrinolysis
breakdown of clots by plasmin
Clot Inactivated plasminogen Activated (by
tPA) plasmin
Substance to activate plasminogen
Thrombin
Tissue plasminogen acticator (tPA)
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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)
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