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Blood is the only type of connective tissue with a liquid matrix (plasma).
Functions of blood include:
Transporting vital substances
Regulating processes for homeostasis
Maintaining stability of interstitial fluid
Distributing heat
Blood volume varies depending on:
Body size
Changes in fluid concentration
Changes in electrolyte concentration
Amount of adipose tissue
Blood constitutes about 8% of body weight:
Adult females: 4-5 liters
Adult males: 5-6 liters
Blood cells are formed mainly in red bone marrow and are referred to as "formed elements."
Red blood cells (RBCs)
White blood cells (WBCs)
Platelets (cell fragments)
Figure 14.1 illustrates blood composition, showcasing various components.
Purpose: Detect blood abnormalities
Plasma:
Clear, straw-colored fluid matrix of blood
Constitutes about 55% of blood volume
Located at the top of centrifuge tube
Red Blood Cells (RBCs):
Comprise 35-46% in females, 40-54% in males
Found at the bottom of the centrifuge tube
The percentage of RBCs is known as the Hematocrit (HCT)
White Blood Cells (WBCs) and Platelets:
Less than 1% of blood volume, located in the "buffy coat" in the middle of the centrifuge tube
Universal precautions are specific safety measures to prevent transmission of bloodborne pathogens in the workplace, particularly:
HIV
Hepatitis B virus
Later included Hepatitis C virus
Assumption: Any patient may have been exposed to bloodborne pathogens
Estimated that 4-7% of new infectious disease cases are from unsafe injections
Recommendations to prevent infection include:
Use of personal protective equipment (gloves, masks)
Use of fume hoods and sharps containers
Safe workplace practices, such as hand-washing
Hematopoiesis is the formation of blood cells (formed elements include RBCs, WBCs, and platelets).
Blood cells originate in red marrow from hematopoietic stem cells (hemocytoblasts).
Hematopoietic Stem Cells:
Give rise to more stem cells
Differentiate into specialized cells in response to growth factors:
Lymphoid Stem Cells: Give rise to lymphocytes
Myeloid Stem Cells: Give rise to all other types of formed elements, including RBCs, other types of WBCs, and platelets
Figure 14.3 displays the process of hematopoiesis, outlining how different blood cells are formed.
RBCs, also known as erythrocytes, have a biconcave disc shape.
Composed of about one-third hemoglobin, which is responsible for oxygen transport:
Oxyhemoglobin: Hemoglobin bound to O2
Deoxyhemoglobin: Hemoglobin without O2
Unique features:
Lack nuclei and mitochondria
Cannot divide
Produce ATP through glycolysis
RBC count is defined as the number of RBCs in a cubic millimeter or microliter (μL) of blood.
Typical ranges can be used to diagnose diseases and evaluate their progress.
Changes in RBC counts are significant as they reflect variations in the blood's oxygen-carrying capacity.
Erythropoiesis is the formation of RBCs.
Occurs in the red bone marrow and is regulated via a negative feedback mechanism.
Low blood O2 levels lead to kidneys and liver releasing erythropoietin (EPO), stimulating RBC production.
RBC developmental stages:
Hemocytoblast → erythroblast → reticulocyte → erythrocyte
Average life span of RBCs is 120 days.
Vitamin B12 and folic acid: Essential for DNA synthesis and growth/division of cells.
Iron: Necessary for hemoglobin synthesis.
Anemia: Condition with reduced oxygen-carrying capacity, stemming from insufficiency of RBCs or hemoglobin.
Vitamin B12: Absorbed in the small intestine; essential for DNA synthesis.
Iron: Absorbed from the small intestine; reused during red blood cell destruction.
Folic Acid: Absorbed from the small intestine; crucial for DNA synthesis.
Primary Cause | Due to | Results in |
---|---|---|
Decreased RBC number | Hemorrhage | Hemorrhagic anemia |
Bacterial infections | Destruction of RBCs due to transfusion incompatibility | Hemolytic anemia |
Deficiency of intrinsic factor | Inadequate vitamin B12 absorption | Pernicious anemia |
Destruction of bone marrow | Medications, cancer, viruses, poisons | Aplastic anemia |
Decreased hemoglobin concentration | Dietary malnourishment, heavy menstruation, persistent ulcers | Iron-deficiency anemia |
Abnormal hemoglobin | Defective gene structure | Sickle cell anemia |
Deficient hemoglobin; RBCs are short-lived | Thalassemia |
Figures depict visual examples of Iron Deficiency Anemia and Sickle Cell Disease.
Caused by a mutation in a single DNA base that codes for hemoglobin.
The mutation results in abnormal hemoglobin structure leading to sticky RBCs that deform into sickle shapes, blocking blood vessels.
Consequences include:
Oxygen deficiency leading to increased sickling, blockages, and severe pain.
Shortened lifespan of RBCs, resulting in anemia and extreme fatigue.
Infants diagnosed at birth receive antibiotics for infection protection in the spleen.
Hydroxyurea increases fetal hemoglobin production, which is more effective at binding oxygen and reduces sickling.
Bone marrow or umbilical cord stem cell transplants can cure the disease, but carry slight risk of death.
Experimental genome mutation corrections and stem cell infusions show promise.
RBCs lose elasticity after months of deforming through narrow capillaries, becoming fragile.
Worn-out RBCs are removed by the spleen or liver:
Macrophages phagocytize ruptured RBCs.
Hemoglobin decomposes into:
Globin chains with heme groups.
Heme groups break down into iron and biliverdin.
Iron is redeployed to red bone marrow via transferrin.
Biliverdin synthesizes into bilirubin.
Biliverdin and bilirubin are secreted as bile pigments.
Globin chains are broken down into amino acids.
Damaged RBCs squeeze through capillaries.
Macrophages in spleen and liver clear damaged RBCs.
Hemoglobin decomposes into heme and globin components.
Heme splits into iron and biliverdin.
Iron is available for hemoglobin synthesis or stored in the liver as ferritin.
Biliverdin converts into bilirubin.
Biliverdin and bilirubin enter bile as pigments.
Globin metabolizes into amino acids by macrophages or returns to plasma.
Figure 14.8 illustrates the life cycle of a red blood cell, highlighting stages of growth and destruction.
WBCs (leukocytes) protect against diseases and have limited lifespans, necessitating continual replacement.
Produced in red bone marrow regulated by hormones like interleukins and colony-stimulating factors.
Types of WBCs (5 in total, divided into categories):
Granulocytes:
Neutrophils
Eosinophils
Basophils
Agranulocytes:
Lymphocytes
Monocytes
Diapedesis: Ability to move between capillary walls to migrate toward infection sites.
Cellular Adherence Molecules: Direct leukocytes to injury locations.
Phagocytosis: Process of engulfing and digesting pathogens; neutrophils and monocytes are major phagocytes.
Inflammatory Response: Restricted spread of infection, promoted by basophils which secrete heparin and histamine.
Positive Chemotaxis: Attraction of WBCs to infection sites through signals from damaged cells.
Figure 14.10 shows the response of white blood cells to bacterial invasion, highlighting their roles in immune defense.
Granulocytes with small light purple granules.
Lobed nucleus comprised of 2 to 5 sections.
First responders to infection sites and strong phagocytes.
Comprise 54-70% of leukocytes; elevated counts signal bacterial infections.
Granulocytes with coarse granules that stain deep red.
Bilobed nucleus shape.
Involved in moderate allergic reactions and defending against parasitic infections.
Make up 1-3% of leukocytes; elevated counts indicate parasitic infestations and allergies.
Granulocytes with large, deep blue-stained granules that obscure nuclei.
Release histamine for inflammation and heparin to prevent clotting.
Comprise less than 1% of leukocytes.
Largest WBCs, characterized by diverse shaped nuclei.
Agranulocytes that leave bloodstream as macrophages.
Comprise 3-9% of leukocytes and can live for weeks to months.
Important phagocytizers of bacteria, debris, and dead cells.
Slightly larger than RBCs with a large nucleus surrounded by a thin cytoplasm layer.
Important in immunity;
T cells: Attack pathogens and tumor cells.
B cells: Produce antibodies.
Comprise 25-33% of leukocytes, with some living for years.
Procedures to assess WBC counts:
Leukocytosis: Increased WBC count, often due to infections or vigorous exercise.
Leukopenia: Decreased WBC count linked to diseases like AIDS and flu.
Differential WBC Count: Lists percentages of each WBC type; can indicate particular diseases (e.g., increased neutrophils in infections).
White Blood Cell Population Change | Possible Illness |
---|---|
Elevated lymphocytes | Hairy cell leukemia, whooping cough, mononucleosis |
Elevated eosinophils | Tapeworm infestation, allergic reactions |
Elevated monocytes | Typhoid fever, malaria, tuberculosis |
Elevated neutrophils | Bacterial infections |
Low helper T cells | AIDS |
Leukemia is a form of cancer affecting white blood cells.
Types of classification include:
Acute: Rapid onset and progression of symptoms.
Chronic: Slow start, often goes undetected for prolonged periods.
Further classified as:
Lymphoid: Cancer of lymphocyte production in lymph nodes.
Myeloid: Cancer affecting granulocytes in red bone marrow.
Symptoms include high WBC counts, fatigue, headaches, and increased bleeding and infection risks.
Treatment options involve traditional therapies (chemotherapy), enzyme-targeting drugs, and bone marrow or stem cell transplants.
Platelets (thrombocytes) are cellular fragments derived from megakaryocytes in red bone marrow.
Produced in response to thrombopoietin.
Characteristics:
Lack a nucleus and are smaller than RBCs.
Normal count ranges from 150,000 to 400,000/µL of blood.
Thrombocytosis: Exceedingly high platelet count.
Thrombocytopenia: Undernormal platelet count.
Function in hemostasis by adhering to damaged vessels and releasing serotonin to promote vascular contraction.
Component | Description | Number Present | Function |
---|---|---|---|
Red blood cell (erythrocyte) | Biconcave disc, lacks nucleus; one-third hemoglobin. | 4,700,000 to 6,100,000 (male); 4,200,000 to 5,400,000 (female) | Transports oxygen and carbon dioxide. |
White blood cell (leukocyte) | Varies; numerous types. | 3,500 to 10,500 | Destroys pathogens and removes worn cells. |
Granulocytes | Double the size of RBCs; containing granules. | Various functions including phagocytosis. | |
Neutrophil | Features lobed nucleus; light purple granules. | 50% to 70% of WBCs present | Phagocytizes small particles. |
Eosinophil | Bilobed nucleus; red-stained granules. | 1% to 4% of WBCs present | Defends against parasitic infections and moderates allergies. |
Basophil | Lobed nucleus; deep blue granules. | Less than 1% of WBCs present | Releases heparin and histamine. |
Agranulocytes | Lack granules; includes monocytes and lymphocytes. | Varies: phagocytes, contributes to immunity. | |
Monocyte | Larger than RBC; varies in nucleus shape. | 3% to 9% of WBCs present | Phagocytizes large particles. |
Lymphocyte | Slightly larger than RBC; large nucleus. | 25% to 33% of WBCs present | Provides immunity via B and T cells. |
Platelet (thrombocyte) | Cellular fragment. | 150,000 to 400,000 per microliter | Helps control blood loss from injured vessels. |
Blood plasma is the clear, straw-colored liquid portion, comprising 55% of blood volume.
92% composed of water.
Functions include:
Transportation of nutrients, gases, hormones, and vitamins.
Regulation of fluid and electrolyte balance and maintenance of pH.
Protein | Percentage of Total | Origin | Function |
---|---|---|---|
Albumins | 60% | Liver | Help maintain osmotic pressure |
Globulins | 36% |
Alpha.globulins: Liver, transport lipids | |
Beta.globulins: Liver, transport lipids | |
Gamma.globulins: Lymphatic tissue, immunity | | | Fibrinogen | 4% | Liver | Key role in blood coagulation |
Most significant blood gases:
Oxygen
Carbon Dioxide
Key plasma nutrients include:
Amino acids
Simple sugars
Nucleotides
Lipids (fats, phospholipids, cholesterol)
NPNs contain nitrogen but are not proteins. They include:
Urea: Byproduct of protein breakdown; 50% of NPNs.
Uric acid: Byproduct of nucleic acid metabolism.
Amino acids: From protein digestion.
Creatine: Energy storage; regenerates ATP in muscles.
Creatinine: Product of creatine metabolism.
BUN: Blood urea nitrogen; a measure of kidney health (high levels indicate poor kidney function).
Plasma contains electrolytes, which are ions that can conduct electricity, absorbed from the intestines or generated by cellular metabolism, including:
Sodium
Potassium
Calcium
Magnesium
Chloride
Bicarbonate
Phosphate
Sulfate
Sodium and chloride are predominant electrolytes.
Hemostasis is the stoppage of bleeding.
Mechanisms to limit or prevent blood loss include:
Vascular spasm
Platelet plug formation
Blood coagulation
These mechanisms are particularly effective for small blood vessel injuries.
Stimulated by small blood vessel injury.
Smooth muscle contracts rapidly, thereby slowing blood loss and possibly closing the vessel completely.
Triggered by stimulation of the blood vessel wall and pain receptor reflexes.
Lasts a few minutes but continues to affect for around 30 minutes, allowing the formation of a platelet plug.
Serotonin released from platelets enhances vasoconstriction.
Platelet Plug Formation: Initiated by platelet exposure to collagen; platelets adhere to rough surfaces, creating a plug.
Blood Coagulation: Main mechanism occurring in 5 to 15 minutes through a cascade of reactions to form a clot.
Coagulation methods:
Extrinsic mechanism
Intrinsic mechanism
Vitamin K is essential for many clotting factors.
Coagulation depends on a balance between procoagulants and anticoagulants, conspicuously culminating in the conversion of soluble fibrinogen into insoluble fibrin threads that entrap blood cells.
Mechanism | Stimulus | Effect |
---|---|---|
Vascular spasm | Direct stimulus to vessel walls; platelets release serotonin | Smooth muscle contracts reflexively, prolonging vasoconstriction |
Platelet plug formation | Exposure of platelets to collagen | Platelets adhere to rough surfaces, forming a plug |
Blood coagulation | Cellular damage and foreign surface contact activate factors | Blood clot formation from a series of reactions, converting fibrinogen into fibrin |
Triggered by blood contacting tissues outside the blood vessels.
Damaged tissues release tissue thromboplastin (factor III).
A cascade of sequential clotting factors is activated.
Thrombin converts fibrinogen to insoluble fibrin threads that aggregate and trap blood cells, forming a clot.
Represents a positive feedback mechanism, promoting further clotting.
Initiated without tissue damage when blood touches a foreign substance (e.g., collagen).
Triggered by the Hageman factor XII (present in blood).
Similar sequence of factor activation leading to the formation of a fibrin mesh to create a blood clot.
Steps | Extrinsic Clotting Mechanism | Intrinsic Clotting Mechanism |
---|---|---|
Trigger | Damage to vessel or tissue | Blood contacts foreign surface |
Initiation | Tissue thromboplastin | Hageman factor |
Series of reactions involving clotting factors | Lead to the production of prothrombin activator | Same pathway |
Conversion | Prothrombin activator converts prothrombin to thrombin | Same conversion process |
Conversion of fibrinogen | Fibrin threads form from fibrinogen | Same conversion process |
Figure 14.18 illustrates the mechanisms of blood clotting focusing on extrinsic and intrinsic pathways.
Component | Source | Mechanism(s) |
---|---|---|
I (fibrinogen) | Synthesized in liver | Extrinsic and intrinsic |
II (prothrombin) | Synthesized in liver; requires vitamin K | Extrinsic and intrinsic |
III (tissue thromboplastin) | Damaged tissue | Extrinsic |
IV (calcium ions) | Plasma electrolyte | Extrinsic and intrinsic |
V (proaccelerin) | Synthesized in liver; released by platelets | Extrinsic and intrinsic |
VII (prothrombin conversion accelerator) | Synthesized in liver; requires vitamin K | Extrinsic |
VIII (antihemophilic factor) | Released by platelets and endothelial cells | Intrinsic |
IX (plasma thromboplastin component) | Synthesized in liver; requires vitamin K | Intrinsic |
X (Stuart-Prower factor) | Synthesized in liver; requires vitamin K | Extrinsic and intrinsic |
XI (plasma thromboplastin antecedent) | Synthesized in liver | Intrinsic |
XII (Hageman factor) | Synthesized in liver | Intrinsic |
XIII (fibrin-stabilizing factor) | Synthesized in liver; released by platelets | Extrinsic and intrinsic |
Note: Factor VI is not an actual clotting factor but a combination of activated factors V and X. |
Clots retract to close the broken blood vessel and squeeze serum from the clot (serum = plasma minus fibrinogen and clotting factors).
Platelet-derived growth factor stimulates repair of blood vessel wall.
Plasmin digests fibrin threads, dissolving the blood clot.
Thrombus: An abnormal clot forming in a vessel.
Embolus: A clot traveling through blood vessels.
Thrombosis: Formation of clots in vital organ supplying vessels.
Infarction: Tissue death due to blocked blood vessels.
Embolism: A clot that lodges in an organ, such as in pulmonary embolism.
Atherosclerosis: Fat accumulation in arterial linings may lead to abnormal clot formation.
Figure 14.19 displays both normal and atherosclerotic arteries highlighting differences in structure and function.
DVT occurs due to pooling of stagnant blood, particularly in deep veins of the legs or pelvis.
Complications include pulmonary embolism from clots traveling to the lungs.
Symptoms include deep muscle pain, cramping, and swelling.
Preventive measures include anticoagulant medications, compression stockings, and movement during long periods of immobility.
Normal blood vessel linings discourage platelet accumulation.
Healthy endothelial cells generate prostacyclin (PGI2) to prevent platelet adhesion.
Fibrin adsorbs thrombin, limiting the clotting reaction spread.
Antithrombin in plasma inactivates thrombin by binding to it and blocking its effect.
Basophils and mast cells secrete heparin to inhibit coagulation.
Factor | Action |
---|---|
Smooth lining of blood vessel | Prevents intrinsic clotting mechanism activation |
Prostacyclin | Inhibits platelet adherence to blood vessel wall |
Fibrin threads | Adsorb thrombin |
Antithrombin in plasma | Interferes with thrombin action |
Heparin from mast cells and basophils | Inhibits prothrombin activator formation |
Disorder | Abnormality |
---|---|
Chronic granulomatous disease | Granulocytes can't produce superoxide to kill bacteria |
Erythrocytosis | Reticulocytes have extra EPO receptors |
Factor V Leiden | Increases risk of abnormal clotting |
Hemophilia (various types) | Lack of specific clotting factors causing bleeding |
Hereditary hemochromatosis | Excess iron absorption; deposits in organs |
Porphyria variegata | Enzyme deficiency causing varied symptoms |
Sickle cell disease | Abnormal hemoglobin crystallizes, causing RBC blockage and anemia |
Von Willebrand disease | Lack of clotting factor, leading to bleeding; less severe than hemophilia |
The discovery of the ABO blood antigen gene in 1910 clarified blood type incompatibilities.
Blood types are determined by proteins (antigens) on red blood cell surfaces, determined by the underlying genetics.
Safe transfusions necessitate knowledge of donor and recipient blood types and cross-matching for agglutination.
Antigens: Molecules that evoke an immune response; foreign antigens trigger antibody production.
Antibodies: Blood plasma proteins that target specific antigens.
Agglutination: RBC clumping from antibody-antigen interactions, typically from transfusion reactions that can cause adverse symptoms like anxiety, breathing difficulties, and pain.
The ABO blood group is characterized by the presence or absence of Antigen A and Antigen B.
Antigens are carbohydrates attached to glycolipids in red blood cell membranes.
Recipients must not have antibodies in their plasma against the donor's RBC antigens to avoid agglutination, with specific examples for blood type compatibility outlined.
Blood Type | Antigen | Antibody |
---|---|---|
A | A | Anti-B |
B | B | Anti-A |
AB | A and B | Neither anti-A nor anti-B |
O | Neither | Both anti-A and anti-B |
Population | Type O | Type A | Type B | Type AB |
---|---|---|---|---|
Caucasian | 45 | 40 | 11 | 4 |
African American | 49 | 27 | 20 | 4 |
American Indian | 79 | 16 | 4 | 1 |
Hispanic | 63 | 14 | 20 | 3 |
Chinese American | 42 | 27 | 25 | 6 |
Japanese American | 31 | 38 | 21 | 10 |
Korean American | 32 | 28 | 30 | 10 |
Figure 14.20 illustrates antigens and antibodies relevant to the four blood types.
Figure 14.21 demonstrates examples of agglutination processes.
Type O: Universal donor; lacks A and B antigens, making it safe for any blood type recipient.
Transfused slowly to avoid complications even with reactions to antibodies.
Type AB: Universal recipient; contains no anti-A or anti-B antibodies allowing for acceptance of all donor blood types.
Blood Type of Recipient | Preferred Blood Type of Donor | Permissible Blood Types of Donor |
---|---|---|
A− | A− | A−, O− |
A+ | A+ | A−, O−, O+ |
B− | B− | B−, O− |
B+ | B+ | B−, O−, O+ |
AB− | AB− | A−, B−, O− |
AB+ | AB+ | AB−, A−, A+, B−, B+, O−, O+ |
O− | O− | None |
O+ | O+ | O− |
Named after the Rhesus monkey, the Rh blood group contains various antigens, with antigen D being the most significant.
Rh positive indicates the presence of the D antigen; Rh negative indicates absence.
Anti-Rh antibodies form solely in Rh-negative individuals in response to Rh-positive RBCs, creating sensitization issues on subsequent transfusions.
Erythroblastosis fetalis or hemolytic disease in newborns occurs when an Rh-positive fetus is carried by an Rh-negative mother, leading to potential complications.
Figure 14.22 depicts mechanisms involved in Rh incompatibility scenarios.
Discuss general characteristics and major functions of blood.
Distinguish between formed elements and the liquid portion of blood.
Describe origin and significance of blood cells.
Explain RBC counts in disease diagnosis and RBC life cycle.
Summarize regulation of RBC production and types of WBC functions.
Describe the function of major plasma components and review hemostatic mechanisms and coagulation steps.