Chapter 19coastalbend.edu/uploadedFiles/CBC/Content/Programs... · – Digestive system cells •...
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Chapter 19 Cardiovascular System:
The Blood
AP2 Chap. 19: Cardiovascular Syst 1
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Cardiovascular System: The Blood
I. Functions of the Blood II. Plasma III. Formed Elements IV. Hemostasis V. Blood Grouping VI. Diagnostic Blood Tests
AP2 Chap. 19: Cardiovascular Syst 2
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Cardiovascular System • Cells req. constant nutrition &
waste removal b/c they are metabolically active
• This system made up of the heart, the blood vessels, & the blood: connects the various tissues of the body. The heart pumps blood thru the blood vessels & the blood delivers nutrients & picks up waste products.
AP2 Chap. 19: Cardiovascular Syst
Fig. 1.3 pg 8
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Blood: Facts & Figures • Blood: Type of CT
– Formed Elements: • 45% make-up • Cells • Cell Fragments
– Plasma • 55% bld vol. • Liquid Matrix
• Total Bld Vol. – ♀ 4-5 Liters – ♂ 5-6 Liters
• 8% of total body Weight
AP2 Chap. 19: Cardiovascular Syst
Figure 19.1 pg 651
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I. Fxns of the blood
AP2 Chap. 19: Cardiovascular Syst 5
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I. Fxns of the blood The blood helps maintain homeostasis in several ways:
1. Transport of gases, nutrients, & waste products. 2. Transport of processed molecules 3. Transport of regulatory molecules 4. Regulation of pH & Osmosis 5. Maintenance of Body Temperature 6. Protection against foreign substances 7. Clot formation
AP2 Chap. 19: Cardiovascular Syst 6
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I. Fxns of the blood
1. Transport of gases, nutrients, & waste products.
• O2: – lungs cells
• CO2: – cells lungs for exhalation
• Ingested nutrients, ions, & H2O: – Digestive system cells
• Waste products: – Cells kidneys for elimination
2. Transport of processed molecules
• Many things are made in one place in the body. They are then carried via the blood to another part for modification & finalization.
• Ex\ – Skin prod’s Vit D – Transferred to liver & kidney to
modify into its active form – Finalized form travels to the
small intestine to promote Ca2+ uptake
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The blood helps maintain homeostasis in several ways:
3. Transport of regulatory molecules • Carries hormones & enz’s that regulate body processes from 1 body part
to another
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I. Fxns of the blood
4. Regulation of pH & Osmosis
• Buffers maintain blood pH • Homeostasis=7.35-7.45 • Osmotic composition:
– Bld is critical for maintaining normal fluid &ion balance
AP2 Chap. 19: Cardiovascular Syst 8
The blood helps maintain homeostasis in several ways:
5. Maintenance of Body Temp.
6. Protection against foreign substances
• Warm bld is transferred from the body core to the body surface where heat is released
• An important part of the immune system is located w/in the blood & helps fight foreign substances such as toxins or microorganisms
7. Clot formation
• Protects against XSV bld loss when bld vessels are damaged
• 1st step in tissue repair & return to fxn when tissues are damaged
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II. Plasma
AP2 Chap. 19: Cardiovascular Syst 9
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II. Plasma • 91% water & 9% other
– Proteins, ions, nutrients, gases, wastes
– Colloid • Plasma Proteins:
Pro’d by liver or bld cells 1. Globulins 2. Albumins 3. Fibrinogen
• Ions: Na, K, Ca, Mg, Cl, Fe, PO4, H, OH-, HCO3
- • Nutrients:
– Vitamins – Glucose, AA’s, Cholesterol,
& triglycerides (aka triacylglycerol )
• Gases: O2, CO2, & N2 10
Figure 19.1 pg 651
• Waste: Urea, Uric Acid, Creatinine, Ammonia Salts, Bilirubin, & lactic acid
• Regulatory Substances
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II. Plasm
a • Water:
– Acts as a solvent & suspending medium • Ions:
– Involved in osmosis, membrane potential, & acid-base balance
• Nutrients: – Vitamins: promote enz activity – Rest: energy & building blocks
• Regulatory Substances: – Enz’s catalyze chem rxns – Hormones stimulate/inhibit body fxns
• Gases – O2
• Req’d for aerobic respiration – CO2
• Waste product of aerobic respiration that can be used as bicarbonate helping buffer bld
– N2 • Inert
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Functions in the plasma:
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II. Plasma Fxn of plasma proteins
1. Globulins: – α
• Protects tissues via inflammation
• Fxns as a transport protein • Converts Fe2+ to Fe3+ for
transport in transferrin • Transports hemoglobin from
damaged RBC’s – β
• Acts as a transport protein • Involved in immunity • Prevents blood loss
– γ • Most antibodies are γ
globulins involved in immunity
2. Albumin: – Partly responsible for
bld viscosity & osmotic pressure
– Acts as a buffer – Acts as a transport
protein 3. Fibrinogen
– Fxns in bld clotting
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II. Plasma Composition
Waste: • Urea, Uric Acid, Creatinine, Ammonia Salts:
– Byproducts of protein metabolism that are excreted by the kidneys
• Bilirubin – Byproduct of RBC breakdown that is excreted by
the liver as part of the bile into the intestine • Lactic Acid
– Byproduct of anaerobic respiration that is converted into glucose by the liver
AP2 Chap. 19: Cardiovascular Syst 13
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III. Formed Elements A. Production of Formed Elements B. Red Blood Cells C. White Blood Cells D. Platelets
AP2 Chap. 19: Cardiovascular Syst 14
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III. Formed Elements: 3 major classes
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Red Blood Cells (Erythrocytes)
RBC’s 700X more than WBC
17X more than platelets
White Blood Cells (Leukocytes)
WBC’s
Platelets (Thrombocytes)
Granulocytes Agranulocytes
Basophil
Eosinophil
Neutrophil
Monocyte
Lymphocyte
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III. F
orm
ed E
lem
ents
P
rod’
n of
form
ed e
lem
ents
• Embryo:
– Tissues like the yoke sac, liver, thymus, spleen, lymph nodes, & red bone marrow (RBM)
• After Birth: – Confined to RBM with
some lymphoid tissue aiding in prod’n of lymphocytes
– Young children almost all bone marrow is RBM
– Adults RBM confined to ribs, sternum, vertebrae, pelvis, proximal femur & humerus (rest replaced by Yellow bone marrow)
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Hematopoiesis (Hemopoiesis)
Figure 19.2 pg 655
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III. Formed Elements RBC’s: Structure
• Biconcave disk with thicker edges than in the center – Allows for greater surface area &
makes movement of gases into the cell more rapid
– Allows for easier bending & folding ’ing its size to allow it to pass more easily thru small bld vessels
• Original cell looses its nucleus & almost all organelles when mature.
• Main Component w/in RBC: – Hemoglobin red pigmented
protein filling 1/3 of the RBC vol. • Minor Components:
– Lipids, ATP & the enz: carbonic anhydrase
AP2 Chap. 19: Cardiovascular Syst 17
Figure 19.3 pg 656
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III. Formed Elements RBC’s: FXN
Primary Fxn O2 transport – Take O2 from the lungs to
the body tissues – 98.5% of O2 in bld linked to
hemoglobin – 1.5% dissolved in plasma – Take CO2 from body tissues
to the lungs • RBC rupturehemolysis • Hemoglobin must be in cell
if not denatures & no longer fxnal
• CO2 Transport in blood – 3 major ways: 1. 7% dissolved in plasma 2. 23% attached to
Hemoglobin 3. 70% transported as
bicarbonate ion (HCO3-)
• Carbonic anhydrase is the enzyme responsible for converting CO2 & H2O into Carbonic Acid wh/dissociates into a H+ & HCO3
- AP2 Chap. 19: Cardiovascular Syst 18
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III. Formed Elements RBC’s: Hemoglobin
• 4 PP-Chain + 4 Heme-groups • Each polypeptide chain (globin) is bound to 1 heme.
– 9 hemoglobin types based on aa sequence (α, β, γ, δ & embryonic)
– Most adult is a combo of 2 α and 2 β • Heme is a red pigment molecule containing an iron atom • 3 types of Hemoglobin exist w/ diff’s in their affinity for O2
1. Embryonic: pro’d up to 3rd mo. of development 2. Fetal: @ 3rd mo fetal replaces embryonic hemoglobin 3. Adult: by birth 60-90% is adult by 2 to 4 almost nothing but
adult AP2 Chap. 19: Cardiovascular Syst 19
Figure 19.4 pg 656
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III. Formed Elements RBC’s: Hemoglobin Iron (Fe)
• Fe is req’d for normal hemoglobin fxn b/c O2 binds to the Fe molecule w/in the heme
• It is usually ingested in diet.
• Exposure to O2, binds 1 O2 to each Heme (oxyhemoglobin) w/o (deoxyhemoglobin)
• AA’s of the globin bind to CO2 : – Carbaminohemoglobin
• Also bind to NO, which fxns as a chemical signal in the body (hormone) & induces the relaxation of smooth muscle
• Thus Hemoglobin may play a role in blood pressure via NO involvement.
AP2 Chap. 19: Cardiovascular Syst 20
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III. Formed Elements: RBC’s Life History of RBC’s
RBC Production
• Lowered bld O2 induced the kidney to release erythropoietin wh/goes to bone marrow & increases RBC prod’n thus increasing bld O2 levels
AP2 Chap. 19: Cardiovascular Syst 21
Figure 19.5 pg 659
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III. Formed Elements: RBC’s Life History of RBC’s
RBC death and Hemoglobin recycling
• RBC’s only live for 110(♀)-120(♂) days
• W/O nuclei they have no way to prod. new proteins or divide thus existing proteins, enz’s, PM components & other structures begin to degenerate & the RBC becomes less able to transport O2 & the PM b/c’s more fragile over time. They can rupture releasing hemoglobin.
• What to do???? 22
Figu
re 1
9.6
pg 6
60
Aged, damaged, or abnormal RBC’s are taken to the spleen, liver & other lymphatic tissue. Here macrophages isolate hemoglobin.
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III. Formed Elements: RBC’s: Life History of RBC’s RBC death and Hemoglobin recycling
• Hemoglobin is separated into Heme & Globin
• Globin is broken down into it’s component AA’s that can be used to make new proteins or metabolized.
• Heme - Fe is released and the rest is converted 1st into biliverdin then to bilirubin – Bilirubin via bld goes to the liver
& excreted w/in bile to the small intestine (colors both feces & urine & reabsorbed bilirubin derivatives)
– Fe: bound to transferrin & carried in bld to:
• Various tissues for storage • Bone marrow to be used in the
production of new hemoglobin. 23 Figure 19.6 pg 660
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III. Formed Elements: WBC’s
AP2 Chap. 19: Cardiovascular Syst 24
Figure 19.7 pg 661
Figure 19.8 pg 662
Figure 19.3 pg 656
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III. Formed Elements: WBC’s • Lack hemoglobin • Have a nucleus • Protect the body
against invading microorganisms & remove dead cells & debris from the body
• Most are motile exhibiting ameboid movement.
• Leave the bld stream & enter the tissue via diapedesis – b/c thin & elongated &
slip btwn or thru the cells of the blood vessel walls
• Chemotaxis: WBC attraction to foreign materials or dead cells w/in the tissue
AP2 Chap. 19: Cardiovascular Syst 25
• At the site of infections WBC’s accumulate & phagocytize bacteria, dirt, & dead cells; then they die:
• Pus buildup of dead WBC’s+ bacteria + fluid + cell debris
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III. Formed Elements: WBC’s 3 major classes
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Red Blood Cells (Erythrocytes)
RBC’s 700X more than WBC
17X more than platelets
White Blood Cells (Leukocytes)
WBC’s
Platelets (Thrombocytes)
Granulocytes Agranulocytes
Basophil
Eosinophil
Neutrophil
Monocyte
Lymphocyte
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III. Formed Elements: WBC’s Granulocytes
Basophil • Nucleus w/ 2 indistinct
lobes; cytoplasmic granules stain blue-purple; 10-12 µm in diameter
• Fxn: – Releases: – Histamine
promotes inflammation
– Heparin prevents clot formation
AP2 Chap. 19: Cardiovascular Syst 27
Eosinophil • Nucleus often bilobed;
cytoplasmic granules stain orange-red to bright red; 11-14 µm diameter
• Fxn: • Releases
chemicals that reduce inflammation
• Attacks certain worm parasites
Neutrophil • Nucleus has 2 to 4 lobes
connected by thin filaments; cytoplasmic granules stain light pink to reddish purple; 10-12 µm diameter
• Fxn • Phagocytizes
microorganisms, Ag-Ab complexes & other substances
• Lysozyme
60-70% WBC
2-4% WBC
0.5-1% WBC
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III. Formed Elements: WBC’s Agranulocytes
Lymphocytes • Round nucleus; cytoplasm
forms a halo around the nucleus; 6-14 µm diameter
• Produces antibodies (Ab’s) & other chemicals responsible for destroying microorganisms; contributes to allergic rxns, graft rejection, tumor control, & reg’n of the immune system
Monocytes • Nucleus can be round,
kidney shaped, or horse shoe shaped; contains more cytoplasm than lymphocyte; 12-20µm diameter
• Phagocytic cell in the bld; leaves the bld & becomes a macrophage, wh/ phagocytizes bacteria, dead cells, cell fragments, & other debris w/in tissue
AP2 Chap. 19: Cardiovascular Syst 28
20-25% WBC
3-8% WBC
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III. Formed Elements: Platelets • Cell fragments
surrounded by plasma membrane & containing granules
• ~ 3µm diameter • Surface displays proteins
that allow platelets to stick to other molecules (glycoproteins)
• These surface molecules & internal granules help control bld loss
• Also contains actin & myosin to cause platelet contraction
• Life 5-7 days
• Essential Functional Roles:
1. Forming platelet plugs, which seal holes in small vessels
2. Promoting the formation & contraction of clots; wh/help seal off larger wounds in bld vessels
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IV. Hemostasis A. Vascular Spasm B. Platelet plug formation C. Coagulation D. Control of Clot formation E. Clot retraction & Dissolution
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IV. Hemostasis
• The stoppage of bleeding to maintain homeostasis.
• 3 major steps to achieve hemostasis
1. Vascular Spasm
2. Platelet plug formation
3. Coagulation
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IV. Hemostasis: 1. Vascular Spasm
• Immediate but temporary constriction of blood vessel resultant from vessel wall smooth muscle contraction.
• Can close small vessels completely to stop bleeding
• Produced by: 1. Nervous System Reflexes
Damage can cause reflexive contraction 2. Chemical Signals
Ex/ platelets release thromboxanes & damaged endothelial cells release endothelian both of wh/ induce contraction
AP2 Chap. 19: Cardiovascular Syst 32
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IV. Hemostasis: 2. Platelet Plug Formation
• Accumulation of platelets that can seal-up small breaks in blood vessels
• Described in steps that actually occur simultaneously
33
Figure 19.9 pg 663
• Platelet Adhesion: • von Willebrand factor (vWF)
binds platelets to collagen in damaged tissue attaching platelets to damaged surface
• Platelet release rxn: • Bound platelets release ADP,
thromboxanes, & other chemicals that activate other platelets
• Platelet aggregation • Activated platelets express
fibrinogen receptors that bind fibrinogen (a plasma protein) wh/ is used to link platelet to platelet with an interlinking fibrinogen.
• Activated platelets also express platelet factor III & coagulation factor V wh/ are imp. to clot formation
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IV. Hemostasis: Coagulation • When a bld vessel is severely
damaged blood clotting (coagulation) results in the formation of a clot.
• Blood clot network of threadlike protein fibers called fibrin that trap blood cells, platelets, & fluid.
• Formation of a blood clot depends on a number of proteins called coagulation factors. – These factors only fxn after
activation wh/is a complex process involving multiple chemical rxns.
– Activation begins with 1. Extrinsic & 2. Intrinsic pathways that converge into the Common Pathway
AP2 Chap. 19: Cardiovascular Syst 34
Figure 19.10 pg 664
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IV. Hemostasis: Coagulation: Clot formation Extrinsic Pathway • Extrinsic is so called b/c
chemicals being released come from damaged tissue and not w/in the blood.
• Tissues release thromboplastin/tissue factor(TF)/F3 (combo of lipoproteins & phospholipids)
• TF in the presence of Ca2+ forms a complex with F7
• This complex activates F10
• This is the beginning of the common pathway
AP2 Chap. 19: Cardiovascular Syst 35
Figure 19.11 pg 665
For simplicity Factor will be abbreviated as F and roman numerals will be numbers
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IV. Hemostasis: Coagulation: Clot formation Intrinsic Pathway • Intrinsic is so called b/c
chemicals being released come directly from the blood.
• Plasma F12 contacts collagen from damaged tissue F12 activation
• Active F12 stimulation F11 activates F9
• Activated F9 joins with F13, platelet phospholipids & Ca2+ to activate F10
• This is the beginning of the common pathway
AP2 Chap. 19: Cardiovascular Syst 36
Figure 19.11 pg 665
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IV. Hemostasis: Coagulation: Clot formation Common Pathway • Extrinsic pathway may influence
the fxn of the intrinsic thus they are not exclusive
• On the platelet surface activated F10, F5, platelet phospholipids, & Ca2+ complex to form Prothrombinase (PT).
• PT converts soluble plasma protein prothrombin into the enz Thrombin (Tn)
• Tn: – Converts soluble plasma protein
fibrinogen into insoluble fibrin wh/ forms the fibrous network of the clot
– Stimulate F13 activation necessary to stabilize the clot
– Also part of + fdbk that stimulates the production of more Tn & platelet activation
AP2 Chap. 19: Cardiovascular Syst 37
Figure 19.11 pg 665
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IV. Hemostasis: Control of clot formation • If clotting got out of control…homeostasis wouldn’t be
maintained and it would lead to death. • Bld has several anticoagulants to prevent unwanted
clotting via inhibition of clotting factors. • Examples:
– Antithrombin • Plasma protein from liver that
slowly inactivates thrombin – Heparin
• w/antithrombin inactivates thrombin
– Prostacyclin • Counteracts prothrombin by
causing vasodilatation & inhibiting coagulation factor release from platelets
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• @ site of injury anticoagulants are outnumbered and thus unable to prevent clotting
• Away from site of injury clotting factors are so dilute that anticoagulants can fxn properly.
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IV. Hemostasis: Clot Retraction & Dissolution
• Clot retraction: formed clot begins condenses into denser compact structure. – Actin & myosin w/in platelets are like smooth
muscle & begin to contract causing retraction – Serum will also be squeezed out of the clot.
• Plasma minus fibrinogen & clotting factors
• Consolidation of the clot pulls edges of damaged bld vessel together helps stop bld flw, reduces infection, & enhances healing.
AP2 Chap. 19: Cardiovascular Syst 39
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IV. Hemostasis: Clot Retraction & Dissolution • Fibrinolysis: process by which a clot is dissolved w/in a
few days of its formation. • Norm bld protein plasminogen is converted into
plasmin: once active it is an enz that hydrolyzes fibrin. • It b/c part of the clot as it is forming. • Activated by: thrombin, F12, tissue plasminogen
activator, urokinase, & lysosomal enz’s released from damaged tissues
AP2 Chap. 19: Cardiovascular Syst 40
Figure 19.12 pg 667
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V. Blood Grouping
ABO Blood Group Rh Blood Group
AP2 Chap. 19: Cardiovascular Syst 41
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V. Blood Grouping • Transfusion: transfer of blood or blood
components from one individual to another • Infusion: introduction of fluid other than blood
(Saline/Glucose sol’n) into the blood. – Used in cases when bld vol needs to be restored to
prevent shock. • Antigen (Ag): Surface protein • Antibody (Ab): protein from the blood plasma
that binds to an antigen and marks that cell for death. – Ab’s are specific to a certain Ag. When Ab’s bind
Ag’s on RBC’s they form molecular bridges attaching multiple RBC’s together. This “clumping” is called Agglutination.
– This complex may also cause hemolysis. 42
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V. Blood Grouping 43
Red Blood Cell
Antigen (Ag)
Antibody (Ab)
In the human there have been 35 blood groups identified, but there are 2 primary groups of antigens that are
displayed on RBC’s
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ABO-Blood Group Variants on Chromosome 9
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Type B Type A Type AB Type O Surface displays
A-Ag’s only Surface displays
B-Ag’s only Surface displays
A & B-Ag’s Codominance
Surface displays No Ags
Rh-Factor Blood Group on Chromosome 1 Rh+
Surface displays Rh-Fator
Rh- Surface displays
No antigens
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Most common blood types that exist
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Type B- Type A- Type AB- Type O-
Type B+ Type A+ Type AB+ Type O+
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Issues w/blood donation & necessity of blood typing: • Ab’s do not develop unless they are exposed to
a foreign Ag. Thus:
46
Frank A-type Blood
Shot Needs a blood transfusion
• Transfused with Type A blood…lives happily every after
• Transfused with Type B blood…his body makes Ab’s against the B-Ag and his blood agglutinates & hemolysis and Frank dies from massive clot formation
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V. Blood Grouping: Ag’s & Ab’s
AP2 Chap. 19: Cardiovascular Syst 47
What would happen to the type AB if an A-Ab was introduced??
Figu
re 1
9.13
pg
668
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Agglutination reaction
AP2 Chap. 19: Cardiovascular Syst 48
Figure 19.14 pg 669
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Hemolytic Disease of a Newborn (HDN)
• Rh- mother gives birth to an Rh+ fetus
• 1st birth: – Everything is okay. Baby is
born with out incident. – During birth mother is exposed
to babies blood and can form antibodies…
• 2nd birth: – Antibodies in the mothers body
attack the baby as a foreign object and can kill it.
• Prevention: – Injection of mother with
RhoGAM soon after each birth. – It takes care of babies blood
before the immune system can respond.
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Your responsibility for the exam! Pg 654: Stem cells & cancer therapy
Pg 658: Effect of carbon monoxide on oxygen transport
Pg 658: Hemoglobin-based Oxygen carriers Pg 663 Clinical importance of activating platelets
Pg 666 How vitamin K helps prevent bleeding Pg 666 Danger of unwanted clots Diagnostic Blood Tests: pg 671-2
Clinical Focus: pg 673-4
AP2 Chap. 19: Cardiovascular Syst 50