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8/8/2019 Biology Blood
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BIOLOGY
PRESENTATION
OF GROUP 2
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1. Edwin Aria B.
(03)
2. Intan Permata K.
(05)
3. Meryne Wandani P..
(07)
MEMBERS OF GROUP 2 :
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CompositionofBlood
Consistsofformedelements (cells)
suspended & carriedinplasma (fluid
part)
Total blood volumeisabout 5L
Plasmaisstraw-colored liquid
consistingofH20 & dissolvedsolutes
Includesions,metabolites, hormones,
antibodies13-7
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19-5
Composition of Blood
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19-6
FunctionsofBlood
Transport of:
Gases, nutrients, waste products
Processed molecules
Regulatory molecules
Regulation of pH and osmosis
Maintenance of body temperature
Protection against foreign substances
Clot formation
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theaverage human has 5 litresofblood
itisatransportingfluid
itcarries vital substancestoall partsofthe body.
bloodblood
X 500
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19-8
Plasma
Liquid part of blood Pale yellow made up of91% water, 9% other
Colloid: Liquid containing suspended
substances that dont settle out Albumin: Important in regulation of watermovement between tissues and blood
Globulins: Immune system or transport
molecules Fibrinogen: Responsible for formation of blood
clots
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19-9
Formed Elements
Red blood cells (erythrocytes) White blood cells (leukocytes)
Granulocytes
Neutrophils
Eosinophils
Basophils
Agranulocytes
Lymphocytes
Monocytes
Platelets (thrombocytes)
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19-10
ProductionofFormed
Elements Hematopoiesis or hemopoiesis: Process of
blood cell production
Stem cells: All formed elements derived
from single population Proerythroblasts: Develop into red blood cells
Myeloblasts: Develop into basophils,neutrophils, eosinophils
Lymphoblasts: Develop into lymphocytes Monoblasts: Develop into monocytes
Megakaryoblasts: Develop into platelets
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19-11
Hematopoiesis
Hematopoiesisisformationofbloodcells
fromstemcellsinmarrow(myeloid
tissue) &lymphoidtissueErythropoiesis
isformationof
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19-12
Erythrocytes
Structure Biconcave, anucleate
Components
Hemoglobin
Lipids, ATP, carbonic
anhydrase
Function
Transport oxygen fromlungs to tissues and
carbon dioxide from
tissues to lungs
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Haemoglobin
gives red bloodgives red bloodcells their colourcells their colour
can carry up to 4can carry up to 4molecules of Omolecules of O22
associates andassociates and
dissociates with Odissociates with O22
contains ironcontains iron
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When there is a high concentration of oxygen e.g in the
alveoli haemoglobin combines with oxygen to formoxyhaemoglobin. When the blood reaches the tissue which
have a low concentration of oxygen the haemoglobin
dissociates with the oxygen and the oxygen is released into
body tissues
Function of HaemoglobinFunction of Haemoglobin
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19-15
Erythropoiesis
Production of red blood cells Stem cells proerythroblasts early erythroblasts
intermediate late reticulocytes
Erythropoietin: Hormone to stimulate RBC
production
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19-16
Hemoglobin Breakdown
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19-17
Leukocytes
Protect bodyagainst
microorganismsandremovedeadcellsand
debris
Movements
Ameboid
Diapedesis
Chemotaxis
Passive Immunity
Active Immunity
Antigen Antibody
Types
Neutrophils: Mostcommon;phagocytic cellsdestroy bacteria
(60%)
Eosinophils: Detoxifychemicals;
reduceinflammation(4%) Basophils: Alergic reactions;
Release histamine, heparin
increaseinflam.response(1%)
Lymphocytes: Immunity 2 types;
b & tCell types. IgG-infection,
IgM-microbes, IgA-Resp & GI,
IgE-Alergy, IgD-immune
response
Monocytes: Become
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LEUKOCYTES
Fig13.3
13-10
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MonocytesMonocytes
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PhagocytesPhagocytes
Monocytes and macrophages
Provide a non-specific response to
infection
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Lymphocytes
Provide a specific immune response toinfectious diseases.
There are 2 types: -
- T-cells- B-cells
They produce antibodies.
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Platelets (thrombocytes)
Aresmallestofformedelements,lacknucleus
Arefragmentsofmegakaryocytes;amoeboid
Constitutemostofmassofbloodclots
Releaseserotoninto vasoconstrict& reduce bloodflowtoclotarea
Secretegrowth factorstomaintainintegrityofblood vessel wall
Survive 5-9days
these hardenformingaclot,or
"scab."
Fig13.3
13-12
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Can occur via 2 pathways: Intrinsic pathway clots damaged vessels & blood left in test tube
Initiated by exposure of blood to negatively charged surface of glass orblood vessel collagen
This activates factor XII (a protease) which initiates a series of clotting factors
Ca2+ & phospholipids convert prothrombin to thrombin
Thrombin converts fibrinogen to fibrin which polymerizes to form a mesh
Damage outside blood vessels releases tissue thromboplastin thattriggers a clotting shortcut (= extrinsic pathway)
CONVERSION OF FIBRINOGEN
TO FIBRIN
13-24
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19-24
Platelet Plug Formation
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Fig13.9
13-25
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19-26
Blood Grouping
Determined by antigens (agglutinogens) on
surface of RBCs
Antibodies (agglutinins) can bind to RBCantigens, resulting in agglutination (clumping)
or hemolysis (rupture) of RBCs
Groups
ABO and Rh
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19-27
Agglutination Reaction
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19-28
ABO Blood Groups
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How common is your blood type?
46.1%
38.8%
11.1%
3.9%
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Blood Transfusions
A blood transfusion is a procedure in which blood is given to a patient through an
intravenous (IV) line in one of the blood vessels. Blood transfusions are done to replace
blood lost during surgery or a serious injury. A transfusion also may be done if a persons
body can't make blood properly because of an illness.
Who can give you blood?
People with TYPE O blood are called
Universal Donors, because they can give
blood to any blood type.
People with TYPE AB blood are called
Universal Recipients, because they canreceive any blood type.
Rh + Can receive + or -
Rh - Can only receive -
Universal Donor
Universal Recipient
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Rh Factors
Scientists sometimes study Rhesus monkeys
to learn more about the human anatomybecause there are certain similarities betweenthe two species. While studying Rhesusmonkeys, a certain blood protein wasdiscovered. This protein is also present in the
blood of some people. Other people, however,do not have the protein.
The presence of the protein, or lack of it, isreferred to as the Rh (forRhesus) factor.
If your blood does contain the protein, yourblood is said to be Rh positive (Rh+). If yourblood does not contain the protein, your bloodis said to be Rh negative (Rh-).
A+ A-
B+ B-AB+ AB-
O+ O-
http://www.fi.edu/biosci/blood/rh.html
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Blood Evidence
Blood samples Can be analyzed to determine blood
type and DNA, which can be matched to possible
suspects.
Blood droplets Can be analyzed to give clues to thelocation of a crime, movement of a victim, and type of
weapon.
Blood spatter Can be analyzed to determine
patterns that give investigators clues to how a crime
might have happened.
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Microscopic
Views
Bird Blood
Cat Blood
Dog Blood
Fish Blood
Frog Blood
Snake BloodHuman Blood
Horse Blood
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19-34
Rh Blood Group
Firststudiedinrhesusmonkeys
Types
Rh positive: Havetheseantigenspresent
onsurfaceofRBCs
Rh negative: Donot havetheseantigens
present
Hemolyticdiseaseofthenewborn(HDN)
Motherproducesanti-Rh antibodiesthat
crossplacentaandcauseagglutination
and hemol sis offetal RBCs
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19-35
Erythroblastosis Fetalis
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19-36
Diagnostic Blood Tests
Type and crossmatch
Complete blood count
Red blood count
Hemoglobinmeasurement
Hematocrit measurement
White blood count
Differential white bloodcount
Clotting
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19-37
BLOOD DISORDERS
Erythrocytosis: RBC
overabundance
Anemia: Deficiency
ofhemoglobin Iron-deficiency
Pernicious
Hemorrhagic
Hemolytic
Sickle-cell
Hemophilia
Thrombocytopenia
Leukemia
Septicemia
Malaria
Infectious
mononucleosis Hepatitis
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Sickle Cell Anemiathat is a desease of red blood cells that
organized of sickle, so its caused the ability to
bind oxygen and carbon dioxide decrease.
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Leukaemiathat is a desease which is marked with an excessive total of white
blood cells beyond normal caused by uncontrol cell division.
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HaemophiliaThat is a descending desease genetically which is marked with
difficulties in blood clotting if a wound occurs.
Anaemiathat is a desease which lacks ofblood cells caused by the lack ofhaemoglobin extent or iron in blood.
h l
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Thalassaemiathat is a hereditary desease which lacks of red blood cells ability to bind
oxygen and carbon dioxide caused by irregular shape.
H
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Hypertensionthat is a desease which is marked with a blood
pressure beyond normal (more than 140 mmHg)
Hypotensionthat is a desease which is marked with a blood
pressure beyond normal (under 100 mmHg)
A h l i
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Atherosclerosisthat is a desease which the arteries
are hardening because deposition ofplaque of fatty mineral.
Arteriosclerosisthat is a desease which the
arteries are hardening because ofcalcium deposition.
L h i
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Leucopheniathat is a desease which
lacks of white blood cells.
Varicosethat is a desease in which the vein is
widening so that it looks bigger and swellingon the skins surface.
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Hematopoiesis
Is formation of blood cells from stem cells inmarrow (myeloid tissue) & lymphoid tissue
Erythropoiesis is formation of RBCs
Stimulated by erythropoietin (EPO) from kidney
Leukopoiesis is formation of WBCs
Stimulatedby variety ofcytokines
= autocrine regulators secreted by immune system
13-13
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Erythropoiesis
2.5 million RBCsare produced/sec
Lifespan of 120
days Old RBCs removed
from blood byphagocytic cells in
liver, spleen, &bone marrow
Iron recycled backinto hemoglobin
production
Fig13.4
13-14
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RBC Antigens & Blood Typing
Antigens present on RBC surface specify blood type
Major antigen group is ABO system
Type A blood has only A antigens
Type B has only B antigens
Type AB has both A & B antigens
Type O has neither A or B antigens
13-15
Click heretoplay
ABO Blood Types
RealMediaMovie
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Transfusion Reactions
People with Type A blood makeantibodies to Type B RBCs, butnot to Type A
Type B blood has antibodies to
Type A RBCs but not to Type B Type AB blood doesnt have
antibodies to A or B
Type O has antibodies to bothType A & B
If different blood types aremixed, antibodies will causemixture to agglutinate
Fig13.5 13-16
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Transfusion Reactions continued
If blood types don't match,
recipients antibodiesagglutinate donors RBCs
Type O is universal donorbecause lacks A & B antigens
Recipients antibodies wont
agglutinate donors Type O RBCs
Type AB is universalrecipient because doesntmake anti-A or anti-Bantibodies
Wont agglutinate donors RBCs
Insert fig. 13.6
Fig13.6 13-17
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Role of Platelets
Platelets don't
stick to intact
endothelium
because ofpresence of
prostacyclin
(PGI2--a
prostaglandin) &NO
Keep clots from
forming & are
vasodilators13-20
Qui
Ti
and aTI
(LZW) decompressorare needed to see this picture.
Fig13.7a
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Role of Platelets
Damage to endotheliumallows platelets to bind
to exposed collagen
von Willebrand factor
increases bond by bindingto both collagen &
platelets
Platelets stick to collagen
& release ADP, serotonin,& thromboxane A2 = platelet release reaction
13-21
Fig13.7b
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Role of Platelets continued
Serotonin &thromboxane A2stimulatevasoconstriction,
reducing blood flow towound
ADP & thromboxane A2cause other platelets to
become sticky & attach &undergo platelet releasereaction
This continues untilplatelet plug is formed
13-22
Fig13.7c
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Platelet plug becomes infiltrated by meshwork of fibrin
Clot now contains platelets, fibrin & trapped RBCs Platelet plug undergoes plug contraction to form more compact plug
Role of Fibrin
13-23
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Dissolution of Clots
When damage is repaired, activated factor XIIcauses activation ofkallikrein
Kallikrein converts plasminogen to plasmin
Plasmin digests fibrin, dissolving clot
13-26
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Anticoagulants
Clotting can be prevented by Ca+2 chelators (e.g.sodium citrate or EDTA)
or heparin which activates antithrombin III (blocks
thrombin) Coumarin blocks clotting by inhibiting activation of
Vit K
Vit K works indirectly by reducing Ca+2 availability
13-27
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Prostaglandins (PGs)
Are produced in almost every organ Belong to eicosanoid family -- all derived from arachidonic acid of
plasma membrane
Fig11.34
11-72
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Have wide variety of functions Different PGs may exert antagonistic effects in tissues
Some promote smooth muscle contraction & some relaxation
Some promote clotting; some inhibit
Promotes inflammatory process of immune system
Plays role in ovulation
Inhibits gastric secretion in digestive system
Prostaglandins (PGs) continued
11-73
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Cyclooxygenase (COX) 1 & 2 are involved in PG synthesis(Fig 11.34)
Are targets of a number of inhibitory non-steroidal anti-inflammatory drugs (NSAIDs)
Aspirin, indomethacin, ibuprofen inhibit both COX 1 & 2 thereby producingside effects
Celebrex & Vioxx only inhibit COX 2 & thus have few side effects
Prostaglandins (PGs) continued
11-74
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