Chapter 19: The Cardiovascular System: Blood

Functions of Blood

________________ Oxygen from lungs to cells, CO2 from cells Nutrients from GI tract Hormones Heat and waste

___________ Homeostasis of body fluids

pH, temperature, osmotic pressure

_______________- from excessive blood loss & disease Clotting WBC Proteins, Ab, interferon, complement

Components, Fig 19.1, table 19.1

_____________ - 55% of whole bloodWater, proteins, others

__________________- 45% RBC = erythrocytes (4.8- 5.4 million/l blood)WBC = leukocytes, 5 types, (5-10,000/ l blood)

Agranulocytes= Lymphocytes, monocytesGranulocytes= Neutrophils, eosinophils, basophils

Platelets = thrombocytes; from megakaryocytes; (150-400,000/l)

Plasma, specific components

WaterSolutes

Proteins- albumin, globulins, clotting factorsAntibodies are _________________- produced during

immune responses against bacteria & viruses

Nutrients- simple sugars, amino acids, fatsElectrolytes- various saltsGases- oxygen and carbon dioxideWaste products- byproducts of metabolism:

urea, uric acid, creatinine, ammonia, bilirubin

Normal blood smear

Physical characteristics

Denser, more viscous than waterTemp = 38°C = 100.4°FSlightly alkaline pH = 7.35 - 7.45___________________________ is blood8% body mass_____________ (1.5 gal) in average male

4-5L (1.2 gal) in avg. ♀

Formation of blood cells Fig 19.3

____________- how formed elements are made Before birth- in yolk sac of embryo In fetus- liver, spleen, thymus and lymph nodes Red bone marrow - 1° site last 3 months of fetal

development & continues to be thru out lifeHighly vascularizedMicroscopic spaces in spongy boneFrom pluripotent stem cellsRate of production in adulthood and becomes

predominantly yellow bone marrow

Marrow sinusoids (enlarged, leaky capillaries) circulation

Red Blood Cells = Erythrocytes

General Structure: biconcave disk, 7-8 μmFunction: ____________________

Hemoglobin (Hb) – oxygen carrying protein that gives blood it’s red color, binds 4 oxygen molecules

______________- % of total blood volume that is occupied by RBCNormal range adults: ♀ 38-46%, ♂ 40-54%

Testosterone stimulates erythropoietin- hormone that stimulates RBC production

Production – new mature RBC must enter the bloodstream at least 2 million/ second to = their rate of destruction

Structural CharacteristicsStructural Characteristics

RBC Physiology

____________________ for oxygen transportNo nucleus, all space for oxygen storageLack mitochondria for ATP generation do not USE

any of the O2 they transportShape facilitates function

↑ surface area ↑ surface for gas diffusion

280 million Hb / RBC, each Hb can bind 4 O2120 day life–wear & tear, no nucleus no repair

Destroyed in spleen and liver & recycled ________ on plasma membrane account for

ABO blood types & Rh factor

Hb = 2α, 2β chains; 1 heme with Fe2+ /chain

Figure 19.5 formation & destruction

Erythropoiesis Figure 19.6

Production of RBC Start in RB marrow w/ proerythroblast

Divides several timesEjects nucleus reticulocyte = immature

Loss of nucleus causes indentation

______________ pass from RB marrow to bloodstream- squeeze thru endothelial cells of capillaries called sinusoids

RBC destruction Fig. 19.5, 6

If erythropoiesis ≠ destruction, neg. feedback loop to ↑ RBC productionIf cellular oxygen is deficient = _________,

stimulates kidney to release erythropoietinHigh altitude – lower O2 content in airCirculatory problems________- # RBC or Hb content low (some causes:)

• Lack of iron• Lack of certain a.a.• Lack Vitamin B12

Breakdown & recycling at liver, spleen, or RB marrow

Erythrocyte Disorders

________________ – disorder characterized by > normal hematocrit (>55%) in which hypertension, thrombosis (clot in an unbroken vessel), & hemorrahage (bleeding) can occur

Anemias- O2 carrying capacity reduced, fatigued, intolerant to cold, may appear pale: Iron deficiency Megoblastic- inadequate Vitamin B12 or folic acid Pernicious- insufficient hemopoiesis Hemorrhagic- excessive loss of RBC Hemolytic- RBC rupture prematurely Thalassemia- Hb deficiency Aplastic- destruction of RB marrow

Erythrocyte disorders (2) Fig 19.14

Sickle-Cell Disease (SCD) – RBC contain Hb-S, an abnormal HbHb-S gives up oxygen to interstitial fluid it forms a

long, rod-like structure, sickle shapeSome degree of ____________Mild ____________- yellowness of skin, eyes,

membranes due to build up of bilirubinJoint, bone pain; breathlessness, rapid h.r., fever,

fatigue due to tissue damage & oxygen debt__________________

2 defective genes = severeone gene = minor problems

Leukocytes = WBC Fig. 19.7, 8

Types: granular and agranularAll have nuclei, no Hb

Functions- each of 5 have specific functionsSee table 19.3

Far less numerous than RBCAvg 5-10,000 cells / μl of blood

________________________ > 10,000 cells / μl of blood• Normal protective response: microbes, strenuous exercise, anesthesia,

surgery________________________ < 5,000 cells / μl of blood

• Never beneficial– caused by radiation, shock, chemotherapy

Cell life = hours to few days, but T & B memory can live for many years once established

Granulocytes fig 19.7, table 19.3

______________________= 60-70% Phagocytosis destruction of bacteria w/ lysozyme, defensins, & strong

oxidants______________________= 2-4%

combat histamine effects in allergic rxns phagocytize A-Ab complexes destroy certain parasitic worms

_______________ = 0.5-1% liberate heparin (prevents clotting) histamine (vasodilate, ↑perm of bv, constricts airway) serotonin in allergic rxns

Agranulocytes fig 19.7, table 19.3

__________________ = 20-25%mediate immune responses- A-Ab rxns B cells develop into plasma cells, secrete AbT cells attack invading viruses, cancer cells,

transplanted tissue cellsNatural killer cells attack wide range of infectious

microbes & certain spontaneous arising tumor cells___________________ = 3-8%

Phagocytosistransform into fixed or wandering macrophages

Emigration (aka diapedesis) Fig 19.8

How WBC leave bloodstreamRolling along the endothelium, stick to it, squeeze

between endothelial cellsPrecise signals stimulate, vary for different types

Adhesion molecules- ____________ tether neutrophils to endothelium & assist in movement to ECF

Neutrophils & macrophages are phagocytic_____________ -microbe secretions attract phagocytes

Neutrophils- quick responders:Lysozyme, strong oxidants, defensins- proteins that

exhibit broad range antibiotic activity bacteria & fungi

Phagocytosis (in ch 22)

Inflammation

Immunity

State of being resistant to injury, particularly by poisons, foreign proteins, & invading pathogens______________– due to an individual’s biological

makeupAntibodies, skin, stomach acid, mucous, coughing,

enzymes in saliva & tears, skin oils ______________ – acquired due to injection of

vaccine, dead or attenuated pathogens or immunoglobulins

______________ – resistance to disease or infection due to one’s immune system functioning to produce antibodies

______________ – acquired by transfer of serum from another animal produced by sensitized lymphocyte, or mother to fetus

Antigen - Antibody

_____________ (A) – substance provoking immunogenicity and reactivity (react w/Ab or cells that result from immune response) On RBC = agglutinogens = glycoproteins or glycolipids Categorized the blood groups: A, B, AB, O; also Rh

____________ (Ab) - protein produced by a plasma cell to specific antigen Combine with Antigen to neutralize, inhibit or destroy it

__________________ – clumping of microorganisms or blood cells due to A-Ab rxn

MHC Antigens

Major _________________ (MHC) antigens – surface proteins on WBC & other nucleated cells that are unique to each person (except identical twins) Used for tissue typing

Leukemias

group of RB marrow cancers, abnormal WBC multiply uncontrollably accumulation of cancerous WBC interferes w/production of RBC,

WBC & plateletsO2 carrying capacity , more susceptible to infection, abnormal clot

Cancerous WBC spread to lymph nodes, liver, & spleen causing enlargement

Anemia, weight loss, fever, night sweats, excessive bleeding, recurrent infections

Cause- unknown, risk factors: radiation, chemotherapy, genetic disorders, environmental factors, microbes

Acute- symptoms develop rapidly (adults or children)Chronic- take years to develop (usually just adults)

Treatment- chemotherapy, radiation, stem cell transplant, interferon, Ab, blood transfusion

Platelet formation

Hemostasis Fig 19.11

1. _____________ – smooth muscle contraction in rxn to damage

2. ______________________ – platelets adhere, activate, liberate contents, aggregation forms plug

3. ___________________ – fibrin threads form4. ________________________ - contraction of fibrin

threads to tighten clot, release factors to strengthen5. ______________ – enzyme digests clot

Fibrinolytic system – dissolves small inappropriate clots Streptokinase – first thromolytic agent for dissolving clots in

coronary arteries, approved 1982

Coagulation time

Time required for blood to coagulate, 2-6 minCan be prolonged due to the following:

__________________ – X chromosome linked disorder resulting in deficiency of clotting factor VIII (type A) or deficiency of factor XI (type B & C)Spontaneous or traumatic subcutaneous intramuscular

hemorrahaging, nose bleeds, blood in urineObstructive jaundice – obstructing bile flowSome anemias and leukemiasSome of infectious diseases

Blood typing Fig 19.12-19.14

Human Blood Groups ABO Blood GroupsRh Blood Groups

Transfusion rxns: Agglutination Hemolysis

Blood Typing Table 19.5 - frequency of typesTable 19.6 - group interactions

Transfusion

RBC only or blood plasma only is transferred into the bloodstream or directly into red bone marrow

INCOMPATIBLE BLOOD TYPE: Agglutination rxn – recipient’s ____________bind to the _____________A-Ab complex activate plasma proteins to the

complement family Make the plasma membrane of donated cells leaky_________________ – rupture of cells, loss of Hb

Rh factor Fig 19.13

Antigen discovered in Rhesus monkeyRh+ have antigen, Rh- do NOT have antigenNormally, plasma does not contain anti-Rh Ab

If Rh- person receives Rh+ transfusion immune system will start to make anti-Rh Ab that will remain in blood. Problem: _____________ of Rh+ occurs later, Anti-Rh Ab that have been building can cause agglutination of donated blood hemolysis

Hemolytic disease of newborn (HDN)- if fetal blood (Rh+) leaks across placenta, exposure to Rh-A mother (Rh-) making anti-Rh, prob – 2nd baby RH+