Blood Phys iology
Cells within the human body are susceptible to changes in temperature, pH, and to
Since most c ells in the body are fixed within tissues they mus t have nutrients and
oxygen brought to them and waste removed.
Blood se rves this transp ortation function.
The bloo d is c lass ified a s a flu id ma trix c onne ctive tiss ue c ons isting of ce lls an d ce ll
fragments surrounded by a liquid matrix which circulates through the heart and blood
The cells and cell fr agme nts a re th e for med elem ents and the m atrix of the bloo d is
Therefore blood can be divided like other connective tissues into a cellular
component and a matrix component.
Formed elements make up about 45% and plasma 55% of the total blood volume.
Blood volume: 4-5 L in females, 5-6 L in males
Functions of the Blood
Distribution and transport (estimate 60 ,000 miles o f vessels in bod y)
RBC transport Oxygen, CO
Carries absorbed nutrients, electrolytes and water from intestines:
Meta bolic Wa ste -urea, exc ess w ater, ions a re carried to the kidney.
Negative - also transports bacteria, viruses, toxins etc.
Regulation and maintenance
From glands to ta rget organs
Transport of various enzymes
Diversion of blood from deeper to superficial cutaneous vessels to cool body
or vice versa to retain heat.
pH / acid-base balance
Blood acts as a buffering system for the body.
Protects against blood loss when tissues / vessels are damaged
Leukocytes protect against disease causing agents.
(1) toxin s, b act eria
III. Major Components of the Circulatory System
Two d ivisions: Cardiovas cular system a nd lymphatic syste m.
Ca rdio vas cula r: He art, bloo d ve sse ls
at rest pumps 5 liters / min.
Completely recirculates the blood every minute.
Ve sse ls
Form a tubular network.
Arteries carry blood away from heart to arterioles
Blood enters capillaries -
(1) thinnest and most numerous of vessels..
(2) exchange of nutrients, fluids and waste occurs in capillaries.
Blood flows into venules which enter into larger veins.
Lymphatic: lymphatic vess els and lymphoid tiss ues in spleen, thymus, tonsils, and
The fluid portion of the blood (plasma) passes through the capillary walls under
hydrostatic pressure (interstitial fluid).
Som e inte rstit ial fluid retu rns t o the bloo d an d so me e nter s the lymph atic
Lymphatic vess els carry interstitial fluid now ca lled lymph back to the venous
Lymph nodes along the way filter and cleanse the blood before it is returned.
IV. Components of the blood.
Plasma - straw colored liquid composed of water and dissolved solutes.
90% w ater - solvent a nd suspe nding medium for blood c omponents
Over 10 0 different solutes - p roteins, ions, nutrients , gases and wa ste
(1) 7% Pro teins
(a) Albumins (58% ) - buffer / maintains osmotic p ressure / visc osity
(b) Globulins (38%) - " & $ -transport lipids and hormones. (-Act as
(c) Fibrinogen (4%) - B lood clotting
(2) 2% Other solutes
(a) Ions - Na+, K+, Ca++, etc.
(b) Nutrients - Glucose, amino acids, cholesterol, triaclglyerol
(c) Waste products - Urea, uric acid, creatinine, ammonia salts.
(d) Gases - Oxygen, CO , Nitrigen
(e) Regulatory substances- enzymes, hormones.
Formed Elements (Cells)
Hematocrit = % of
blood composed of
Leukocytes (W BC) - 5
bas oph ils
lymphocytes a nd
Eryt hroc ytes - red bloo d ce lls
Numbers : Female - 4.3 to 5.2 million / mm3 and M ale 5.1 to 5.8 million / mm3.
Shape “biconcave disks” - increases surface area
7 um in diameter and 2.2 um thick.
Contains he moglobin and iron.
No nucleus, very few organelles.
Carry oxygen to tissues and carbon dioxide away from tissues.
Func tion d epe nde nt on hemo glob in
Hem oglo bin
(1) Stru ctur e:
(a) Composed of 4 protein chains, 2 alpha chains and 2 beta chains.
(b) Each chain contains an iron containing heme group.
(c) iron in these heme gro ups is critical for oxygen to bind to the
hemo glob in
(d) Each hemoglobin is capable of binding 4 oxygens.
Considerations: Each blood cell contains 280 million
hemoglobin molecules . Each R BC there fore has the c apability
to bind over 1 billion oxygen molecules.
(2) The majority of CO (70%) is c arried in the blood as bicarb onate ions
(a) CO + H O W H CO W HCO - + H+
(b) catalyzed by carbonic anhydrase in the RBC
(3) Ca rbo n mon oxid e bin ds t o He moglo bin fro ming a sta ble
carboxyhe moglobin - result O can’t bind to hemoglobin and d eath
(1) RBC’s are produced within the bone marrow. Through a process called
(2) Most blood cells derive from a common ancester cell known as a
(3) Und er a ppr opr iate con ditio ns th e he moc ytob last differ entia tes into a cell
known as a proerythroblast (early erythrocyte forming cell) etc.
(a) Ste m ce ll >
(b) proerythrob last >
(c) early (baso philic) erythroblast >
(d) intermediate (polychromatic)erythroblast > (hemoglobin production
(e) late erythroblast (loss of nucleus) >
(5) Changes that occur d uring RBC d evelopment:
(a) decrea se in size, loo se nucleus a nd many of its organe lles including
mitoc hond ria
(6) Regulation of production
(a) pro duc tion r equ ires :
folate and B12 for cell division and
iron for hemoglobin to be produced.
(b) Erythrocyte production is stimulated by low blood oxygen
Cause s: decrea sed or d efective erythroc ytes, dise ases o f the
lungs, high altitude, cardiovascular delivery problems,
increased de mands for oxygen (endurance exercise).
(c) Decreased blood oxygen causes increased erythropoietin release
from the kidneys.
erythropoietin stimulates bone marrow to produce more
erythrocytes and increas e the rate o f maturation.
Fate and destruction of RBC’s:
(1) As RBC circulate they eventually become ragged and worn out as they
squeeze through capillaries.
(a) (RBC cannot produce new proteins - no nucleus)
(b) Typical life span 100 - 120 days.
(2) As RBC ’s squee ze through the narrow c apillaries of the spleen (or liver)
the worn out cells become trapped and broken down by fixed
(3) Breakdown products are recycled as follows:
(a) Macrophages engulf and destro y worn out R BCs in sp leen and
(b) Hem oglo bin is split into heme and glob in
(c) Globin is broken d own into amino a cids which c an be use d to
synthesize other proteins.
(d) Heme (iron + por phyr in) liberates it’s iron core which is recycled.
a) Fe3+ is pic ked up a nd tr ans por ted in blo od b y a p lasm a pr ote in
called tran sfer rin
b) Fe is carried to marrow for synthesis of Hb in new RBC or
c) Is stored in muscle or liver where iron detaches from
transferrin and binds to an iron sto rage pro tein called ferrit in.
d) Up on re leas e fro m sto rage , iron ca n rea ttac hes to tr ans ferrin
e) Iron is then transported to bone marrow where RBC
pre curs ors tak e it up thro ugh re cep tor m edia ted end ocy tos is
for use in producing new hemoglobin molecules.
f) Erythropoiesis in red bone marrow results in the production of
RBC which enter the circulation.
(4) Por phyr in -
(a) Non iron portion of heme (prophyrin) is converted to bilive rdin
(b) biliverdin is converted to bilirub in (orange pigment)
(c) bilirubin enters the blood stream and is transported to the liver.
(d) Wit hin the liver, bilirub in is s ecr ete d by the liv er c ells in to b ile
which pas ses into the small inte stine
(e) In the large inte stine bacteria convert bilirubin into urobilinogen
Some of the U robilinogen is abso rbed ba ck into the bloo d and
converted to urobilin (yellow pigment) and is excreted in the urine
(g) Mos t urobiligen is elimina ted in fece s in the form o f stercob ilin
which gives feces its characteristic color.
Jaundice - ye llowish staining of skin and s clera caus es by buildup o f bilirubin.
Disorders of Erythrocytes
Anemias (deficiency of hemoglobin in blood)
Result of either a decrease in hemoglobin / RBC or in the number of RBCs.
Symptoms : pale, lethargic, shortness of breath, tired.
Aplas tic anem ia: inability of red bone marrow to produce RBCs
(1) caused by:
(a) damage to Red bone marrow by chemicals, drugs, radiation
(b) Iron defic ienc y - R BC s ar e sm aller than norm al.
(c) Folate deficiency - ne cessa ry for DNA replication - poo r pregnant
women and alcoholics
Pernic ious anem ia - Vitman B12 deficiency - Vitamin B12 is necessary for
production of folate.
Hem orhagic a nemia - results from loss o f blood. Ie. U lcers, mens tration.
Hem olytic anem ia - erythrocytes rupture or are destroyed at an increased
(1) caused by:
(a) genetic membrane problems,
(b) snake venom,
(c) immune diseases,
(d) heart valve problems.
Thalasemia - defective hemoglobin production
(1) insufficient globin production - genetic disorder
(2) Sickle cell anemia - a bnormal shap ed hemoglob in
(a) cells are rigid, fragile and sickle shaped
(b) death by age 30.
(c) pro tec tive a gains t mala ria
i) caused by a proto zoan (plas modium)
carried by a nopheles mo squito
protozoan develops in the RBCs releases toxins that cause
RBCs to rupture.
Bro ad c lass ificat ion o f whit e blo od c ells
4,000 -11,00 0 / mm3 (5-9,000 considered normal range)
Diapedesis - can cross capilary bounderies to fight infection
Ameboid mo tion -cytoplasmic fluid moveme nt
Positive chemotaxis - ability to follow chemical trail through the body
Characterized as granulocytes or agranulocytes
Granulocytes - twice the size of RBC, cytoplasmic granules present, survive 12h
to 3 days.
Ne utro phils
(1) Appea rance -se e lab hando ut
(a) 2-5 lobes , cytoplas mic granules that sta in slightly pink
(c) 54 t o 62 % o f whit e ce lls
(a) most common WBC
(b) chemically attracted to sites fo infection
(c) good at fighting bacte rial and fungal infections
(d) contain peroxidases and other hydrolytic enzymes
(e) contain defens ins which act to digest foreign subs tances a nd
punc ture hole s in b act eria
Num ber s inc rea se r apid ly wit h men ingitis and app end icitis
Eos inop hils
(a) bilobed nucleus
(b) cytoplasmic granules that stain red or bright red
(c) 11-14 um
(d) 1-3 % o f whit e blo od c ells
(a) most effective in working against parasitic worms such as tape
worms, flukes, pinwo rms, and ho okwo rms
(b) release chemical that reduce inflammation
(c) secrete enzymes that break down clots.
Bas oph ils
(a) two indistinct lobes
(b) cyto plas mic gr anule s st ain b lue-p urple
(c) 10-12 um
(d) less than 1% of w hite c ells
(a) contain and re lease histamine
(b) act as a chemoattractant to attract other WBC
(c) release he parin - prevents clots
(a) only slightly larger than RBC
(b) roun d nuc leus nea rly fills c ell.
(d) 25- 33% of w hite b lood cells
(a) Genera lly found in lymphoid tissue
(b) provides specific immune response
i) T-lymphocytes act directly against virus infected cells and tumor
B-Lymphocyte s produc e plasma c ells which give rise to
(a) Nucleus round, kidney of horseshoe shaped
(b) contains more cytoplasm tha n lymphocyte
(d) 3-9 % o f whit e ce lls
(a) Once activated transform into macrophages which attack and digest
everything in their way (dead cells, bacteria, etc.)
Responsible for blood clot formation and are not cells at all but are fragments of cells.
Cytoplasmic fragment surrounded by a plasma membrane containing granules
130,0 00 to 40 0,000 / mm3
Enables c lotting
Releases seratonin which causes vasoconstriction
Hemostasis (prevention of bloo d loss) by c lotting
Can be divided into three stages (vascular sp asm, plate let plug formation,
(1) Once a blood ves sel has be en injured the first and mo st immediate
respons e is for the blood vessel to s tart to spa sm.
(a) smooth muscle contraction
(2) Va scu lar s pas m is c aus ed b y ner vous sys tem r eflex es a nd b y che mica ls
(thromboxane s, endo thelin)
Platele t plug form ation
(1) Sea ls up sma ll bre aks in blo od v ess els
(a) platelet adhesion
i) Vo n willib rand ’s fa cto r from end othe lial w all
bind s pla tele ts to colla gen in ves sel w all.
(b) platelet activation
i) release ADP and thromboxanes
casca de of chemica l release by o ther platelets
(c) Activated platelets also bind fibrinogen
i) causes platelet aggrega tion.
Forms a plug.
(d) Platelets also release p latelet factor III and coagulation factor V.
i) important in clot formation (discussed later).
(3) Aspirin inhibits plug formation by block ing prostiglandin and
(1) blood clot formation
(a) fibrin protein fibers trap blood cells, platelets and fluid.
(b) Formation depends o f a number of factors
(c) Coagulation fac tors are no rmally inactive
(d) Injury causes activation of clotting factors
(e) Activation depends on surface proteins on activated platlets.
(2) Process: (three main stages) Fig. 19.10
(a) formation of prothrombinase by two p athways
(b) convers ion of prothrom bin to thromb in (by prothrombinase)
(c) convers ion of fibrinog en to fibrin by th romb in
(d) 2 pathways for the formation of prothrombinase
i) Extrinsic pathway - begins with factors released outside of
plasma in dama ged tissue
a) Thro mbo plas tin (tissue factors ) released by damage d tissue
b) Thromboplastin complexes with Factor VII to activate Factor
c) Factor X complexes with Factor V platelet phos pholipids and
Ca+ to activate prothrombinase.
Intrinsic pathway - begins with factors inside (intrinsic to )
a) damage to blood vessels exposes collagen in C. T.
b) factor XII is activated by collagen
c) activated factor XII a ctivates factor XI
d) Factor XI ac tivates factor IX
e) IX joins w ith factor VIII, p latelet phosp holipids and C a+ to
activate factor X
f) Factor X complexes with Factor V platelet phos pholipids and
Ca+ to activate prothrombinase.
Control of clot formation
Anticoagulants prevent blood from clotting outside of the injury area.
(1) Anticoagulants can counteract low levels of clotting factors.
(2) Antic oag ulant s inc lude : antit hrom bin a nd he par in
Fibrin meshwork adheres to the walls of the vessel
(1) Plat elet s co ntain act in and myos in
(2) bind to fibrin and pull it tight causing retraction