Biology 2213 Review Sheet for Test #1 Dr. James Adams
Chapter 17: Blood
-- a Connective Tissue
Matrix (plasma): 55% of blood volume (with dissolved fibrous proteins)
Cells: 45% of blood volume, almost all RBC's (<1% WBC's & platelets)
I. Distribution -- O2, nutrients, nitrogenous wastes, hormones
II. Regulation -- body heat, fluid volume, pH
III. Protection -- Platelets (blood loss), WBC=s, antibodies, complement
Matrix -- Plasma: 90% water, 10% Solutes (Table 17.1, pg. 644)
Electrolytes: inorganic ions -- sodium and associated chloride, many others
Nitrogenous substances: urea and others, mostly waste products
Gases: CO2 (mostly as bicarbonate ion), not much O2 since most is inside RBC's
Plasma proteins (8% by weight): albumins (for osmotic balance), transport proteins,
antibodies, fibrinogen (inactive form of fibrin for clots)
Osmolarity of plasma quite constant.
Formed Elements: All come from stem cells (hemocytoblasts)
in red bone marrow
Called formed elements because only leukocytes are complete cells
I. Erythrocytes (red blood cells, RBC=s) -- carry O2 (attached to Hb)
lack all organelles, including nucleus and mitochondria (makes sense -- why?);
hemoglobin (Hb) makes up 33% of cell mass; spectrin in membrane makes cells pliable
size and shape contribute to exchange of gases, including the 20% of CO2 they carry
approx. 5,000,000 RBC's/microliter of blood (major contributor to viscosity of blood)
Hemoglobin: 4 globin subunits, each with an Fe containing heme group (porphyrin ring)
Each RBC contains 250,000,000 Hb; one cell can therefore carry 1 billion O2
Production (hematopoiesis): 15 days in red blood marrow (where in adults?); released and
mature in two days (from reticulocytes); production/destruction remarkably constant
(±two million per second turnover). SEE Fig. 17.5, pg. 647.
Hormonal regulation (erythropoietin [from kidney -- WHY?], testosterone); nutrients
required for produciton (organics, iron, B-vitamins). Since production is so rapid, B12
vitamin deficiency often first indicated by reduced RBC procution (pernicious anemia)
RBC's in turn destroyed in spleen/liver/ bone marrow (100 - 120 day lifespan). Hb turnover
rapid as well -- iron must be stored/transported (ferritin/transferrin) for reuse; rest of
heme destroyed and eliminated (released in bile [bilirubin] into small intestine); globin
RBC disorders: Anemias (know pernicious, sickle-cell), polycythemia (blood doping)
II. Leukocytes (white blood cells, WBC=s) -- major immune system cells; production
(of some) dramatically increases with infection/injury
Types: (Most to least numerous: N, L, M, E, B) -- recognize these for lab practical
Will discuss these in much greater detail in the Immune system chapter (21)
1. Neutrophils (PMNL's): active bacterial and fungal phagocytes
2. Eosinophils: respond to allergens (inflammation) and macroendoparasites
3. Basophils (& mast cells): release histamines/heparin
1. Lymphocytes: T- mature in thymus; attack virus-infected/tumor cells
B- produce antibodies
These cells are SPECIFIC; with each individual attacking a very specific
invader; different invader, different lymphocytes
2. Monocytes: become macrophages ("big eaters") upon leaving the bloodstream
Production (leukopoiesis): in red bone marrow; hormonal control: colony-stimulating
factors (CSF=s) released by several cell types (mainly other WBC's - why?); granulo-
cytes stored in red bone marrow, short life-spans; agranulocytes in lymphoid tissues,
with long life-spans. Must know myeloid and lymphoid stem cells, and which WBC's
come from them. SEE Fig. 17.11, pg. 655.
WBC disorders: Leukemia (cancerous), mononucleosis (viral)
III. Thrombocytes (platelets [not true cells]) -- fragments of megakaryocytes; form platelet
plug during clotting (to be discussed, below)
Production: thrombopoietin (produced by the liver). SEE Fig. 17.12, pg. 657.
Hemostasis/Maintenance of blood flow (stoppage of blood flow through wound)
Three Steps: NOTE: chemicals you need to know are in BOLD
1. vascular spasms -- damaged blood vessels constrict; normal response of smooth
muscle in vessel walls, and response to several chemicals (see below)
2. platelet plug formation -- intact endothelial cells normally release NO and prostacyclin
that prevent platelets from sticking; however, platelets stick to damaged tissue edges,
and, in turn, release a number of chemicals themselves (see below), which induce
more platelets to stick (ADP and thromboxane); chems. also promote a wide
variety of other clot enhancing phenomena, including vascular spasms
(thromboxane) and coagulation.
3. Coagulation (clotting) -- cascade of events (pgs. 658-659), several steps involve Ca+2.
Vitamin K involved in making several clotting proteins in the liver.
Two pathways: intrinsic, involving PF, and extrinsic, involoving TF -- see Fig. 17.14, pg. 659.
Both feed into common pathway: Prothrombin activator --> (pro-)thrombin -->
Complete in 3-6 minutes.
Clot Retraction: platelets contract (actin/myosin); pull edges of wound together
Fibrinolysis: tissue-plasminogen activator --> plasmin(-ogen). Interestingly, thrombin can also
activate plasminogen; will explain in class.
Prevention of undesirable clotting: antithrombin, heparin -- found on endothelial cells
Healing: Platelet derived growth factor (PDGF)
1. Thromboembolic disorders: persistent clots (thrombus, embolus)
2. Bleeding disorders: Thrombocytopenia (reduced platelet #), liver damage, hemophilia
Transfusions and Blood Groups: A/B Antigens (agglutinogens) and anti-A & anti-B. Table 17.4.
antibodies (agglutinins; unique because they are produced without exposure to antigens)
Blood types; who is universal donor/acceptor, and why?
We will do a lab on blood typing
Rh blood groups
Diagnostic Blood tests: blood is the most frequently tested tissue of the body -- WHY?
Chapter 18: Heart A & P
Heart (the transport system pump); in mediastinum
ANATOMY: See also "Circulatory System Structures -- to know" sheet for lab
Landmarks: Apex/base; ant/post interventricular sulci; atrioventricular (coronary) sulcus
Coverings: visceral (epicardium)/parietal pericardium (serous); fibrous pericardium.
Heart Wall: epicardium (as above)/mycardium with elastic CT skeleton/endocardium
Chambers, valves and associated vessels: Know right and left atria and ventricles; interatrial
septum with fossa ovalis, interventricular septum; fossa pectinate muscles (in atria),
trabeculae carneae with papillary muscles/chordeae tendineae in ventricles; superior/inferior
vena cavae (entering R atrium), pulmonary trunk (exiting R ventricle), pulmonary arteries
and veins (entering L atrium), aorta (exiting L ventricle); atrioventricular [tricuspid (R) and
bicuspid (mitral) (L)] valves, semilunar [pulmonary (R) and aortic (L)] valves
Systemic/pulmonary circuits (know where oxygenated and deoxygenated)
( Simplified diagram of flow ) (will be handed out in class)
Cardiac circulation: Arteries-- right coronary artery, and its branches: marginal and posterior
interventricular artery (in posterior interventricular sulcus); left coronary artery, and its
branches; anterior interventricular (in anterior interventricular sulcus) and circumflex artery.
Veins -- Great and middle (draining anterior and posterior respectively), which feed into
coronary (cardiac) sinus, which, in turn, empties into R atrium
PHYSIOLOGY: Cells called fibers -- they tend to branch and all form intercalated disks
numerous gap junctions (heart a functional syncytium); contain lots of mitochondria. Difs.
from skeletal muscle: some cardiac cells autorhythmic, heart contracts as a unit; no tetanic
contractions in heart muscle (long refractory period); heart almost exclusively aerobic
Membrane potential (from chap 2); Na+, K+, Cl-, A.A.-; action potential (from chap 11)
Cardiac muscle contraction: ("fast") Na+ channels involved, as is typical for AP, but "slow"
Ca+2 channels also involved (Ca+2 also enters from extracellular fluids), increases
refractory period; makes tetany virtually impossible. Actual contraction typical of
muscle -- Ca+2 release from SR, binds to troponin . . . (as in chap 9)
Intrinsic conduction system: autorhythmic cells-- use fast Ca+2 channels for depolarization
sinoatrial (SA) node (the pacemaker); atrioventricular (AV) node (delays impulse so
atria contract before ventricles) -- see Fig. 18.13, Page 687: AV node
feeds into AV bundle, R & L bundle branches, and subendocardial conducting network
(Purkinje fibers) distribute impulse to walls of ventricles synchronously, with papillary
muscles contracting just ahead of rest of ventricles to tighten chordae tendineae.
Nodal system determines synchronicity of heartbeat
Modifying the basic rhythm:
External (ANS, hormonal) stimulation required to accelerate/decelerate heart rate (H.R.)
Cardiac centers in medulla oblongata -- see Fig. 18.14, page 688.
Sympathetic nervous system (including adrenal gland): release norepinephrine (also
called noradrenalin) -- speeds H.R.
Parasympathetic (mainly vagus nerve): releases acetylcholine -- slows H.R.
Cardiac cycle: systole and diastole, with associated heart sounds (valves); know basic
sequence of events (pgs. 693 - 696)
Cardiac output (C.O.): (stroke volume) x (heart rate) [S.V. x H.R.]
Regulation of S. V.: preload and the Frank-Starling Law, contractility, afterload
Regulation of H. R.: autonomic nervous system controls (as above, hormonal controls
(thyroxine, epinephrine), ions, physical factors (age, gender, etc.). All, of course,
influence blood pressure as well.* (see below)
C.O. remains remarkably consistent throughout adult life (avg. of 5.25 l/min.), which
means anything that changes either S.V. or H.R. will inversely affect the other.
Chapter 19: Vessels
60,000 miles of vessels in the body; arteries/veins just conduits, exchange in capillaries
Walls of vessels three-layered:
1. tunica intima (interna) -- endothelium (simp. squam.); slick, continuous with endo-
cardium; sparse conn. tissue basement membrane
2. tunica media -- circularly arranged smooth muscle, w/vasomotor nerve fibers, and
elastin fibers; partly regulates blood flow/pressure (vasodilation/-constriction);
thickest in big arteries, non-existent in capillaries/small veins, thinner and ill-defined
in larger veins
3. tunica externa (adventitia) -- loosely woven collagen with nerves; thickest in large
veins. Contains networks of smaller vessels, the vaso vasorum, which branch into
tunica media as well.
Arteries: carry blood away from the heart
1. Elastic (conducting)-- large lumen; closest to heart; withstand large pressure fluctuations,
and act as auxilliary pumps; arterial pulse
2. Muscular (distributing) -- small to medium-sized; carry blood to specific organs
3. Arterioles -- diameter <0.3mm down to 10 microns; smaller lose tunica externa; fine
control of blood flow here
Capillaries: 8-10 microns (barely bigger than diameter of RBC); tunica intima (endothelium) only
1. Continuous capillaries -- blood-brain barrier; skin; muscles, etc.. Numerous pinocytotic
2. Fenestrated capillaries -- pores increase permeability; mucosa of intestine, glomerulus in
kidney; hypothalamus; many other places.
3. Capillary sinuses -- sluggish flow allows cleaning by special phagocytes
Thoroughfare channels and capillary beds, with numerous precapillary sphincters
Veins: Low pressure; have very important one-way
1. Venous sinuses -- flattened endothelium only (intracranial [dural sinuses], coronary)
2. Venules -- no tunica media, except in largest; shunt blood to veins
3. Veins -- all layers (tunics), but thinner than arteries (particularly media), with larger
lumen than arteries; up to 65% of blood in veins at one time (blood reservoirs)
Because of low pressure, have modifications to aid in blood movement (see below*)
one way valves, large lumen (low resistance), respiratory/muscular "pumps"
Vascular Anastomoses -- more common between veins
Physiology of Circulation: blood flow -- from high
to low pressure areas, flow velocity (rate), P/R
blood pressure, resistance -- know definitions; relationship: F = Δ
Resistance: influenced by blood vessel diameter and length, and viscosity; the only regulated
one of these is the diameter. Resitance is greatest in small diameter vessels (most
friction), especially arterioles and capillaries hence, most resistance peripheral (P.R.)
Systemic blood pressure (B.P.): greatest at heart, highest at systole (lower with diastole),
declines further from heart, near zero at vena cavae -- pressure gradient
(see fig. 19.7, pg. 716)
*Factors aiding venous return: B.P. gradient, valves, muscular/respiratory pumps, mild
venoconstriction (with sympathetic stimulation)
*Maintaining B.P.: regulation of cardiac output
(see above), blood volume, P.R.
Regulation of B.P.: anything that influences the above factors influence B.P.
I. Short Term controls
A. Neural controls: sympathetic/parasympathetic stimulation
1. The cardiovascular/vasomotor centers in the medulla -- vasomotor tone
2. Baro-(presso-)receptor reflexes -- carotid and aortic
3. Chemoreceptors responding to various chemicals -- CO2 & pH (& O2)
4. Higher brain centers (emotional influences, etc.)
B. Hormonal controls: adrenal hormones ([nor-]epinephrine), ANP, ADH, NO
II. Long Term controls: largely involve changing volume of blood
A. Renal regulation:
1. Direct mechanism
2. Indirect mechanism: involves renin/angiotensin/aldosterone
Further involves, as you would expect, ADH from above
For summary of effects of different factors on smooth muscle in the walls of blood vessels, see
Fig. 19.16, page 727.
to special areas (specific organs); at rest/during
exercise (Fig. 19.15, pg. 726)
metabolic controls: concentration of various substances in blood -- CO2 , H+ (& O2),
adenosine. Involves NO or endothelin release from endothelium
myogenic controls: Fast flow results in stretch of tunica media and automatic constric-
tion response of smooth muscle cells; slow flow results in opposite response.
Different regional flow: skeletal muscle, brain, skin, lungs, heart, kidneys
Flow rate (velocity): (see Fig. 19.18, pg. 730) fastest in large arteries, slowest in capillaries
(largest cross-sectional area), faster again in veins. This is exactly what you would want --
Capillary fluid dynamics: fenestrated capillaries; SEE pgs. 732-733.
involves hydrostatic pressure (on plasma) forcing fluid out at arteriole end of capillary bed
and (colloid) osmotic pressure (due to concentrated plasma solutes [particularly albumins]
left behind) pulling fluid back in at the venule end of the cap. bed, resulting in a Net Filtration
Pressure (NFP) that is outward at the arteriole end and inward at venule end of the capillary
bed. Not all fluid leaving a fenestrated cap bed at arteriole end returns at venule end --
explains need for another fluid "pick up" system -- the Lymphatic system (the next chapter
and on the next test!).
(Circulatory pathways: Pages 736 - 758. You will find out in
lab which specific vessels
you will need to know for lab practical)