Blood Physiology
Components of Blood
Hematology – study of blood, blood-forming tissues, and the disorders associated
with them
Blood – liquid connective tissue surrounded by an extracellular matrix called blood
plasma; thick, viscous, slightly sticky; bright red when saturated with oxygen, dark
red if not; constitutes about 20% of ECF; 8% of total body mass
38˚C – temperature of blood
5 to 6 L – volume in adult male
4 to 5 L – volume in adult female
Functions of Blood
 Transportation – oxygen from the lungs to cells and carbon dioxide from
cells to the lungs; nutrients from GI tract; hormones from endocrine glands;
wastes to various organs for elimination
 Regulation – helps regulate pH through buffers (chemicals that convert
strong acids/bases to weak ones)
 Protection – blood can clot to avoid excessive loss from cardiovascular
system; WBC carry phagocytosis
Venipuncture – withdrawal of blood from vein using a needle and collecting tube
Median cubital vein – common site for venipuncture
Finger or Heel stick – often used in infants
Arterial stick – withdrawn from artery; determine the level of oxygenated blood
1. Blood plasma – 91.5% water, 8.5% solutes (7% plasma proteins and 1.5%other
solutes)
 Plasma proteins – proteins in blood
o Albumin – smallest, most numerous
o Globulin – immunoglobulins: attack viruses and bacteria; alpha
and beta globulin: transports iron, lipids and fat-soluble vitamins
o Fibrinogen – blood clotting
*Hepatocytes – liver cells that synthesize most of plasma proteins
2. Formed elements
 RBC/Erythrocytes – biconcave discs (for diffusion of gas molecules); lack
nucleus and mitochondria (generate ATP anaerobically); live only about 120
days; cannot reproduce; cytosol contains hemoglobin (oxygen-carrying
protein; red pigment; 33% of cell weight)
*280M hemoglobin molecules are in each RBC
o Heme – ring-like nonprotein pigment; bound to 4 chains; has iron
ion at the center that binds to oxygen
o Globin – 4 polypeptide chains (2 alpha, 2 beta)
Hematocrit – percentage of total blood volume occupied by RBCs
Nitric oxide – binds to oxygen; released NO causes vasodilation (increase in blood
vessel diameter; improves blood flow)
Erythropoiesis – production of RBCs from red bone marrow with precursor cells
called proerythroblast; cell near the end of development ejects its nucleus and
becomes reticulocyte which develops into mature RBCs in 1 to 2 days after release
*release of nucleus is the cause of RBCs biconcave shape
Hypoxia – cellular oxygen deficiency; stimulates the kidney to release more
erythropoietin, which speeds development of proerythroblasts
Blood doping – also artificially induced polycythemia; enhances RBC
production by injecting epoetin alfa (drug used to treat anemia); increase viscosity
of blood; makes the blood
 WBC/Leukocytes – have nuclei; combats pathogens
o Granular Leukocytes Leukocytosis – increase in WBC; normal, protective response to
o Neutrophil – phagocytosis; pale lilac; also stresses
polymorphonuclear leukocytes (PMNs) because they
have several differently shaped nuclear lobes Leukopenia – abnormally low level of WBC
o Eosinophil – combats effects of histamine by releasing
Emigration/Diapedesis – process on which WBC leave the
histaminase; destroys parasitic worms; red-orange; its
bloodstream; WBCs roll along the endothelium, stick to it and then
granules does not obscure its nucleus
squeeze between endothelial cells
*high eosinophil count indicates an allergic condition or a
Adhesion Molecules – help WBCs stick to endothelium
parasitic infection
 Selectins – stick to carbohydrates on the surface of
o Basophil – liberate heparin, histamine and serotonin that
neutrophils
intensify inflammatory response; involved in allergic
 Integrins – tether neutrophils to the endothelium
reactions; similar in function to mast cells; round and
 Defensin – protein in neutrophils; exhibit broad range of
blue-purple; its granules obscure the nucleus
antibiotic activity
o Agranular Leukocytes
o Lymphocyte – major cells in immune system battles;
Chemotaxis – phenomenon wherein chemicals released by
antigen-antibody reaction; stains sky-blue; classified as
microbes attract phagocytes
large or small lmyphocytes
 B cells – secrete antibodies destroying bacteria  Platelets/Thrombocytes – form platelet plug; release chemicals that
 T cells – attack viruses, cancer cells and promote vascular spasm and blood clotting; irregularly disc-shaped; has
transplanted tissue cells many vesicles but no nucleus; 150,000 to 400,000 platelets are present in
 NK cells – attack infectious microbes and arising each mL of blood; have a short life span of about 5 to 9 days
tumor cells
o Monocyte – kidney-shaped or horseshoe-shaped, blue- Complete Blood Count (CBC) – counts of RBCs, WBCs and platelets
gray and foamy-appearance due to azurophilic granules
which are lysosomes; take longer to reach the site of  14-20 g/100mL – normal hemoglobin in infants
infection but arrive in large numbers; phagocytosis after  12-16 g/100mL – normal hemoglobin in females
transforming into fixed/wandering macrophages  13.5-18 g/100mL – normal hemoglobin in males
 Fixed macrophages - reside in particular
Bone Marrow Transplant – replacement of cancerous or abnormal bone marrow to
granules
establish normal blood cell counts; defective bone marrow is destroyed by
 Wandering macrophages - roam the tissue,
chemotherapy and radiation; removed from the iliac crest of the hip bone; injected to
gather at site of infection
recipient’s ven like transfusion; patient is extremely vulnerable to infection

Graft-versus-host disease - transplanted bone marrow may produce T

cells that can attack host cells

Immunosupressive drugs – reduce level of immune system activity;

taken forever by transplant patients

Major Histocompatibility (MHC) antigens – cell identity Cord-blood Transplant – stem cells are obtained from the umbilical cord after birth
markers in WBC with a syringe and then frozen
 Hemostasis Pathways

Hemostasis – sequence of response that stops bleeding; prevents hemorrhage (loss
of large amount blood from vessels)
Mechanisms to reduce Blood Loss
1. Vascular spasm – when arteries are damaged, smooth mm in their walls
contract
2. Platelet plug – has enzymes that produce thromboxane A2; has fibrin-
stabilizing factor (help strengthen blood clot); has platelet-derived growth
factor (PDGF) which causes proliferation of vascular endothelial cells
 Platelet adhesion to damaged blood vessels
 Platelets become activated and extend many projections that
enable them to interact with one another and begin to liberate their
vesicles or the platelet release reaction
Liberated ADP and thromboxane A2 – activates
nearby platelets
1. Extrinsic pathway – occurs rapidly; tissue factor (TF) or
thromboplastin leaks into the blood from cells outside blood vessels and
initiates formation of prothrombinase
 TF, in the presence of calcium ions, activates factor X
 factor X combines with factor V to form prothrombinase
TF – mixture of lipoproteins and phospholipids released from the surface of
damaged cells
2. Intrinsic pathway – occurs more slowly; activators are either in direct
contact with blood or contained within the blood
 if endothelial cells become damaged, blood can come in contact with
collagen fibers
 contact with collagen fibers activates clotting factor XII that eventually
activates clotting factor X
 once factor X is activated, it combines with factor XII to form
prothrombinase

Serotonin and Thromboxane A2 – function as

vasoconstrictors
 Release of ADP makes other platelets in the area sticky and the
stickiness causes them to adhere to the originally activated
platelets. This gathering of platelets is called platelet
aggregation

Platelet plug - mass formed by the accumulation and attachment of large numbers
of platelets; become quite tight when reinforced with fibrin threads

3. Blood clotting/Coagulation – process of gel formation

Thrombosis – result if the blood clots too easily
Hemorrhage – if blood takes too long to clot
Clotting factors – include calcium ions, inactive enzymes
synthesized by hepatocytes and various molecules associated with
platelets

Stages of Blood Clotting

1. Formation of prothrombinase by Extrinsic or Intrinsic pathway (Common

pathway)
2. Prothrombinase converts prothrombin into enzyme thrombin
3. Thrombin converts soluble fibrinogen into insoluble fibrin which forms the
threads of the clot

Clot Retraction – consolidation or tightening of the fibrin clot; fibrin threads
gradually contract as platelets pull on them; some serum can escape but formed
elements cannot
Vitamin K – fat-soluble vitamin absorbed through the lining of intestines; required
for the synthesis of 4 clotting factors
*uncontrolled bleeding – due to vitamin K deficiency
Fibrinolytic system – dissolves small, inappropriate clots or when damage is
already repaired
Fibrinolysis – dissolution of clot
 Plasminogen – inactive plasma enzyme incorporated to a clot; can be
activated into plasmin or fibrinolysin
 Prostacyclin – opposes the action of thromboxane A2
 Antithrombin – blocks the action of several factors (XII, X, II)
 Heparin – by mast cells; blocks thrombin; often administered during
hemodialysis
 Warfarin – antagonist to Vitamin K; blocks synthesis of 4 clotting factors;
slower than heparin
 Activated protein C (APC) – inactivates the 2 major factors not blocked by
antithrombin; enhances activity of plasminogen
Intravascular Clotting – within the cardiovascular system; may form when blood
flows too slowly or stasis
Thrombosis – clotting in an unbroken blood vessel
Thrombose – the clot itself
Embolus – a blood clot, bubble of air, fat from broken bones or a piece of debris
transported by the bloodstream
Pulmonary embolism – embolus lodges in the lungs
Aspirin – inhibits vasoconstriction and platelet aggregation by blocking thromboxane
A2 synthesis
Thrombolytic agents – chemicals injected to the blood to dissolve blood clots and
restore circulation
Streptokinase – dissolves clots in the coronary arteries
Tissue plasminogen activator (t-PA) – used to treat heart and brain
attack victims caused by blood clots
Blood Groups and Blood Types
Agglutinogens – antigens ion the surface of erythrocytes
Agglutinins – antibodies in blood plasma
1. ABO Blood group – based on two glycolipid antigens (A and B)
 Anti-A antibody – reacts with antigen A
 Anti-B antibody – reacts with antigen B
Transfusion – transfer of whole blood or blood components into the bloodstream or
directly into the red bone marrow
Agglutination – clumping of RBCs; an antigen-antibody response due to
incompatible transfusion; activates plasma proteins of complement family
Hemolysis – rupture of RBCs and release of hemoglobin into plasma; it is because
complement molecules make the membrane of the donated RBCs leakier
 2. RH Blood group – named after RH factor (the RH antigen) which was
first found in Rhesus monkey
 Rh positive – people who has Rh antigen
 Rh negative – people without

*immune system starts to make anti-Rh antibodies when Rh- person receives
blood from Rh+

Hemolytic Disease of the Newborn (HDN) – due to Rh incompatibility; may arise

during pregnancy; when the mother is Rh- and the baby is Rh+; mother’s immune
system responds by making anti-Rh antibodies

ABO Blood typing – drops of blood are mixed with different antisera (solutions
that contain antigen)

Determining RH factor – drop of blood is mixed with antiserum containing

antibodies that will agglutinate RBCs

Rh+ blood agglutinates

Rh- blood does not agglutinate

Medical Conditions

Anemia – oxygen-carrying capacity of blood is reduced

 Iron-deficiency anemia – most common

 Megoblastic anemia – inadequate intake of Vit B12 or folic acid; red bone
marrow produces large, a
 Pernicious anemia – insufficient hemopoiesis; inability of stomach to
produce intrinsic factor
 Hemorrhagic anemia – excessive loss of RBC through bleeding
 Hemolytic anemia – RBC plasma membrane ruptures prematurely
 Thalassemia – deficient hemoglobin synthesis
 Aplastic anemia – destruction of red bone marrow due to toxins, gamma
radiations or medications
 Sickle-cell disease (SCD) – inherited; RBCs contain Hb-S (abnormal
hemoglobin which forms rodlike structures that bend the RBC to sickle
shape); sickle cells rupture easily and die in about 10-20 days; cannot keep
pace with hemolysis; cause K ions to leak out
*Low level of K ions kill malaria parasites Hemochromatosis – excessive absorption of iron and excess iron deposit

Hemophilia – bleeding occur spontaneously; known as the royal disease Medical terms

Leukemia – group of red bone marrow cancers; acute or chronic

Cyanosis – bluish/dark purple skin discoloration due to increased methemoglobin
(hemoglobin not combined with oxygen)

Jaundice – yellowish discoloration of sclerae of eyes, skin and mucous membrane

due to excess biliburin (yello-orange pigment)

Venesection – opening of a vein from blood withdrawal

Phlebotomy – therapeutic bloodletting; removal of blood to lower its viscosity; by a

phlebotomist

Hemato/Hemopoiesis – process at which blood cells are formed