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BLOOD
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River of life
Transport everything that must be carried from one place to another
within the body (nutrients(sugar, protein), hormones, wastes(metabolic)
& body heat) through blood vessels
Only fluid tissue in the body (Tissue –group of cells with same function)
Connective Tissue – cells, extracellular matrix(plasma)
Has both solid and liquid components

COMPONENTS OF BLOOD

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Complex connective tissue in which living blood cells (Formed
elements) are suspended in nonliving matrix (Plasma)
Collagen and elastin fibers are absent but dissolved proteins become
visible fibrin strands in blood clotting
Erythrocytes/RBC

reddish mass at the bottom

formed elements that function in oxygen transport
Buffy Coat

Thin whitish layer at the junction between RBC and plasma

Contains the remaining formed elements, leukocytes (WBC
that protect body) and platelets (cell fragments that stop
bleeding)
Hematocrit – percentage/blood fraction of RBC in blood

PHYSICAL REPRESENTATION OF BLOOD
Sticky opaque fluid with a characteristic metallic state
Salty metallic taste because of Iron
Color depends on the amount of oxygen (oxygenation of RBC) it is
carrying

Scarlet – oxygen rich

Dull red – oxygen poor
Heavier than water and because of its formed elements
5 times thicker (viscous) because of RBCs
Slightly alkaline (pH- 7.35-7.45)
Temperature slightly higher than body temperature (38 C or 100.4 F)
because one of its function is to remove heat
Accounts for approximately 8% of the body weight
5 to 6 liters (6 quarts) – healthy man
Plasma
90% water – liquid part of blood
Straw-colored due to dissolved substances

Nutrients(glucose, fatty acid, AA, vitamins)

salts(electrolytes Na(osmotic), K(pH buff), Ca, MG, Cl,
bicarbonate(membrane permeability))

respiratory gas (O2 CO2)

hormones(steroid and thyroid hormone)

plasma proteins

waste products of cell metabolism (urea)
Plasma proteins

Most abundant solutes in plasma

Mostly made by the liver (except antibodies & protein based
hormones)

Joan is pretty

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Cannot be used by cell as source of energy/fuel/metabolic
nutrients (sugar, amino acids can be used as fuel)

Composition of plasma varies continuously (after eating, etc)

Albumin – acts as a carrier to shuttle certain molecules
through circulation ;; important blood (ph) buffer ;; contribute
to osmotic pressure of blood (which acts to keep water in
bloodstream)

Clotting proteins(Fibrinogens)– help stem blood loss when a
blood vessel is injured

Antibodies(Globulins) – help protect body from pathogens

Not taken up by the cells to be used as food fuels/metabolic
nutrients, as are other solutes such as glucose, fatty acids
and oxygen
Composition of plasma varies continuously as cells remove or add
substances to the blood
Composition of plasma is kept relatively constant by various
homeostatic mechanisms of the body

When blood proteins drop to undesirable levels, the liver is
stimulated to make more

When blood starts to become too acid (acidosis) or too basic
(alkalosis), respiratory system and kidneys restores it to
normal slightly alkaline pH
Helps to distribute body heat, a by-product of cellular metabolism

FORMED ELEMENTS
Erythrocytes
Red blood cells
Ferry oxygen to all cells of the body
“fit” between cell structure and function
Differ from other blood cells (biconcave) because they are
Anucleate(lack nucleus) and contain few organelles
Literally “bags” of hemoglobin molecules
Hemoglobin

Iron bearing protein

Transport bulk of the oxygen that is carried in the blood

Also binds with a small amount of CO2

A single RBC contains about 250 million hemoglobin
molecules (billion oxygen)

Each hemoglobin molecules can bind 4 oxygen molecules

The more hemoglobin the RBCs contain, the more oxygen
they will be able to carry

Contain to a-chain and 2 b-chain

12-18 grams of hemoglobin per 100 ml of blood

Hemoglobin is slightly higher for men than women
Lack mitochondria and make ATP by anaerobic respiration, they do not
use up any oxygen they are transporting making them efficient oxygen
transporters
Small flexible cells shaped like biconcave discs (flattened sheets with
depressed centers on both sides
Look like miniature donuts because of their thinner centers
Their small size and peculiar shape provide a large surface area
relative to their volume, making them ideally suitable for gas exchange
Outnumbers WBC by 1000 to 1

5 million per mm3 (cubic millimeter)

Number of RBC/mm3 increases, viscosity increases

Number of RBC decreases, blood thins and flows more
rapidly
More hemoglobin molecules the RBCs contain, the more oxygen they
will be able to carry
Destined to die (3-4 months life span) because they don’t have any
nucleus so no proteins (also doesn’t have ER and mitochondria)

brick red cytoplasmic granules  number increases during allergies and infections by parasitic worms(flatworms. parasites and tumor cells Diapedesis – ability of WBC to slip in and out of blood vessels where there is infection (unlike RBCs are confined in bloodstream) Circulatory system is simply their means of transportation to areas of the body where their services are needed for inflammatory and immune response Positive Chemotaxis – ability to locate areas of tissue damage and infection in the body by responding to certain chemicals that diffuse from damaged cells Once they have “caught the scent” the WBCs move through tissue spaces by AMOEBOID MOTION (they form flowing cytoplasmic extensions that help them move along) Leukocytosis  Total WBC count is above 11000 cells/mm3  Indicates that a bacterial/viral infections is stewing in the body Leukopenia  Abnormally low WBC count  Caused by certain drug (corticosteroids and anticancer agents) Classified into 2 major groups  Granulocytes  Agranulocytes Joan is pretty A. has fine granules that are difficult to see. lysosome-like..Homeostatic Imbalance Anemia . dark purple nucleus that occupies most cell volume (spherical/slightly dented)  Cytoplasm pale blue and appears as thin rim around nucleus  Produces ANTIBODIES  Only slightly larger than RBCs  Tend to take up residence in lymphatic tissues  Not phagocytic Monocytes  Largest of the WBCs  More abundant gray-blue cytoplasm and blue purple distinctive U/kidney shaped nucleus (resemble lymphocytes)  When they migrate into the tissues. oval or kidney shaped) Lymphocytes  Large. 2. dark blue  Large histamine-containing granules that stain dark blue  Histamine – inflammatory chemical that makes blood vessels leaky and attracts other WBCs to inflammatory site Agranulocytes Lack visible cytoplasmic granules Nucleus closer to norm (spherical. movable army that helps defend the body against damage by bacteria.red  blue-red nucleus that resembles an old fashioned telephone receiver (figure 8 or bilobed)  sport coarse. as during vigorous exercise.decrease in the oxygen carrying ability of the blood  May be a result of:  Lower than normal number of RBCs  Hemorrhagic anemia – losing blood because of external/internal cut . they change into macrophages with huge appetites  Macrophages – important in fighting chronic infections (tuberculosis) .blue  Rarest  U or S shaped nucleus with constrictions. 2. tapeworms) ingested in food(raw fish) or entering via skin Basophils . 1. deep purple nucleus has 3-7 lobes connected by thin strands of nucleoplasm  Avid phagocytes at sites of acute infections  Particularly partial to bacteria and fungi (which they kill during a respiratory burst that deluges the phagocyte invaders with a potent brew of oxidizing substances (bleach. gatric ulcer  Hemolytic anemia . anxiety or other stressful situation  The stiff. deformed erythrocyte rupture easily and dam up in small blood vessels (interfere with oxygen delivery and can cause extreme pain)  Single nucleotide GAG(Glutamine)  GTG (Valine)  Havoc results from a change in just 1 AA in 2-4 polypeptide chains  Sickle cell trait – sickling gene that can be passed on Polycythemia  Excessive or abnormal increase in number of RBC  May result from bone marrow disease/cancer(polycythemia vera)  May be normal physiologic response to living at high altitudes where air is thinner and less oxygen I available (secondary polycythemia)  Causes blood to flow sluggishly and impairs circulation  Blood becomes more viscous/thicker Leukocytes White blood cells Crucial to body defense against disease 4000 to 11000 WBC/mm3 (in book– 4800-10800) Account for less than 1% of total blood volume Only “complete cells” in blood (contain nuclei and usual organelles) Form a protective. B.. 1. viruses. vit B 12) that would be needed in production to RBC  Aplastic anemia – reduction of production of RBC in bone marrow bec cancer(leukemia)  Abnormal or deficient hemoglobin content in the RBCs  Sickle cell anemia  Iron deficiency anemia – iron binds oxygen to hemoglobin Sickle Cell Anemia  The abnormal hemoglobin formed becomes spiky and sharp when the RBCs unload oxygen molecules or when the oxygen content of the blood is lower than normal. phagocytic cells **** most abundant to least – Never Let Monkeys Eat Bananas . hydrogen peroxide and others)) Eosinophils . folic acid. Granulocytes Granule-containing WBCs Have lobed nuclei (which typically consist of several rounded nuclear areas connected by thin strands of nuclear malt) Granules stain with Wright’s stain Neutrophils – both red and blue  Most numerous of the WBCs  Multilobed nucleus  Fine granules respond to both acidic and basic stains  Cytoplasm stains pink.RBCs are rupturing  Pernicious anemia – secondary to lack of particular nutrient(iron. 3.

ribs. proximal epiphysis) Developing RBCs divide many times then begin synthesizing huge amounts of hemoglobin Mag-ipon muna ng hemoglobin which is a protein yung nucleus When enough hemoglobin has been accumulated. skull. ribs.anucleate so they are unable to synthesize proteins. platelets and injured tissues Blood loss at the site id permanently prevented when fibrous tissue grows into the clot and seals the hole in the blood vessel Three major phases/stages: 1. Within 2 days. sternum and proximal epiphyses of humerus and femur Each type of blood cell is produced in different numbers in response to changing body needs and different stimuli (hormones) Formation of Red blood Cells Hemocytoblast  Proerythroblast  Erythroblast Stimulated by hormones RBCs. a series of reactions is set in motion to accomplish HEMOSTASIS or stoppage of bleeding Fast and localized Involves many substances found in plasma. grow or divide RBCs fall apart/fragment in 100-120 days Remains are eliminated by phagocytes in spleen. sternum. Vascular Spasms/Vasoconstriction  Immediate response to blood vessel injury is vasoconstriction (which causes blood vessels to go to spasms)  Spasms narrow the blood vessel at that point. pelvic bone. prodding it to “high gear” to turn out more RBCs Overabundance of erythrocytes/excessive amount of oxygen – depresses erythpoietin release and RBC production It is not the number of RBCs in blood that controls RBC production Control is based on their ability to transport enough oxygen to meet the body’s demands Formation of White Blood Cells and Platelets Stimulated by hormones Colony Stimulating Factors (CSFs) & interleukins  Prompt red bone marrow to turn out leukocytes  Marshall up an army of WBCs to ward off attacks by enhancing the ability of mature leukocytes to protect body  Released in response to specific chemical signals in environment (inflammatory chemicals & certain bacteria and their toxins) Thrombopoietin  hormone that accelerates the production of platelets from megakaryocytes Flat bones of Ilium/Sternum – injection for blood marrow Bone Marrow Biopsy – microscopic examination HEMOSTASIS Normally. liver and other body tissues Lost cells are replaced continuously by division of hemocytoblasts in the red bone marrow (flat bones. they ejected ER and become fully functioning erythrocytes (mature) 3-5 days – entire developmental process from hemocytoblasts to mature RBS Erythropoietin  Hormone that controls rate of production of erythrocyte (normally small amount of it circulates in the blood and RBCs are formed at a fairly constant rate)  produced in the kidneys (sometimes liver)  step up their release of it when blood levels of O2 begin to decline  targets bone marrow. blood flows smoothly past intact lining (endothelium) of blood vessels If blood vessel breaks.000/mm³ Needed for the blood clotting process that occurs in plasma when blood vessels are ruptures/broken HEMATOPEOSIS Blood cell formation Occurs in red bone marrow/myeloid tissue from a common stem cell (HEMOCYTOBLAST)  Forms 2 descendants  Lymphoid stem cell: lymphocytes  Myeloid stem cell: all other classes of formed elements Adult – tissue is found on flat bones of skull and pelvis. nucleus and most organelles are ejected out (cell collapses inward) producing the young Joan is pretty - - RBC called RETICULOCYTE (bec it still contains ER) (usually found in bone marrow but sometimes blood  hemorrhagic anemia) Reticulocyte enter the bloodstream to begin their task of transporting oxygen. decreasing blood loss until clotting can occur .Homeostatic Imbalance Leukemia – excessive production of abnormal WBCs  Literally “white blood”  Bone marrow becomes cancerous and huge number of WBCs are turned out rapidly  Severe anemia and bleeding problems might result Platelets Thrombocyte Not cells in strict sense Fragments of multinucleated cells called MEGAKARYOCYTE (pinch off thousands of anucleate platelet “pieces” that quickly seal themselves off from the surrounding fluids) Appear as dark staining irregularly shaped bodies scattered among other blood cells Normal platelet count: 300.

Platelet plug forms/Platelet Aggregation  Platelets are repelled by intact endothelium. abnormal/severe bleeding episodes occur  Vitamin K (needed by liver cells to produce the clotting factor) is deficient  vit K supplements  If liver function is severely impaired (hepatitis & cirrhosis) only whole blood transfusions are helpful (transfusions of concentrated platelets provide temporary relief from bleeding) Hemophilia  Several different hereditary bleeding disorders that result from lack of any clotting proteins  Bleeder’s disease  Males are usually the victims (x chromosoms)  Begin early in life  Repeated bleeding  Given a transfusion of fresh plasma or injections of the purified clotting factor they lack  Victims of blood transmitted viral disease (hepatitis and AIDS-acquired immune deficiency syndrome is a condition of depressed immunity) BLOOD GROUPS AND TRANSFUSIONS Body can only compensate loss of blood at certain limit Losses of 15-30% .pallor & weakness Losses over 30% . chills. heparin and dicumarol/warfarin(common rat poison – internal bleeding) Bleeding Disorders Thrombocytopenia Joan is pretty     - - Platelet deficiency Results from an insufficient number of circulating platelets Petechiae – small purplish blotches on the skin Can arise from any condition that suppresses the bone marrow cancer. too much fibrinogen means bleeding  Within an hour. physical blows or accumulation of fatty malt) Slowly flowing blood/Blood pooling – another risk factor especially in immobilized patients because clotting factors are not washed away as usual and accumulate so that clot formation becomes possible Antiplatelet/Anticoagulants – used against thrombus prone patients .2F) for 35 days Human Blood Groups Antigen  genetically determined proteins in the plasma membrane of RBC  identify each person as unique  substance that the body recognizes as foreign  it stimulates the immune system to release antibodies or use other means to mount a defense against it  foreign proteins (part of viruses or bacteria that invaded the body)  Each of us can tolerate our own antigen  Another’s antigen will be recognized as foreign  antibodies act Antibodies  “recognizers”  Present in plasma that attach to RBCs bearing surface antigens different from those on the patient’s RBC  Agglutination and/or hemolysis – caused by binding of antibodies causing the foreign RBC to clump . Coagulation/Blood Clotting  Injured tissues are releasing TISSUE FACTOR which interact with PF3 (phospholipid that coats the surfaces of platelets)  This combination interacts with other blood protein clotting factors and Ca2+ to form an activator that leads to formation of THROMBIN (enzyme)  Thrombin joins soluble FIBRINOGEN proteins into long hairlike molecules of insoluble FIBRIN (meshwork that traps RBCs and forms the basis for the clot) forms red thrombus .. the platelets become sticky and cling to damage site  Anchored platelets release chemicals that enhance the vascular spasms and attract more to the site  Platelet plug/White thrombus – small mass formed as more platelets pile up 3. radiation or certain drug Impaired liver function  Liver unable to synthesize its usual supply of clotting factors. aspirin.. hypertension Thrombus  Too much coagulation/excessive clot formation  Clot that develops and persists in in an unbroken blood vessel  If it is large enough. nausea and vomiting . the triggering factors are rapidly inactivated to prevent widespread clotting (Solid blood) Then endothelium regenerates and clot breaks down Placing a sterile gauze (provides rough surface to which platelets can adhere)/applying pressure(fracture cells.. squeezing serum (plasma minus the clotting proteins) from the mass and pulling the ruptures edges of the blood vessels closer together Blood clots in 3-6 minutes Once clotting cascade has started. - Other factors causing spasms: direct injury to smooth muscle cells. increasing release of tissue factor locally) would speed up clotting process Disorders of Hemostasis Undesirable Clotting Risk factor: High cholesterol level. the clot begin to retract. stimulation of local pain receptors & release of serotonin by anchored platelets) 2. but when it is broken so that the undelying collagen fibers are exposed.severe shock (fatal) Whole body transfusions are routinely given to replace substantial blood loss and to treat severe anemia or thrombocytopenia Blood bank mixes blood and anticoagulant to prevent clotting Treated blood – stored (ref at 4C/39. leads to clogging of small blood vessels throughout body  During next few hours. may lead to death of heart muscle or heart attack Embolus  If thrombus breaks away from the vessel wall and floats freely in blood stream  Usually no problem unless it lodges a blood vessel too narrow for it to pass through  Cerebral Embolus (brain) – stroke May be caused by anything that roughens endothelium of a blood vessel and encourage clinging of platelets (severe burns. foreign RBCs are lysed (ruptured) and their hemoglobin released into bloodstream Most devastating consequence of severe transfusion – freed hemoglobin molecules may block kidney tubules (causing kidney failure and death) May also cause: fever. it may prevent blood from flowing to the cells beyond the blockage  Coronary Thrombosis – blockage in blood vessels serving in heart.

donor 30 common RBC antigens in the body – so each person’s blood can be classified into diff blood groups ABO blood groups based on which antigen a person inherits (type A or B)  Absence of both: type O (most common)  Presence of both: type AB  Presence of each yield each types: A & B Antibodies from during infancy against ABO antigens not present in your won RBCs RH Blood groups Named because 1 of the 8 Rh antigens (agglutinogen D)  Rhesus monkeys Usually we’re Rh+ Rh+ . O Uni.- - ABO BLOOD GROUP Blood Group AB B A O - -  Prevent kidney damage . O O Uni. B.person receives Rh+.their RBCs carry Rh antigen Unlike ABO antibodies.individuals If Rh. after transfusion his immune system becomes sensitized and begins production of antibodies (anti-Rh+) Hemolysis  Rupture of RBCs Joan is pretty Does not occur with first transfusion because it take time for body to react and start making antibodies  Second time and after.women carrying Rh+ babies  First is healthy delivery  Then forms anti-Rh+ bodies destroying babies RBC producing condition called HEMOLYTIC DISEASE OF THE NEWBORN (baby becomes anemic and hypoxix and cyanotic)  Treated with RhoGAM – immune serum BLOOD TYPING Testing blood by mixing it with 2 different types of immune serum (antiA and anti-B) Person A mixed with anti A serum – Agglutination occurs Person b – Agglutination with anti-B serum No Agglutination at all – Type O Cross matching: testing for agglutination of donor RBC’s by the recipient’s serum and of the recipient’s RBC by the donor’s serum Developmental Aspects Before birth blood cell formation – liver and spleen 7 months – red marrow Congenital blood defects include various types of hemolytic anemias and hemophilias Fetal Hemoglobin has greater ability to pick up O2 that the adult Hemoglobin Physiologic jaundice reflects liver immaturity of infants Excessive leukocytosis may be indicative of malignancy or leukemia (common in the very young and very old) Elderly are at risk for pernicious anemia MADE BY JOAN PRETTY <3 .infusing fluids to dilute and dissolve the hemoglobin and diuretics to flush it out of the body in urine RBC Antigens (agglutinogens) A B B A None Plasma antibodies (agglutinins) None v Anti A Anti B Anti A & Anti B Blood can receive A. recipient B. AB. O A. Anti-Rh antibodies are not automatically formed and present in the blood of Rh. patient’s antibodies attack and rupture the donor’s Rh+ antibodies Hemolytic disease of the newborn (erythroblastosis fetalis) Rh.