Ch. 17 Blood Slides mostly © Marieb & Hoehn 9 th ed. Other slides by WCR

Ch. 17Blood

Slides mostly © Marieb & Hoehn 9th ed.Other slides by WCR

© 2013 Pearson Education, Inc.

Blood Composition

• Blood– Fluid connective tissue– Plasma – non-living fluid matrix– Formed elements – living blood "cells"

suspended in plasma• Erythrocytes (red blood cells, or RBCs) • Leukocytes (white blood cells, or WBCs) • Platelets


Blood Composition

• Spun tube of blood yields three layers– Plasma on top (~55%)– Erythrocytes on bottom (~45%)– WBCs and platelets in Buffy coat (< 1%)

• Hematocrit– Percent of blood volume that is RBCs – 47% ± 5% for males; 42% ± 5% for females


Figure 17.1 The major components of whole blood.

Withdraw bloodand place in tube.

Centrifuge theblood sample.

Plasma• 55% of whole blood• Least dense component

Buffy coat• Leukocytes and platelets• <1% of whole bloodErythrocytes

• 45% of whole blood (hematocrit)• Most dense component

Formedelements

Slide 1

21


Physical Characteristics and Volume

• Sticky, opaque fluid with metallic taste

• Color varies with O2 content

– High O2 - scarlet; Low O2 - dark red

• pH 7.35–7.45

• ~8% of body weight

• Average volume– 5–6 L for males; 4–5 L for females


Functions of Blood

• Functions include– Distributing substances– Regulating blood levels of substances– Protection


Distribution Functions

• Delivering O2 and nutrients to body cells

• Transporting metabolic wastes to lungs and kidneys for elimination

• Transporting hormones from endocrine organs to target organs


Regulation Functions

• Maintaining body temperature by absorbing and distributing heat

• Maintaining normal pH using buffers; alkaline reserve of bicarbonate ions

• Maintaining adequate fluid volume in circulatory system


Protection Functions

• Preventing infection – Antibodies– Complement proteins– WBCs


Blood Plasma• 90% water

• Over 100 dissolved solutes– Nutrients, gases, hormones, wastes, proteins,

inorganic ions– Electrolytes most abundant solutes by

number– Plasma proteins most abundant solutes by

mass• Remain in blood; not taken up by cells• Proteins produced mostly by liver• 60% albumin; 36% globulins; 4% fibrinogen


Albumin

• 60% of plasma protein

• Functions– Substance carrier– Blood buffer– Major contributor of plasma osmotic pressure


Formed Elements

• Only WBCs are complete cells

• RBCs have no nuclei or other organelles

• Platelets are cell fragments

• Most formed elements survive in bloodstream only few days

• Most blood cells originate in bone marrow and do not divide


Figure 17.2 Photomicrograph of a human blood smear stained with Wright's stain.

Platelets Erythrocytes Monocyte

Neutrophils Lymphocyte


Erythrocytes

• Biconcave discs, anucleate, essentially no organelles

• Diameters larger than some capillaries

• Filled with hemoglobin (Hb) for gas transport

• Contain plasma membrane protein spectrin and other proteins– Spectrin provides flexibility to change shape

• Major factor contributing to blood viscosity


2.5 µm

7.5 µm

Top view

Side view (cut)

Figure 17.3 Structure of erythrocytes (red blood cells).


Erythrocytes

• Structural characteristics contribute to gas transport – Biconcave shape—huge surface area relative

to volume– >97% hemoglobin (not counting water)– No mitochondria; ATP production anaerobic;

do not consume O2 they transport

• Superb example of complementarity of structure and function


Erythrocyte Function

• RBCs dedicated to respiratory gas transport

• Hemoglobin binds reversibly with oxygen

• Normal values – Males - 13–18g/100ml; Females - 12–16

g/100ml


Hemoglobin Structure

• Globin composed of 4 polypeptide chains– Two alpha and two beta chains

• Heme pigment bonded to each globin chain– Gives blood red color

• Heme's central iron atom binds one O2

• Each Hb molecule can transport four O2

• Each RBC contains 250 million Hb molecules


Figure 17.4 Structure of hemoglobin.

Globin chains

Hemegroup

Globin chains

Hemoglobin consists of globin (two alpha and two betapolypeptide chains) and four heme groups.

Iron-containing heme pigment.


Hematopoiesis

• Blood cell formation in red bone marrow– Composed of reticular connective tissue and

blood sinusoids

• In adult, found in axial skeleton, girdles, and proximal epiphyses of humerus and femur


Figure 17.5 Erythropoiesis: formation of red blood cells.

Stem cell Committed cell Developmental pathway

Phase 1Ribosome synthesis

Phase 2Hemoglobin accumulation

Phase 3Ejection of nucleus

Hematopoietic stemcell (hemocytoblast) Proerythroblast

Basophilicerythroblast

Polychromaticerythroblast

Orthochromaticerythroblast Reticulocyte Erythrocyte


Regulation of Erythropoiesis

• Too few RBCs leads to tissue hypoxia

• Too many RBCs increases blood viscosity

• > 2 million RBCs made per second

• Balance between RBC production and destruction depends on– Hormonal controls – Adequate supplies of iron, amino acids, and B

vitamins


Hormonal Control of Erythropoiesis

• Hormone Erythropoietin (EPO)– Direct stimulus for erythropoiesis – Always small amount in blood to maintain

basal rate• High RBC or O2 levels depress production

– Released by kidneys (some from liver) in response to hypoxia

• Dialysis patients have low RBC counts


Stimulus: Hypoxia(inadequate O2

delivery) due to O2-carryingability of bloodrises.

Enhancederythropoiesisincreases RBC count. Kidney (and liver to

a smaller extent)releases erythropoietin. Erythropoietin

stimulates redbone marrow.

Figure 17.6 Erythropoietin mechanism for regulating erythropoiesis.

Homeostasis: Normal blood oxygen levels

IMBALANCE

IMBALANCE• Decreased RBC count• Decreased amount of hemoglobin• Decreased availability of O2

Slide 1

1

2

3

4

5


Dietary Requirements for Erythropoiesis

• Nutrients—amino acids, lipids, and carbohydrates

• Iron– Available from diet– 65% in Hb; rest in liver, spleen, and bone marrow– Free iron ions toxic

• Stored in cells as ferritin and hemosiderin• Transported in blood bound to protein transferrin

• Vitamin B12 and folic acid necessary for DNA synthesis for rapidly dividing cells (developing RBCs)


Fate and Destruction of Erythrocytes

• Life span: 100–120 days– No protein synthesis, growth, division

• Old RBCs become fragile; Hb begins to degenerate

• Get trapped in smaller circulatory channels especially in spleen

• Macrophages engulf dying RBCs in spleen


Fate and Destruction of Erythrocytes

• Heme and globin are separated– Iron salvaged for reuse– Heme degraded to yellow pigment bilirubin– Liver secretes bilirubin (in bile) into intestines

• Degraded to pigment urobilinogen• Pigment leaves body in feces as stercobilin

– Globin metabolized into amino acids• Released into circulation


Raw materials aremade available in bloodfor erythrocyte synthesis.

Aged and damagedred blood cells are engulfedby macrophages of spleen,liver, and bone marrow; thehemoglobin is broken down.

New erythrocytesenter bloodstream;function about 120days.

Erythropoietin and necessaryraw materials in blood promoteerythropoiesis in red bone marrow.

Erythropoietin levels rise in blood.

Low O2 levels in blood stimulatekidneys to produce erythropoietin.

Figure 17.7 Life cycle of red blood cells.

Hemoglobin

Heme Globin

Bilirubin ispicked upby the liver.

Iron is storedas ferritin orhemosiderin.

Aminoacids

Iron is bound to transferrinand released to bloodfrom liver as neededfor erythropoiesis.

Bilirubin is secreted intointestine in bile whereit is metabolized tostercobilin by bacteria.

Circulation

Food nutrients(amino acids, Fe,B12, and folic acid)are absorbed fromintestine and enterblood.

Stercobilinis excretedin feces.

Slide 11

2

3

4

5

6



New erythrocytesenter bloodstream;function about 120days.

Slide 5

Erythropoietin and necessaryraw materials in blood promoteerythropoiesis in red bone marrow.

Erythropoietin levels rise in blood.

Low O2 levels in blood stimulatekidneys to produce erythropoietin.1

2

3

4


Raw materials aremade available in bloodfor erythrocyte synthesis.

Aged and damagedred blood cells are engulfedby macrophages of spleen,liver, and bone marrow; thehemoglobin is broken down.


Hemoglobin

Heme Globin

Bilirubin ispicked upby the liver.

Iron is storedas ferritin orhemosiderin.

Aminoacids

Iron is bound to transferrinand released to bloodfrom liver as neededfor erythropoiesis.

Bilirubin is secreted intointestine in bile whereit is metabolized tostercobilin by bacteria.

Circulation

Food nutrients(amino acids, Fe,B12, and folic acid)are absorbed fromintestine and enterblood.

Stercobilinis excretedin feces.

Slide 75

6


Erythrocyte Disorders

• Anemia– Blood has abnormally low O2-carrying

capacity– Sign rather than disease itself

– Blood O2 levels cannot support normal metabolism

– Accompanied by fatigue, pallor, shortness of breath, and chills


Causes of Anemia

• Three groups– Blood loss– Low RBC production– High RBC destruction


Causes of Anemia: Blood Loss

• Hemorrhagic anemia– Blood loss rapid (e.g., stab wound)– Treated by blood replacement

• Chronic hemorrhagic anemia– Slight but persistent blood loss

• Hemorrhoids, bleeding ulcer

– Primary problem treated


Causes of Anemia: Low RBC Production

• Iron-deficiency anemia– Caused by hemorrhagic anemia, low iron

intake, or impaired absorption– Microcytic, hypochromic RBCs– Iron supplements to treat



• Pernicious anemia– Autoimmune disease - destroys stomach

mucosa

– Lack of intrinsic factor needed to absorb B12

• Deficiency of vitamin B12

– RBCs cannot divide macrocytes

– Treated with B12 injections or nasal gel

– Also caused by low dietary B12 (vegetarians)



• Renal anemia– Lack of EPO– Often accompanies renal disease– Treated with synthetic EPO



• Aplastic anemia– Destruction or inhibition of red marrow by

drugs, chemicals, radiation, viruses– Usually cause unknown– All cell lines affected

• Anemia; clotting and immunity defects

– Treated short-term with transfusions; long-term with transplanted stem cells


Causes of Anemia: High RBC Destruction

• Hemolytic anemias– Premature RBC lysis– Caused by

• Hb abnormalities• Incompatible transfusions• Infections


Causes of Anemia: High RBC Destruction

• Sickle-cell anemia– Hemoglobin S

• One amino acid wrong in a globin beta chain

– RBCs crescent shaped when unload O2 or blood O2 low

– RBCs rupture easily and block small vessels• Poor O2 delivery; pain


Figure 17.8 Sickle-cell anemia.

Val His Leu Thr Pro Glu Glu …

1 2 3 4 5 6 7 146

Normal erythrocyte has normalhemoglobin amino acid sequence in the beta chain.

Val His Leu Thr Pro Val Glu …

1 2 3 4 5 6 7 146

Sickled erythrocyte results from asingle amino acid change in thebeta chain of hemoglobin.


Leukocytes

• Make up <1% of total blood volume– 4,800 – 10,800 WBCs/μl blood

• Function in defense against disease– Can leave capillaries via diapedesis– Move through tissue spaces by ameboid

motion and positive chemotaxis

• Leukocytosis: WBC count over 11,000/mm3

– Normal response to infection


Leukocytes: Two Categories

• Granulocytes – Visible cytoplasmic granules– Neutrophils, eosinophils, basophils

• Agranulocytes – No visible cytoplasmic granules– Lymphocytes, monocytes

• Decreasing abundance in blood– Never let monkeys eat bananas


Figure 17.9 Types and relative percentages of leukocytes in normal blood.

Formedelements

(All total 4800–10,800/ µl)

GranulocytesNeutrophils (50–70%)

Eosinophils (2–4%)

Basophils (0.5–1%)

AgranulocytesLymphocytes (25–45%)

Monocytes (3–8%)

Platelets

Leukocytes

Erythrocytes

(not drawnto scale)

DifferentialWBC count


Granulocytes

• Granulocytes– Larger and shorter-lived than RBCs– Lobed nuclei– Cytoplasmic granules stain specifically with

Wright's stain– All phagocytic to some degree


Neutrophils

• Most numerous WBCs

• Also called Polymorphonuclear leukocytes (PMNs or polys)

• Granules stain lilac; contain hydrolytic enzymes or defensins

• 3-6 lobes in nucleus; twice size of RBCs

• Very phagocytic—"bacteria slayers"


Eosinophils

• Red-staining granules

• Bilobed nucleus

• Granules lysosome-like– Release enzymes to digest parasitic worms

• Role in allergies and asthma

• Role in modulating immune response


Basophils

• Rarest WBCs

• Nucleus deep purple with 1-2 constrictions

• Large, purplish-black (basophilic) granules contain histamine– Histamine: inflammatory chemical that acts as

vasodilator to attract WBCs to inflamed sites

• Are functionally similar to mast cells


Figure 17.10a Leukocytes.

Granulocytes

Neutrophil: Multilobed nucleus, pale red and blue cytoplasmic granules


Figure 17.10b Leukocytes.

Granulocytes

Eosinophil: Bilobed nucleus, red cytoplasmic granules


Figure 17.10c Leukocytes.

Granulocytes

Basophil: Bilobed nucleus, purplish-black cytoplasmic granules


Agranulocytes

• Agranulocytes– Lack visible cytoplasmic granules– Have spherical or kidney-shaped nuclei


Lymphocytes

• Second most numerous WBC

• Large, dark-purple, circular nuclei with thin rim of blue cytoplasm

• Mostly in lymphoid tissue (e.g., lymph nodes, spleen); few circulate in blood

• Crucial to immunity


Monocytes

• Largest leukocytes

• Abundant pale-blue cytoplasm

• Dark purple-staining, U- or kidney-shaped nuclei


Monocytes

• Leave circulation, enter tissues, and differentiate into macrophages– Actively phagocytic cells; crucial against

viruses, intracellular bacterial parasites, and chronic infections

• Activate lymphocytes to mount an immune response


Agranulocytes

Lymphocyte (small):Large sphericalnucleus, thin rim ofpale blue cytoplasm

Figure 17.10d Leukocytes.


Agranulocytes

Monocyte: Kidney-shaped nucleus, abundant pale blue cytoplasm

Figure 17.10e Leukocytes.


Leukopoiesis

• Production of WBCs– Stimulated by 2 types of chemical

messengers from red bone marrow and mature WBCs

• Interleukins (e.g., IL-3, IL-5)• Colony-stimulating factors (CSFs) named for WBC

type they stimulate (e.g., granulocyte-CSF stimulates granulocytes)


Stem cells

Committedcells

Developmentalpathway

Hematopoietic stem cell(hemocytoblast)

Myeloid stem cell Lymphoid stem cell

Myeloblast Myeloblast Myeloblast Monoblast B lymphocyteprecursor

T lymphocyteprecursor

Promyelocyte Promyelocyte Promyelocyte Promonocyte

Eosinophilicmyelocyte

Basophilicmyelocyte

Neutrophilicmyelocyte

Eosinophilicband cells

Basophilicband cells

Neutrophilicband cells

Granularleukocytes

Agranularleukocytes

Eosinophils Basophils Neutrophils Monocytes B lymphocytes T lymphocytes

Macrophages (tissues) Plasma cells Effector T cells

Some become Some become

(a) (b) (c) (d) (e) (f)

Some become

Figure 17.11 Leukocyte formation.


Platelets• Cytoplasmic fragments of

megakaryocytes• Form temporary platelet plug that helps

seal breaks in blood vessels• Circulating platelets kept inactive and

mobile by nitric oxide (NO) and prostacyclin from endothelial cells lining blood vessels

• Age quickly; degenerate in about 10 days• Formation regulated by thrombopoietin


Figure 17.12 Formation of platelets.

Stem cell Developmental pathway

Hematopoietic stemcell (hemocytoblast)

Megakaryoblast(stage I megakaryocyte)

Megakaryocyte(stage II/III)

Megakaryocyte(stage IV)

Platelets


Table 17.2 Summary of Formed Elements of the Blood (1 of 2)


Table 17.2 Summary of Formed Elements of the Blood (2 of 2)


Hemostasis

• Fast series of reactions for stoppage of bleeding

• Requires clotting factors, and substances released by platelets and injured tissues

• Three steps1. Vascular spasm

2. Platelet plug formation

3. Coagulation (blood clotting)


Hemostasis: Vascular Spasm

• Vasoconstriction of damaged blood vessel

• Triggers– Direct injury to vascular smooth muscle– Chemicals released by endothelial cells and

platelets – Pain reflexes

• Most effective in smaller blood vessels


Hemostasis: Platelet Plug Formation

• Positive feedback cycle• Damaged endothelium exposes collagen

fibers– Platelets stick to collagen fibers via plasma

protein von Willebrand factor– Swell, become spiked and sticky, and release

chemical messengers• ADP causes more platelets to stick and release

their contents • Serotonin and thromboxane A2 enhance vascular

spasm and platelet aggregation


Hemostasis: Coagulation

• Reinforces platelet plug with fibrin threads

• Blood transformed from liquid to gel

• Series of reactions using clotting factors (procoagulants)– # I – XIII; most plasma proteins– Vitamin K needed to synthesize 4 of them


Figure 17.13 Events of hemostasis. Slide 5

Step 1 Vascular spasm• Smooth muscle contracts, causing vasoconstriction.

Step 2 Platelet plugformation• Injury to lining of vessel exposes collagen fibers; platelets adhere.

• Platelets release chemicals that make nearby platelets sticky; platelet plug forms.

Step 3 Coagulation• Fibrin forms a mesh that traps red blood cells and platelets, forming the clot.

Collagenfibers

Platelets

Fibrin


Coagulation: Overview

• Three phases of coagulation– Prothrombin activator formed in both

intrinsic and extrinsic pathways– Prothrombin converted to enzyme thrombin– Thrombin catalyzes fibrinogen fibrin


Coagulation Phase 1: Two Pathways to Prothrombin Activator

• Initiated by either intrinsic or extrinsic pathway (usually both)– Triggered by tissue-damaging events– Involves a series of procoagulants


Coagulation Phase 1: Two Pathways to Prothrombin Activator

• Intrinsic pathway– Triggered by negatively charged surfaces

(activated platelets, collagen, glass)– Uses factors present within blood (intrinsic)

• Extrinsic pathway– Triggered by exposure to tissue factor (TF) or

factor III (an extrinsic factor)– Bypasses several steps of intrinsic pathway,

so faster


Coagulation Phase 2: Pathway to Thrombin

• Prothrombin activator catalyzes transformation of prothrombin to active enzyme thrombin

• Once prothrombin activator formed, clot forms in 10–15 seconds


Coagulation Phase 3: Common Pathway to the Fibrin Mesh

• Thrombin converts soluble fibrinogen to fibrin

• Fibrin strands form structural basis of clot

• Fibrin causes plasma to become a gel-like trap for formed elements

• Thrombin (with Ca2+) activates factor XIII which:– Cross-links fibrin– Strengthens and stabilizes clot


Figure 17.14 The intrinsic and extrinsic pathways of blood clotting (coagulation). (1 of 2)

Intrinsic pathway Extrinsic pathwayVessel endotheliumruptures, exposingunderlying tissues(e.g., collagen)

Tissue cell traumaexposes blood to

Platelets cling and theirsurfaces provide sites formobilization of factors

Tissue factor (TF)

XII

XIIa

Ca2+

VIIXI

XIa

IX Ca2+

VIIa

IXa

VIII

VIIIa

IXa/VIIIa complex TF/VIIa complex

X

Xa

Ca2+

PF3 Va V

Prothrombinactivator

PF3

released byaggregated

platelets

Phase 1


Figure 17.14 The intrinsic and extrinsic pathways of blood clotting (coagulation). (2 of 2)

Phase 2

Prothrombin (II)

Thrombin (IIa)

Phase 3

Fibrinogen (I)(soluble)

Fibrin(insolublepolymer)

Cross-linkedfibrin mesh

XIIIa

XIII

Ca2+


Figure 17.15 Scanning electron micrograph of erythrocytes trapped in a fibrin mesh.


Fibrinolysis

• Removes unneeded clots after healing

• Begins within two days; continues for several

• Plasminogen in clot is converted to plasmin by tissue plasminogen activator (tPA), factor XII and thrombin

• Plasmin is a fibrin-digesting enzyme


Factors Limiting Clot Growth or Formation

• Two mechanisms limit clot size– Swift removal and dilution of clotting factors – Inhibition of activated clotting factors

• Thrombin bound onto fibrin threads

• Antithrombin III inactivates unbound thrombin

• Heparin in basophil and mast cells inhibits thrombin by enhancing antithrombin III


Disorders of Hemostasis

• Thromboembolic disorders: undesirable clot formation

• Bleeding disorders: abnormalities that prevent normal clot formation

• Disseminated intravascular coagulation (DIC)– Involves both types of disorders


Thromboembolic Conditions

• Thrombus: clot that develops and persists in unbroken blood vessel– May block circulation leading to tissue death

• Embolus: thrombus freely floating in bloodstream

• Embolism: embolus obstructing a vessel– E.g., pulmonary and cerebral emboli

• Risk factors – atherosclerosis, inflammation, slowly flowing blood or blood stasis from immobility


Anticoagulant Drugs

• Aspirin– Antiprostaglandin that inhibits thromboxane A2

• Heparin– Anticoagulant used clinically for pre- and

postoperative cardiac care

• Warfarin (Coumadin)– Used for those prone to atrial fibrillation– Interferes with action of vitamin K

• Dabigatran directly inhibits thrombin

Dagatriban and related anticoagulants are based on molecules which leeches create and use to help them suck blood. Medicinal leeches are still used by some physicians, for example to promote blood flow around skin grafts and after reattachment surgery. Buy at http://www.leechesusa.com/.

http://www.leechesusa.com/


Bleeding Disorders

• Thrombocytopenia: deficient number of circulating platelets– Petechiae appear due to spontaneous,

widespread hemorrhage – Due to suppression or destruction of red bone

marrow (e.g., malignancy, radiation, drugs)– Platelet count <50,000/μl is diagnostic – Treated with transfusion of concentrated

platelets


Bleeding Disorders

• Impaired liver function– Inability to synthesize procoagulants – Causes include vitamin K deficiency,

hepatitis, and cirrhosis– Impaired fat absorption and liver disease can

also prevent liver from producing bile, impairing fat and vitamin K absorption


Bleeding Disorders

• Hemophilia includes several similar hereditary bleeding disorders – Hemophilia A: most common type (77% of all cases);

factor VIII deficiency– Hemophilia B: factor IX deficiency – Hemophilia C: mild type; factor XI deficiency

• Symptoms include prolonged bleeding, especially into joint cavities

• Treated with plasma transfusions and injection of missing factors– Increased hepatitis and HIV risk


Transfusions

• Whole-blood transfusions used when blood loss rapid and substantial

• Packed red cells (plasma and WBCs removed) transfused to restore oxygen-carrying capacity

• Transfusion of incompatible blood can be fatal


Human Blood Groups

• RBC membranes bear 30 types of glycoprotein antigens – Anything perceived as foreign; generates an immune

response– Promoters of agglutination; called agglutinogens

• Mismatched transfused blood perceived as foreign– May be agglutinated and destroyed; can be fatal

• Presence or absence of each antigen is used to classify blood cells into different groups


Blood Groups

• Antigens of ABO and Rh blood groups cause vigorous transfusion reactions

• Other blood groups (MNS, Duffy, Kell, and Lewis) usually weak agglutinogens


ABO Blood Groups

• Types A, B, AB, and O• Based on presence or absence of two

agglutinogens (A and B) on surface of RBCs

• Blood may contain preformed anti-A or anti-B antibodies (agglutinins)– Act against transfused RBCs with ABO

antigens not present on recipient's RBCs

• Anti-A or anti-B form in blood at about 2 months of age; adult levels by 8-10


Table 17.4 ABO Blood Groups


Rh Blood Groups

• 52 named Rh agglutinogens (Rh factors)

• C, D, and E are most common

• Rh+ indicates presence of D antigen– 85% Americans Rh+


Rh Blood Groups

• Anti-Rh antibodies not spontaneously formed in Rh– individuals– Anti-Rh antibodies form if Rh– individual

receives Rh+ blood, or Rh– mom carrying Rh+ fetus

• Second exposure to Rh+ blood will result in typical transfusion reaction


Transfusion Reactions

• Occur if mismatched blood infused• Donor's cells

– Attacked by recipient's plasma agglutinins– Agglutinate and clog small vessels– Rupture and release hemoglobin into

bloodstream

• Result in– Diminished oxygen-carrying capacity– Diminished blood flow beyond blocked

vessels– Hemoglobin in kidney tubules renal failure


Transfusions

• Type O universal donor– No A or B antigens

• Type AB universal recipient– No anti-A or anti-B antibodies

• Misleading - other agglutinogens cause transfusion reactions

• Autologous transfusions– Patient predonates

Documents

Ch. 17 Blood Slides mostly © Marieb & Hoehn 9 th ed. Other slides by WCR