Ch+14++Blood+S25

Page 1: Copyright Notice

  • Copyright 2022 © McGraw Hill LLC. All rights reserved. No reproduction or distribution without the prior written consent of McGraw Hill LLC.


Page 2: Characteristics of Blood

Blood Overview

  • 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

  • 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)


Page 3: Blood Composition

  • Figure 14.1 illustrates blood composition, showcasing various components.


Page 4: Components of Centrifuged Blood Samples

Centrifugation of Blood Samples

  • 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


Page 5: Clinical Application 14.1 Universal Precautions with Blood

Safety Measures for Healthcare Workers

  • 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


Page 6: Hematopoiesis (Origin of Formed Elements)

Formation of Blood Cells

  • 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


Page 7: Hematopoiesis of Blood Cells

  • Figure 14.3 displays the process of hematopoiesis, outlining how different blood cells are formed.


Page 8: Red Blood Cells (RBCs)

Characteristics and Function

  • 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


Page 9: Red Blood Cell Counts

RBC Count Measurement

  • 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.


Page 10: Red Blood Cell Production and Its Control

Erythropoiesis

  • 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.

Nutritional Requirements for Erythropoiesis

  • 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.


Page 11: Dietary Factors Affecting Red Blood Cell Production

Key Nutrients for RBC Production

  • 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.


Page 12: Types of Anemia

Classification of Anemia

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


Page 13: Figures 14.6 & 14B

Illustrations

  • Figures depict visual examples of Iron Deficiency Anemia and Sickle Cell Disease.


Page 14: Treating Sickle Cell Disease

Sickle Cell Disease Overview

  • 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.

Treatments

  • 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.


Page 15: Death and Destruction of Red Blood Cells

Lifecycle of RBCs

  • 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.


Page 16: Major Events in Red Blood Cell Breakdown

Summary of RBC Breakdown Events

  1. Damaged RBCs squeeze through capillaries.

  2. Macrophages in spleen and liver clear damaged RBCs.

  3. Hemoglobin decomposes into heme and globin components.

  4. Heme splits into iron and biliverdin.

  5. Iron is available for hemoglobin synthesis or stored in the liver as ferritin.

  6. Biliverdin converts into bilirubin.

  7. Biliverdin and bilirubin enter bile as pigments.

  8. Globin metabolizes into amino acids by macrophages or returns to plasma.


Page 17: Life Cycle of a Red Blood Cell

  • Figure 14.8 illustrates the life cycle of a red blood cell, highlighting stages of growth and destruction.


Page 18: White Blood Cells

Overview of WBCs

  • 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


Page 19: Functions of White Blood Cells

Key Functions of WBCs

  • 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.


Page 20: WBC Response to Bacterial Invasion

  • Figure 14.10 shows the response of white blood cells to bacterial invasion, highlighting their roles in immune defense.


Page 21: Types of WBCs: Neutrophils & Eosinophils

Neutrophils

  • 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.

Eosinophils

  • 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.


Page 22: Types of WBCs: Basophils & Monocytes

Basophils

  • 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.

Monocytes

  • 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.


Page 23: Types of WBCs: Lymphocytes

Lymphocytes Overview

  • 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.


Page 24: White Blood Cell Counts

Measurement of WBCs

  • 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).


Page 25: Abnormal White Blood Cell Numbers

WBC Population Changes and Related Illnesses

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


Page 26: Clinical Application 14.2: Leukemia

Overview of Leukemia

  • 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.


Page 27: Blood Platelets

Overview of Platelets

  • 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.


Page 28: Cellular Components of Blood

Blood Components Overview

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.


Page 29: Blood Plasma

Overview of Plasma

  • 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.


Page 30: Plasma Proteins

Key Plasma Proteins

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 |


Page 31: Gases and Nutrients

Important Blood Components

  • Most significant blood gases:

    • Oxygen

    • Carbon Dioxide

  • Key plasma nutrients include:

    • Amino acids

    • Simple sugars

    • Nucleotides

    • Lipids (fats, phospholipids, cholesterol)


Page 32: Nonprotein Nitrogenous Substances (NPNs)

Overview of NPNs

  • 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).


Page 33: Plasma Electrolytes

Electrolytes in Plasma

  • 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.


Page 34: Hemostasis

Definition and Process

  • 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.


Page 35: Vascular Spasm

Role in Hemostasis

  • 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.


Page 36: Platelet Plug Formation and Coagulation

Mechanisms of Clot Formation

  • 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.


Page 37: Hemostatic Mechanisms

Overview of Mechanisms

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


Page 38: Extrinsic Clotting Mechanism

Process Overview

  • 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.


Page 39: Intrinsic Clotting Mechanism

Activation Process

  • 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.


Page 40: Blood Coagulation Steps

Key Steps in Coagulation

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


Page 41: Blood Clotting Mechanisms

Visual Representation

  • Figure 14.18 illustrates the mechanisms of blood clotting focusing on extrinsic and intrinsic pathways.


Page 42: Clotting Factors

Overview of Clotting Factors

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.


Page 43: Fate of Blood Clots

Post-Clot Formation

  • 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.


Page 44: Abnormal Blood Clot Formation

Definitions and Conditions

  • 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.


Page 45: Normal and Atherosclerotic Arteries

  • Figure 14.19 displays both normal and atherosclerotic arteries highlighting differences in structure and function.


Page 46: Clinical Application 14.3 Deep Vein Thrombosis (DVT)

Overview of DVT

  • 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.


Page 47: Prevention of Coagulation

Mechanisms of Prevention

  • 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.


Page 48: Factors that Inhibit Blood Clot Formation

Key Inhibitors

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


Page 49: Inherited Disorders of Blood

Overview of Disorders

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


Page 50: Blood Groups and Transfusions

Overview of Blood Typing

  • 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.


Page 51: Antigens and Antibodies

Key Definitions

  • 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.


Page 52: ABO Blood Group and Transfusion Compatibility

ABO System Basics

  • 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.


Page 53: ABO Blood Group Frequencies

Population Percentages

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


Page 54: ABO Blood Type Frequencies in the US

Population Distribution

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


Page 55: Antigens and Antibodies of Blood Types

  • Figure 14.20 illustrates antigens and antibodies relevant to the four blood types.


Page 56: Agglutination Visuals

  • Figure 14.21 demonstrates examples of agglutination processes.


Page 57: Universal Donor and Recipient

Blood Type Characteristics

  • 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.


Page 58: Blood Type Compatibility Table

Preferred and Permissible 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−


Page 59: Rh Blood Group

Overview and Implications

  • 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.


Page 60: Rh Incompatibility Illustration

  • Figure 14.22 depicts mechanisms involved in Rh incompatibility scenarios.


Page 61: Important Points in Chapter 14: Outcomes to be Assessed 14.1

Blood Characteristics

  • Discuss general characteristics and major functions of blood.

  • Distinguish between formed elements and the liquid portion of blood.


Page 62: Important Points in Chapter 14: Outcomes to be Assessed 14.2

Blood Cells

  • 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.


Page 63: Important Points in Chapter 14: Outcomes to be Assessed 14.3

Blood Plasma & Hemostasis

  • Describe the function of major plasma components and review hemostatic mechanisms and coagulation steps.

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