cardiovascular system; blood miss nurul

8/14/2019 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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cardiovascular system; blood miss nurul

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