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SCIT 1408 Applied Human Anatomy and Physiology II - Blood Ch 17
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Transcript of SCIT 1408 Applied Human Anatomy and Physiology II - Blood Ch 17
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Blood
Figure 17.10
The only fluid tissue
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Blood Composition Blood: a fluid connective tissue composed of
Plasma Formed elements
Erythrocytes (red blood cells, or RBCs) Leukocytes (white blood cells, or WBCs) Platelets
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Blood Composition Hematocrit
Percent of blood volume that is RBCs 47% ± 5% for males 42% ± 5% for females
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Components of Whole Blood
Figure 17.1
Plasma expanders restore blood volume, not O2
Packed cells restore O2, maybe not volume
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Physical Characteristics and Volume Blood is a sticky, opaque fluid with a metallic taste Color varies from scarlet (> O2) to dark red (<O2) The pH of blood is 7.35–7.45 Temperature is 38C Blood accounts for approximately 8% of body
weight Average volume: 5–6 L for males, and 4–5 L for
females
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Functions of Blood Delivers Oxygen to tissues- from lungs Picks up Carbon dioxide from the tissues- to
lungs
Distribution Regulation Protection
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Functions of Blood
1. Distribution of : O2 and nutrients to body cells
Metabolic wastes to the lungs and kidneys for elimination
Hormones from endocrine organs to target organs
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Functions of Blood
2. Regulation of Body temperature by absorbing and distributing
heat Normal pH using buffers Adequate fluid volume in the circulatory system
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Protection Hemostasis
Activating plasma proteins & platelets Clot formation when a vessel is broken
Immune functions Antibodies- B cells Activating complement proteins Activating WBCs to defend the body against
foreign invaders - Tcells
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Blood Plasma Nitrogenous by-products of metabolism—lactic
acid, urea, creatinine Nutrients—glucose, carbohydrates, amino acids
Electrolytes—Na+, K+, Ca2+, Cl–, HCO3–
Respiratory gases—O2 and CO2
Hormones
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Blood Plasma 90% water Proteins are mostly produced by the liver
60% albumin 36% globulins 4% fibrinogen
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Formed Elements Erythrocytes, leukocytes, and platelets make up the
formed elements WBCs - cells RBCs - no nuclei, few organelles; “a sack of hgb” platelets - cell fragments; “thrombocytes”
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Megakaryocyte
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Components of Whole Blood
Figure 17.2
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Erythrocytes (RBCs)
Figure 17.3
No nucleus
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Erythrocytes Structural characteristics contribute to gas transport
Biconcave shape—huge surface area relative to volume
> 97% hemoglobin (not counting water) No mitochondria; ATP production is anaerobic; no
O2 is used in generation of ATP A superb example of complementarity of structure
and function!
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Structure of Hemoglobin
Figure 17.4
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Hemoglobin (Hb) Oxyhemoglobin – oxygen bound to Hgb (or Hb)
Deoxyhemoglobin - oxygen dissociates from hgb & diffuses into tissues (reduced Hgb)
Carbaminohemoglobin – carbon dioxide bound Hgb
PLAY InterActive Physiology ®: Respiratory System: Gas Transport, pages 3–13
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Erythrocyte Function RBCs are dedicated to respiratory gas transport Hemoglobin binds reversibly with oxygen
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Hematopoiesis Hematopoiesis
Red bone marrow of the: Axial skeleton (sternum) and girdles (iliac crest) Epiphyses of the humerus and femur
Hemocytoblasts give rise to all formed elements “Pluripotent cell” or stem cell
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Production of Erythrocytes: Erythropoiesis
Figure 17.5
Bone marrow
Peripheral Circulation
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Regulation of Erythropoiesis
Normal RBC: 4.2-6.1 x 106/ ul whole blood < RBCs = tissue hypoxia > RBCs = > blood viscosity
Erythropoietin (kidneys) – stimulates RBC production RBC production Requires:
iron amino acids B vitamins
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Homeostasis: Normal blood oxygen levels
IncreasesO2-carryingability of blood
Erythropoietinstimulates redbone marrow
Reduces O2 levelsin blood
Kidney (and liver to a smallerextent) releases erythropoietin
Enhancederythropoiesisincreases RBC count
Stimulus: Hypoxia due todecreased RBC count,decreased amount of hemoglobin, or decreased availability of O2
Start
Imbalance
Imbalance
Erythropoietin Mechanism
Figure 17.6
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Hemoglobin
Aminoacids
Globin
Raw materials aremade available inblood for erythrocytesynthesis.
Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis
Food nutrients,including aminoacids, Fe, B12,and folic acidare absorbedfrom intestineand enter blood
Heme
Circulation
Iron storedas ferritin,hemosiderin
Bilirubin
Bilirubin is picked up fromblood by liver, secreted intointestine in bile, metabolizedto stercobilin by bacteriaand excreted in feces
Erythropoietin levelsrise in blood.
Erythropoietin and necessaryraw materials in blood promoteerythropoiesis in red bone marrow.
New erythrocytesenter bloodstream;function about120 days.
Low O2 levels in blood stimulatekidneys to produce erythropoietin.
Aged and damaged redblood cells are engulfed bymacrophages of liver, spleen,and bone marrow; the hemoglobinis broken down.
1
2
3
4
5
6
Figure 17.7
RBC life cycle- (recycle 80-120 days)
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Anemias - < RBC (normocytic) Hemorrhagic anemia Hemolytic anemia Aplastic anemia
Signs/symptoms include fatigue, paleness, shortness of breath, and chills
Erythrocyte Disorders – Types of Anemia
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Iron-deficiency anemia : (microcytic) (from hemorrhagic anemia) < dietary iron Impaired iron absorption
Pernicious anemia : (macrocytic) Deficiency of vitamin B12
Lack of intrinsic factor needed for absorption of B12
Treatment is intramuscular injection of B12; application of Nascobal
Types of Anemia : Decreased Hemoglobin Content
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Types of Anemia: Abnormal Hemoglobin Thalassemias –
defective globin chain gene(s) Many forms Mediterranean decent
Sickle-cell anemia defective globin chain gene with a single aa
substitution This defect causes RBCs to become sickle-shaped
in < oxygen & > oxygen demand situations
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1 2 3 4 5 6 7 146
1 2 3 4 5 6 7 146
(a) Normal erythrocyte has normal hemoglobin amino acid sequence in the beta chain.
(b) Sickled erythrocyte results from a single amino acid change in the beta chain of hemoglobin.
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Polycythemia Polycythemia – excess RBCs that increase blood
viscosity Three main polycythemias are:
Polycythemia vera Secondary polycythemia – test pilots Blood doping – atheletes
RX: phlebotomies
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Leukocytes (WBCs) Normal WBC: 5-10,000/ ul whole blood
< WBC - leukopenia from bone marrow suppression leads to infection never normal
> WBC – leukocytosis; > 11,000/ul From: infection, exercise, stress, leukemia
Diapedesis- leaks from blood into tissues
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Percentages of Leukocytes
Figure 17.9
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Granulocytes All have granules, segmented nuclei, and are
phagocytic
Neutrophils – “segs”; first ones to site of inflammation
Eosinophils Basophils
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(a) Neutrophil; multilobed nucleus
(b) Eosinophil; bilobed nucleus, red cytoplasmic granules
(c) Basophil; bilobed nucleus, purplish-black cytoplasmic granules
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Neutrophils 50-70% total WBC > Neutrophils – bacterial infections Very active in inflammation
diapedesis
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1–4% of WBCs Red-orange granules (acidophilic) > : allergies, parasitic infections
Eosinophils
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0.5% of WBCs purplish-black (basophilic) granules;
Histamine
Called mast cells in tissues
Basophils
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(d) Small lymphocyte; large spherical nucleus
(e) Monocyte; kidney-shaped nucleus
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25-45% WBCs > in viral infections Large, dark-purple, circular nuclei with a thin rim
of blue cytoplasm Are found mostly enmeshed in lymphoid tissue
(some circulate in the blood) T cells and B cells
T cells function in cell mediated immune response B cells produce antibodies in humoral immune
response
Lymphocytes
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4–8% WBC largest leukocytes Macrophages in tissue Phagocytosis, antigen processing or presentation,
inflammation
Monocytes
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Leukocytes
Figure 17.10
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Leukopoiesis- interleukins & (CSFs) Interleukins are numbered (e.g., IL-1, IL-2),
whereas CSFs are named for the WBCs they stimulate (e.g., granulocyte-CSF stimulates granulocytes)
Macrophages and T cells are the most important sources of cytokines – cytotoxic factors
Many hematopoietic hormones are used clinically to stimulate bone marrow
Production of Leukocytes
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(a) (b) (c) (d) (e)
Hemocytoblast
Myeloid stem cell Lymphoid stem cell
Myeloblast MyeloblastMyeloblast Lymphoblast
Stem cells
Committedcells
Promyelocyte PromyelocytePromyelocyte Promonocyte Prolymphocyte
Eosinophilicmyelocyte
Neutrophilicmyelocyte
Basophilicmyelocyte
Eosinophilicband cells
Neutrophilicband cells
Basophilicband cells
Develop-mentalpathway
Eosinophils NeutrophilsBasophils
Granular leukocytes
Plasma cells
Some become
Monocytes Lymphocytes
Macrophages (tissues)
Agranular leukocytesSome become
Figure 17.11
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Leukocytes Disorders: Leukemias Leukemias- WBC cancers
Myelocytic leukemia – myeloblasts Lymphocytic leukemia – lymphocytes Acute leukemia- blast-type cells; children Chronic leukemia – more mature cells; adults
Childhood leukemia has high cure rate
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Megakaryocyte
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Stem cell Developmental pathway
Hemocytoblast Megakaryoblast Promegakaryocyte Megakaryocyte Platelets
Figure 17.12
Genesis of Platelets The stem cell for platelets is the hemocytoblast The sequential developmental pathway is as
shown.
Bone marrow
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Hemostasis “blood stop” – 3 Phases Involved
1. Vascular spasms – immediate vasoconstriction in response to injury
2. Platelet plug formation
3. Coagulation – cascade of rxns ending in fibrin clot
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Platelet Plug Formation Platelets do not stick to each other or to blood vessels Upon damage to blood vessel endothelium platelets:
With the help of von Willebrand factor (VWF) adhere to collagen
Are stimulated by thromboxane A2 Stick to exposed collagen fibers and form a platelet plug Release serotonin and ADP, which attract still more
platelets The platelet plug is limited to the immediate area of injury
by prostacyclin
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A set of reactions in which blood is transformed from a liquid to a gel
Coagulation follows intrinsic and extrinsic pathways The final three steps of this series of reactions are:
Prothrombin activator is formed Prothrombin is converted into thrombin Thrombin catalyzes the joining of fibrinogen
into a fibrin mesh
Coagulation
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Coagulation
Figure 17.13a
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Detailed Events of Coagulation
Figure 17.13b
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Clot Retraction and Repair Clot retracts within 30-60’
Proteins in platelets squeeze serum from clot Repair
Platelet-derived growth factor (PDGF) – repairs vessel wall
Fibroblasts form a connective tissue patch Stimulated by vascular endothelial growth factor
(VEGF), endothelial cells multiply and restore the endothelial lining
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Fibrinolysis & Control of Clot Formation
As soon as clot is formed, a fibrinolytic process begins to:
1. inhibit growth of clot
2. to break down the clot (within 2 days)
tPA- tissue plasminogen activator = clot buster Two mechanisms prevent clot growth
Swift removal of clotting factors Inhibition of activated clotting factors
Hemostasis vs Fibrinolysis
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Unnecessary clotting is prevented by endothelial lining the blood vessels
Platelet adhesion is prevented by: The smooth endothelial lining of blood vessels- no
plaques, rough spots
Heparin and PGI2 secreted by endothelial cells
Vitamin E quinone, a potent anticoagulant
INFLAMMATION may lead to > clots
Factors Preventing Undesirable Clotting
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Hemostasis Disorders:Thromboembolytic Conditions Thrombus – a clot that develops and persists in an
unbroken blood vessel Thrombi can block circulation, resulting in tissue
death Coronary thrombosis – thrombus in blood vessel of
the heart
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Hemostasis Disorders:Thromboembolytic Conditions Embolus – a clot on the move (in blood)
Can be fat, cancer cells, etc.
Thromboembolus- blood clot on the move Pulmonary emboli can impair the ability of the
body to obtain oxygen Cerebral emboli can cause strokes
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Substances used to prevent undesirable clots: Aspirin – inhibits prostaglandin - thromboxane A2
Heparin – an anticoagulant used clinically for pre- and postoperative cardiac care
Warfarin – used for those prone to atrial fibrillation
Prevention of Undesirable Clots
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Disseminated Intravascular Coagulation (DIC): widespread clotting in intact blood vessels
Poor prognosis
Residual blood cannot clot- thrombin tied up in clot Blockage of blood flow and severe bleeding follows Most common in:
Septic shock A complication of pregnancy Incompatible blood transfusions
Hemostasis Disorders
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Thrombocytopenia – platelets < 50,000/ul Petechiae Caused by suppression or destruction of bone
marrow (e.g., malignancy, radiation) Treated with whole blood transfusions, plasma
exchanges
Hemostasis Disorders: Bleeding Disorders
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Liver disease- Can’t make procoagulants Can’t make vitamin K
Gene defects in genes for clotting factors: Hemophilia A - factor VIII Hemophilia B – factor IX Hemophilia C – factor XI (mild)
Hemostasis Disorders: Bleeding Disorders
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Blood Transfusions Whole blood transfusions are used:
When blood loss is substantial In treating thrombocytopenia
Packed red cells (cells with plasma removed) are used to treat anemia
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RBC membranes have glycoprotein antigens on their external surfaces
These antigens are: Unique to the individual Recognized as foreign if transfused into another
individual Promoters of agglutination and are referred to as
agglutinogens Presence or absence of these antigens is used to
classify blood groups
Human Blood Groups
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Humans have 30 varieties of naturally occurring RBC antigens
ABO and Rh antigens are Landsteiner group Other blood groups (M, N, Dufy, Kell, and Lewis)
Blood Groups
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ABO Blood Groups
Table 17.4
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There are eight different Rh agglutinogens, three of which (C, D, and E) are common
Presence of the Rh agglutinogens on RBCs is indicated as Rh+
Anti-Rh antibodies are not spontaneously formed in Rh– individuals
However, if an Rh– individual receives Rh+ blood, anti-Rh antibodies form
A second exposure to Rh+ blood will result in a typical transfusion reaction
Rh Blood Groups
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Hemolytic Disease of the Newborn Erythroblastosis fetalis or HDN: Rh+ antibodies
of a sensitized Rh– mother cross the placenta and attack and destroy the RBCs of an Rh+ baby
Usually first birth ok RhoGAM – blocks antibodies against Rh+ fetus RX- pre-birth transfusions; exchange transfusions
after birth
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Life threatening- mismatched blood is infused Antigens (cells) & antibodies (plasma) agglutinate:
Diminished oxygen-carrying capacity Clumped cells that impede blood flow Ruptured RBCs- release hgb Hgb ppts in kidneys- renal failure
Transfusion Reactions
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Blood type being tested RBC agglutinogens Serum Reaction
Anti-A Anti-B
AB A and B + +
B B – +
A A + –
O None – –
Blood Typing
Unknown cells Known antisera
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SerumAnti-A
RBCs
Anti-BType AB (containsagglutinogens A and B;agglutinates with bothsera)
Blood being tested
Type A (containsagglutinogen A;agglutinates with anti-A)
Type B (containsagglutinogen B;agglutinates with anti-B)
Type O (contains noagglutinogens; does notagglutinate with eitherserum)
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Restoring Fluid Volume Hypovolemic shock Restore fluid volume-Plasma, plasma expanders
Dextran, plasminate, human serum albumin
OR the following may be better Normal saline Electrolyte solution – Ringer’s
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Diagnostic Blood Tests CBC
# RBCs, WBCs, Hgb, Hct, MCV, MCHC Differential
Microscopic examination reveals variations in size and shape of RBCs, indications of anemias
Hct Serum chemistry analysis can provide a
comprehensive picture of one’s general health status in relation to normal values; i.e. blood glucose
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Diagnostic Blood Tests Differential WBC count Prothrombin time and platelet counts assess
hemostasis SMAC, a blood chemistry profile Complete blood count (CBC)
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Developmental Aspects- Hematopoiesis Fetal blood cells – formed in yolk sac, liver, spleen By 7th month- in red bone marrow Fetus – HbF; > affinity for oxygen than adult
hemoglobin
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Developmental Aspects Age-related blood problems result from disorders
of the heart, blood vessels, and the immune system Increased leukemias are thought to be due to the
waning deficiency of the immune system Abnormal thrombus and embolus formation
reflects the progress of atherosclerosis