BIOL 0800 Reading- Chapter 12 Flashcards Preview

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Flashcards in BIOL 0800 Reading- Chapter 12 Deck (263):

What are the two components of blood?

Formed elements and plasma


What is hematocrit?

The percentage of blood volume that is erythrocytes


At any given moment, what percentage of blood volume is in the capillaries?

Only about 5%, even though that's the percentage that's doing most of the work


What is the pulmonary circuit?

Blood pumped from right ventricle to lungs to left atrium into systemic circulation


What is the systemic circuit?

Blood pumped from the left atrium to the organs/tissues to the right atrium


What is the aorta?

Where the blood leaves the left ventricle to go to systemic circulation


What is microcirculation?

Arterioles, capillaries, and venules


What is the inferior vena cava? And superior?

Brings all the veins together to bring the blood back to right atrium from below the heart; superior brings back all the blood from above the heart


What is the pulmonary trunk?

Brings blood from the right ventricle to the lungs via two pulmonary arteries (one to each lung)


What is the pulmonary vein?

Brings blood back from the lungs to the left atrium


What pattern does the branching of the capillaries create, and why?

Delivers blood to peripheral organs and tissues in parallel so that each only receives a fraction of the bloodflow


How does circulation to the liver and anterior pituitary gland differ from regular circulation?

Blood passes through two capillary beds in series connected by veins before returning to the heart (called a portal system)


What is a portal system?

When blood passes through two capillary beds in series, connected by veins, before returning to the heart


What is the equation relating flow rate, hydrostatic pressure, and resistance?

F = deltaP/R


What is the equation for resistance?

(8Lviscosity)/(pi*r^4) = R


How are blood viscosity and hematocrit related?

Increase in hematocrit increases blood viscosity


How does flow change if the radius of the blood vessel is halved?

Decreases by 16x, since R = 16x


What are the pericardium, epicardium, and myocardium?

The fibrous sac enclosing the heart; the inner layer of the pericardium; the wall of the heart


What is the difference between the left and right AV valves?

LAB RAT: left is bicuspid, right is tricuspid


How do pressure differences interact with AV valves?

If atrial pressure is greater, valve opens; If ventricular pressure is higher during contraction, valve is forced shut


What is the pulmonary valve?

From the right ventricle to the pulmonary trunk


What is the aortic valve?

From the left ventricle to the aorta


What are the two semilunar valves?

From the ventricles to their respective vessels


What is the conducting system of the heart?

The cells that don't contract but control normal heart excitation; in electrical contact with cardiac muscle cells via gap junctions


How do sympathetic postganglionic fibers interact with the heart?

Innervate the entire heart: release epi/norepi to beta-adrenergic receptors in atria and ventricles


How do parasympathetic fibers interact with the heart?

Innervate only the atria: release acetylcholine to muscarinic receptors on the atria


Where does initial depolarization of the myocardium begin?

SA node: conducting system cells near the right atrium near the entrance of the superior vena cava


Where is the SA node?

Near the right atrium by the entrance of the superior vena cava


Describe the path of depolarization triggered by the SA node.

Travels to atria (contract at virtually the same time); then to AV node at base of right atrium, which propagates to the ventricle slowly; then down the interventricular septum through the bundle of His; then to Purkinje fibers, which depolarizes both ventricles from the apex up, squeezing blood out


What is the AV node?

Located at base of right atrium; depolarized after atrial contraction; propagates the action potential slowly, allowing the atria to finish contracting before the ventricles contract


Where does the action potential go after leaving the AV node?

To the bundle of His: AV bundle; separates into right and left bundle branches that separate at the apex of the heart (bottom) to enter the left and right wall


What are the Purkinje fibers?

Fibers that rapidly distribute the impulse through the ventricles and make contact with ventricular myocardial cells to depolarize the rest of the ventricle


In what direction does ventricular contraction occur?

From apex to base, aka up the heart as if squeezing blood out


What two parts of the conducting system are the only conductive link between the aria and ventricles?

The AV node and Bundle of His


How do ion concentrations differ during cardiac action potentials from normal ones?

Na permeability up to depolarize and K permeability down; but then no repolarization: K permeability stays low and Ca permeability increases: stays depolarized around 0 mV


Why is there no rapid repolarization in cardiac action potentials?

K channels stay closed, and Ca permeability increases


Why does Ca permeability increase during cardiac action potentials?

Initial depolarization opens Ca channels and influx of Ca: L-type Ca channels


What are L-type Ca channels?

Channels in the myocardial cells that open during initial depolarization to allow an influx of Ca into the cell to balance the eflux of K out after Na influx; modified DHP receptors which were voltage-sensitive for skeletal muscle contraction


Which has a shorter plateau phase, atrial or ventricular cells?



What is pacemaker potential?

The gradual depolarization from the plateau caused by Ca influx from L-type Ca channels


What are the three ion channel mechanisms that contribute to pacemaker potential?

K channels, F-type channels, and T-type Ca channels


What are F-type channels?

Funny channels: nonspecific cation channels that open at negative membrane potential values: conduct an inward depolarizing Na current


What are T-type Ca channels?

Ca channels that open briefly and contribute to inward Ca current to boost depolarization in pacemaker potential


Why do SA node cells initiate action potentials rather than AV node cells, if they're similar in shape?

Because pacemaker currents of SA node cells are brought to threshold more rapidly than AV node cells


Why is the AV node so slow at propagating cardiac excitation?

Because depolarization in nodal cells is caused by Ca influx from L-type Ca channels, which depolarize the membrane more slowly than voltage-gated Na channels do


What is the P wave?

Corresponds to atrial depolarization


What is the QRS complex?

Corresponds to ventricular depolarization


What is the T wave?

Ventricular repolarization


Why isn't atrial repolarization evident in an EKG wave?

Because it occurs at the same time as the QRS complex


What is Lead I?

Right hand (-) to left hand (+), ground at right ankle


What is Lead II?

Right hand (-) to left ankle (+), ground at right ankle


What is Lead III?

Left hand (-) to left ankle (+), ground at right ankle


How do augmented leads work?

Combine two electrodes into a single central electrode


What is Lead aVR?

Left arm and leg (-) to right arm (+); points up toward right shoulder [combines Lead III]


What is Lead aVL?

Right arm and left leg (-) to left arm (+); points up toward left shoulder [combines Lead II]


What is Lead aVF?

Right arm and left arm (-) to left leg (+); points down [combines Lead I]


What is the difference between partial block and complete block in EKG readings?

Partial block is when AV node damage permits only every other impulse to the ventricles; Complete block is when there is no synchrony between atrial and ventricular electrical activity and the ventricles are contracted by the slow bundle of His activity


How does excitation-contraction coupling with in cardiac muscle cells?

The Ca influx from L-type Ca channels during prolonger depolarization triggers greater release of Ca from ryanodine receptors in the SR, for standard thin filament binding and crossbridge cycling


Is ventricular muscle capable of contraction summation?

No: because of long absolute refractory period


What is the absolute refractory period of the heart?

The period during and following an action potential when the heart can't be re=excited: due to prolonger plateau of depolarization


What is systole?

The period of ventricular contraction and blood ejection


What is diastole?

The period of ventricular relaxation and blood filling


What are the two parts of systole?

IVC and ejection


What are the two parts of diastole?

IVR and filling


When is the only time during the cardiac cycle that all valves are closed?



What is EDV?

The amount of blood in the ventricle after ventricular diastole


What is ESV?

The amoutn of blood remaining after ejection


What is stroke volume?



What is a typical stroke volume for an adult at rest?

135-65 = 70 mL


How does the T wave correspond to action potentials?

Represents the end of the plateau phase of the action potential: onset of ventricular repolarization


What is the dicrotic notch?

The decrease and rebound of aortic pressure caused when the aortic valve closes (since aortic pressure is greater than the relaxing ventricular pressure), due to blood rebounding against the valve


How does typical pulmonary artery sys/dias differ from systemic?

Much lower: 25/10 vs 120/80


What is "lub?"

The first heart sound: closing of the AV valves, onset of systole


What is "dup?"

The second heart sound: closing of the pulmonary and aortic valves: onset of diastole


What is stenosis?

Abnormally narrowed valves


What is cardiac output?

The volume of blood each ventricle pumps, in L/min: volume of blood flowing through either the systemic or pulmonary circuit per minute


What is the formula for cardiac output?

CO = HR x SV


What is a normal cardiac output for a resting adult?

5.0 L/min


What is typical total blood volume?

5.0 L


Without any nervous system input, what is resting heart rate? Why is typical resting heart rate different?

100 bpm; but more parasympathetic input than sympathetic, so closer to 70 bpm


How does sympathetic NS increase heart rate?

Increases pacemaker potential slope by increasing F-type channel permeability: faster depolarization, SA nodal cells reach threshold faster, heart rate increases


How does parasympathetic NS decrease heart rate?

Decreases pacemaker potential slope due to reduction of inward current, so threshold is reached slowly and heart rate decreases; increased SA node cell permeability to K+


What are the three main factors that affect stroke volume?

Changes in EDV, changes in sympathetic NS input magnitude, and changes in afterload


What is preload?

The volume of blood in the ventricles just before contraction


What is afterload?

The arterial pressures against which the ventricles pump


What is the Frank-Starling mechanism?

Stroke volume increases as EDV increases


Why does the Frank-Staling mechanism work?

Because greater EDV stretches the ventricular sarcomeres before contraction, allowing a more forceful contraction later on, which puts out more SV


Why does cardiac muscle cell force increase more steeply as a function of sarcomere length than in skeletal muscle cells?

Because stretching the sarcomeres toward optimum length decreases spacing between thick/thin filaments (allows more crossbridge binding), and increases sensitivity of troponin for Ca and increases Ca release from the SR


What is the significance of the FS mechanism?

At any given heart rate, venous return increase forces an increase in cardiac output by increasing EDV and thus SV


How do epi/norepi increase contractility?

Act on beta-adrenergic receptors


What is ejection fraction?



What is standard EF?

Between 50% and 75%


What are the cellular mechanisms that regulate sympathetic myocardial contractility?

Adrenergic receptors activate G-protein coupled cascades (to produce cAMP and activate a protein kinase), which phosphorylates proteins to enhance contracility (L-type Ca channels, ryanodine receptors and proteins in the SR membrane, thin filament proteins (troponin), thick filament proteins, and Ca pump proteins)


Does parasympathetic NS activity affect ventricular contraction?

Not really: little parasympathetic innervation of ventricles


How does afterload affect stroke volume?

Greater load (increased arterial pressure) reduces stroke volume, because it's harder to push blood through against the pressure


What is echocardiography?

Beaming ultrasonic waves at the heart and electronically plotting the echoes


What is cardiac angiography?

Requires temporary threading of a thin flexible tube (catheter) through an artery/vein into the heart and injecting a radio-opaque contrast material for tracking


What is the formula for compliance?

Compliace = delta V / delta P


What is systolic pressure?

The maximum arterial pressure reached during peak ventricular ejection


What is diastolic pressure?

The minimum arterial pressure that occurs just before ventricular ejection begins


What is pulse pressure?

The difference between systolic and diastolic pressures


What are the three most important factors in determining pulse pressure?

Stroke volume, speed of ejection of stroke volume, and arterial compliance


How does SV affect pulse pressure?

Greater SV increases pulse pressure


How does speed of ejection affect pulse pressure?

Greater speed of ejection increases pulse pressure


How does arterial compliance affect pulse pressure?

Greater compliance decreases pulse pressure


What is mean arterial pressure?

The average pressure in the cardiac cycle


How do you calculate MAP?

DP + (1/3)(SP-DP)


Why is MAP the most important measure of arterial pressure?

Because it's the pressure driving blood into the tissues averaged over the entire cardiac cycle


Does compliance have a major influence on the MAP?

No: compliance affects SP and DP inversely, so it averages out to the same MAP


How does a sphygmomanometer work?

Increase pressure on arteries to greater than SP to cut them off, and slwoly opens up to allow spurts of blodo through at peaks of SP: when you hear the Korotkoff's sounds, you know that's the peak SP, and then when the sounds go away, there's continuous flow, signifying DP


What are the two major roles of arterioles?

Determining relative blood flow to organs at any given MAP, and determining MAP itself


What is the equation for blood flow through any organ?

F = (MAP- venous pressure)/ Resistance of organ


What does flow difference throughout the body depend on?

Relative resistance of respective arterioles, not MAP, because MAP is the same throughout the body


What is intrinsic tone?

The spontaneous contractile activity of ateriolar smooth muscle


What is the result of an increase in contractile force above the intrinsic tone?

Vasoconstriction (and the opposite would eb vasodilation)


What are the two mechanisms controlling vascon or vasodil?

Local controls and extrinsic (or reflex) controls


What are local controls?

Mechanisms independent of nerves or hormones by which organs/tissues alter their own arteriolar resistances and self-regulate their blod flows


What does self-regulation of blood flow by autocrine/paracrine substance through local control include?

Active hyperemia, flow autoregulation, reactive hyperemia, and local response to injury


What is active hyperemia?

When metabolic activity of organs/tissues is increased due to increased blood flow


What is active hyperemia a result of?

Arteriolar dilation in the more active organ or tissue


What are the factors that cause arteriolar smooth muscle to relax in active hyperemia?

Local chemical changes in the ECF surrounding the arterioles


What is one of the most obvious chemical changes when tissues become more active?

Decrease in local oxygen concentration


What chemical factors increase when metabolism increases?

Carbon dioxide, hydrogen ions, adenosine from ATP breakdown; K ions from repeated repolarization; eicosanoids from membrane phospholipid breakdown; bradykinin (peptide generated locally from kininogen by action of kallikrein enzyme); NO released by endothelial cells


What is flow autoregulation?

The change in resistance in the direction of maintaining blood flow as constant in the face of pressure change


What is the mechanism for flow autoregulation?

Arterial pressure decrease lowers blood flow and oxygen supply while increasing other chemical factors (carbon xioide, potassium, adenosine, etc.) just like in metabolic activity: results in vasodilation


Can flow autoregulation involve vasoconstriction? When?

Yes, when arterial pressure increases: removes local vasodilator chemical factors faster than they are produced, and increases oxygen concentration: causes constriction to maintain relatively constant local flow


What is the myogenic response?

The direct responses of arteriolar smooth muscle to stretch, caused y changes in Ca movements into smooth muscle cells through stretch-sensitive Ca channels


Describe myogenic responses to increased and decreased stretch.

Increased stretch: caused by increased arterial pressure, leads to greater contraction; Decreased stretch: caused by decreased arterial pressure, causes smooth muscle tone decrease


What is reactive hyperemia?

When organ/tissue has its blood supply completely occluded and causes a profound transient increase in blood flow as soon as occlusion is released


Reactive hyperemia is essentially an extreme form of what other local control mechanism?

Flow autoregulation


What happens during reactive hyperemia?

No blood flow causes dilation because of low oxygen and high vasodilator chemical factors, so blood flow increases greatly once occluson ends


What are the four main mechanisms of external control of vasocon/dil?

Sympathetic nerves, parasympathetic nerves, noncholinergic/nonadrenergic autonomic neurons, and hormones


How do sympathetic nerves affect arterial pressure?

Release norepi to alpha-adrenergic receptors on vascular smooth muscle to cause vasoconstriction


What is significant about the receptors for norepinephrine on the heart and on the arterioles?

Heart is beta-adrenergic, and arterioles is alpha-adrenergic: if you're going to block sympathetic nervous system activity on heart by beta-adrenergic blocking, then it won't affect the arteriolar constriction


What is the effect of the parasympathetic NS on arteriolar innervation?

Basically none. Ha ha ha.


How do noncholinergic/nonadrenergic automatic neurons affect the vasocon/dil?

Release other vasodilator substances like NO, especially in GI system


How does epinephrine interact with arteriolar receptors?

Binds to alpha receptors for vasoconstriction, but also to beta-2 receptors for relaxation, especially in the skeletal muscle


What two hormones constrict most arterioles?

Angiotensin II and vasopressin (ADH)


What hormone is a potent vasodilator?

Atrial natriuretic peptide


What kind of cells near smooth muscle cells can also affect vasoconstriction/dilation?

Endothelial cells


What is an important paracrine vasodilator released by endothelial cells?

NO, which used to be called EDRF


What vasodilator is released by endothelial cells, especiall in response to blood clotting?

Prostacyclin, or PGI2


What is one of the most important vasoconstrictor paracrine agents released by endothelial cells?

Endothelin1 or ET-1


What is the effect of increased shear stress on release of NO, PGI2, and ET-1?

Increased release of NO and PGI2, but less ET (more vasodilation, less vasoconstriction)


What is flow-induced arterial vasodilation?

When shear stress changes the release of NO, PGI2, and ET-1 to result in vasodilation


What is angiogenesis?

Growth of new capillaries


What is angiostatin?

A peptide that inhibits vessel growth and can reduce tumor size


What are intercellular clefts?

The narrow water-filled spaced between the flat cells of endothelial capillary walls


What are metarterioles?

Vessels that connect arterioles to venules that also deliver blood to capillaries, instead of directly through arterioles


What is the precapillary sphincter?

The site at which a capillary exits from a metarteriole


How does flow velocity change from arterioles to capillaries?

Slows down: allows for diffusion of nutrients


How quickly can ions and small polar molecules move across the capillaries?

Quickly: water-filled channels in capillary walls


How quickly can lipid-soluble molecules move across capillary walls?

Very quickly: pass right through the membrane


How quickly can proteins cross the capillary walls?

Slowly: small amounts of specific proteins like some hormones can cross by vesciel transport


How do leakiness of brain and liver capillaries differ?

Brain is very tight and not leaky; liver is very leaky to allow for protein resorption


What is bulk flow in the capillaries?

The exchange of plasma and interstitial fluid (there's lots more interstitial fluid than plasma)


What is the direction of bulk flow between plasma and interstitial fluid? Why?

Plasma out of the capillaries into the interstitial fluid, because interstitial fluid hydrostatic pressure is lower than capillary blood pressure


Why doesn't all the plasma filter out into the interstitial space?

Hydrostatic pressure differences favoring filtration is offset by an osmotic force opposing filtration


What is filtration for capillaries?

In the presence of a hydrostatic pressure difference cross the capillary wall, the capillary wall acts like a porous filter that allows protein-free plasma to move by bulk flow from capillary plasma to interstitial fluid through water filled channels


Why is there an osmotic flow of water into capillaries?

Because capillary plasma has a lower osmolarity due to the presence of nonpermeable protein colloids


What is net filtration pressure?

NFP = capillary pressure + interstitial fluid protein concentration - interstitial hydrostatic pressure - plasma protein concentratioin


What are the four Starling forces?

Pc, piIF, Pif, piC


What is capillary hydrostatic pressure, Pc?

Favors fluid movement out of the capillary


What is interstitial hydrostatic pressure Pif?

Favors fluid movements into the capillary


What is osmotic force due to plasma protein concentration, pi C?

Favors fluid movement into the capillary


What is osmotic force due to interstitial fluid protein concentration, pi IF?

Favors fluid movement out of the capillary


What is the capillary filtration coefficient?

The measure of how much fluid will filter per mmHg net filtration pressure; major factor in kidney capillaries, whereas usually not under physiological control


How does pulmonary capillary fluid dynamics differ?

Low pressure, low resistance system: so normal pulmonary capillary hydrostatic pressure (movement out of capillary into interstitium) is less, and is offset by greater protein concentration in the lung interstitium: Starling forces facor filtratio, but have an active lymphatic system for drainage


Why is there swelling during injury?

Histamines dilate arterioles and increase capillary pressure and filtration; endothelial cells distort and widen intercellular clefts which increases plasma protein interstitium concentration


What is the average driving pressure from the peripheral veins to the right atrium?

10-15 mmHg


What is the major function of veins?

To act as low-resistance conduits for blood flow from the tissues to the heart


Why is venous pressure important?

Determines venous return to the heart, which is a major determinant of EDV and SV


What does smooth muscle on veins do?

Innervated by sympathetic neurons that release norepinephrine to contract the venous smooth muscle: increases pressure and drives blood towards the heart


What three factors affect venous pressure?

Venous constriction, skeletal muscle pump, and respiratory pump


What is the skeletal muscle pump?

During skeletal muscle contraction, the veins in the muscle are partially compressed


What is the respiratory pump?

The diaphragm lowers during inspiration, increasing abdominal pressure and intraabdominal vein pressure; while the thorax pressure decreases intrathoracic vein and right atrium pressure: enhances venous return during inspiration


What are lymphatic capillaries?

Like capillaries, but are permeable to all interstitial fluid constituents, including protein


What is the main function of lymphatic vessels?

To carry interstitial fluid back into cardiovascular system


Where does the lymph fluid come from?

When blood moves through the capillaries, filtration is larger at the arterial end and lower at the venous end, but more large at the arterial end, so there's a net loss of about 4 L of fluid per day.


What is the formula for mean arterial pressure?

Cardiac output times total peripheral resistance


What is total peripheral resistance?

The sum of the resistances to flow offered by all the systemic blood vessels


Which is lower, total pulmonary vascular resistance, or total peripheral resistance?



What are baroreceptor reflexes?

Reflexes that bring about homeostatic adjustments to MAP


How do baroreceptor reflexes generally work?

Changes in autonomic nerve activity, and secretion of hormones (epinephrine, angiotensin II, and vasopressin)


What is the carotid sinus?

The branching nerve endings of the carotid arteries that are highly sensitive to stretch/distortion


What are the arterial baroreceptors?

The carotid sinuses and aortic arch baroreceptors


How is the rate of discharge of the carotid sinus related to the MAP?

Directly proportional


What is the medullary cardiovascular center?

The primary integrating center for the baroreceptor reflexes: interconnected neurons in the medulla oblongata


What does the medullary cardiovascular center do?

Receives input from baroreceptors to determine the rate of action potential firing of parasympathetic neurons to the heart and sympathetic neurons to the heart/arterioles/veins


How are concentrations of angiotensin II and vasopressin affected by decreased arterial pressure?

Increased concentrations


How is arterial baroreceptor discharge related to medullary cardiovascular center activity?

Increased baroreceptor discharge leads to decreased sympathetic outflow; decreased baroreceptor discharge (lower pressure) leads to increased sympathetic outflow


What is the single most important long-term determinant of blood pressure?

Blood volume


What happens to stroke volume, heart rate, cardiac output, total peripheral resistance, and mean arterial pressure during hemorrhage?

SV, CO, and MAP are restored to near-normal levels, and HR and TPR are increased to pre-hemorrhage levels


What is autotransfusion?

When, during hemorrhage, there is net flux of interstitial fluid into the capillaries because of blood loss and decreased blood volume, to restore blood volume to near-normal levels


What is erythropoeisis?

Maturation of immature red blood cells to restore blood volume


What are the three types of shock?

Hypovolemic (decrease in blood volume), low-resistance (decrease in T{R), and cardiogenic (extreme decrease in cardiac output)


Why do you feel faint upon standing up quickly?

Reduced venous return causes a drop in EDV and decreased ventricle stretch, reducing stroke volume and cardiac output and blood pressure


What happens to the heart during exercise?

MAP increases, pulse pressure increases, stroke volume increases, cardiac output increases, heart rate increases, TPR DECREASES


What are four factors promoting venous return during exercise?

Increased skeletal muscle pump activity, increased respiratory pump, sympathetic increase in venous tone, greater ease of blood flow from arteries to veins through dilates skeletal muscle arterioles


What is the main difference between prolonged cardiac activity and exercise like weight-lifting?

At a certain point, blood flow to the muscle decreased with weight-lifting, since the contraction cuts off blood flow


What are some factors limiting increase in cardiac output during reaching VO2 max?

Rapid heart rate which reduces diastolic filling time, inability of peripheral factors factoring venous return to increase ventricular filling further in the short time


What is diastolic dysfunction?

When ventricle walls have reduced compliance and can't fill normally, leading to reduced EDV and stroke volume


What is systolic dysfunction?

Myocardial damage results in a decrease in cardiac contractility, lowering stroke volume at any given EDV: manifested as decrease in ejection fraction


What is pulmonary edema?

Accumulation of fluid in the interstitial spaces of the lung due to left ventricular failure


What is hypertrophic cardiomyopathy?

Increase in thickness of the heart muscle and disruption of the myocytes and conducting cells in the cardiac walls: interferes with ejection and may cause arrhythmias


What is ischemia?

Insufficient blood flow


What is nitroglycerin?

Used as a vasodilator because breaks down into NO


What are the three main classes of plasma proteins?

Albumins, globulins, and fibrinogen


What is the most abundant class of plasma protein?

Albumins: synthesized by the liver


What is the site of erythrocyte production?

Bone marrow


What are reticulocytes?

Young erythrocytes that still have a few ribosomes that produce a weblike appearance


What characterizes unusually high erythrocyte production?

A higher percentage of reticulocytes in the blood stream, since they usually get broken down pretty quickly


Do RBCs have nuclei or most organelles?



What is the major breakdown product of hemoglobin?

Bilirubin, which is returned to circulation and gives plasma its yellowy color


Which element in hemoglobin does oxygen bind to?



What is ferritin?

A protein that binds the iron store, mainly in the liver


What does transferrin do?

Delivers almost all plasma iron to bone marrow to be incorporated into RBCs


Why is folic acid necessary?

Required for synthesis of thymine, so for DNA formation and cell division, especially of RBCs


What is intrinsic factor, and what is it necessary for?

Protein that allows absorption of vitamin b12, which is required for folic acid actioin


Why do men have a higher hematocrit than women?

Testosterone stimulates erythropoeitin


What is polycythemia?

When there are more RBCs than normal; increases blood viscosity


What are polymorphonuclear granulocytes?

The three classes of WBCs with multilobed nuclei and abundant membrane-surrounded granules


What are the three classes of polymorphonuclear granulocytes?

Eosinophils, basophils, and neutrophils


What are the two other classes of leukocytes?

Monocytes (larger, one nucleus, less granules) and lumphocytes (large nucleus)


Where are WBCs produced?

Bone marrow


What are pluripotent hematopoietic stem cells?

Undifferentiated cells that can give rise to any kind of blood cell in the bone marrow


What is a megakaryocyte?

Large bone marrow cells that form platelets when their cytoplasm pinch off


What ate hematopoeitic growth factors?

Protein hormones and paracrine agents that proliferate and differentiate various progenitor cells and inhibit apoptosis


What is hemostasis? And hematoma?

Stoppage of bleeding; accumulation of blood in the tissues that occurs as a result of bleeding from vessels


What is the immediate inherent response when a blood vessel is injured?

Constriction: slows blood flow, glues cells closer together


What does staunching of blood flow during injury depend on?

Formation of a platelet plug and blood coagulation (clotting)


What is the von Willebrand factor?

A plasma protein secreted by endothelial cells and platelets that helps platelets adhere to collagen fibers to forma bridge between damaged vessel walls and the platelets


What is platelet activation during injury?

When the binding of platelets to collagen triggers the platelets to release their vesicle contents that induce changes in the platelets to result in platelet aggregation


What is platelet aggregation?

When platelet activation causes new platelets to adhere to old ones to create a platelet plug in the damaged vessel


What is thromboxane A2?

An eicosanoid synthesized when platelets adhere together; released into ECF, acts locally; stimulates more platelet aggregation and release of their secretory vesicle contents


What are platelet plugs for?

Sealing small breaks in blood vessel walls


What happens to the blood vessels when there is a break and platelet plugs form?

Vasoconstrict to reduce blood flow to the damaged area


Why doesn't the platelet plug continue to expand once started?

Because the arachidonic acid that's used by platelet cells to make thromboxane A2 to stimulate platelet aggregation is also used by normal endothelial cells to produce PGI2, which inhibits platelet aggregation


What is PGI2?

Inhibits platelet aggregation; also called prostacyclin


What is blood coagulation?

Clotting: the transformation of blood into a solid gel called a clot/thrombus; consists mostly of fibrin


What is the make component of a blood clot?

A protein called fibrin


What is the dominant hemostatic defense to vessel damage?

Clotting: supplements the platelet plug


What is the first specific step in the clotting cascade?

Prothrombin is converted by an enzyme into thrombin (also an enzyme), which catalyzes the reaction of splitting peptides from fibrinogen until it turns into fibrin


How is fibrin made?

Prothrombin is converted into thrombin, which detaches peptides from fibrinogen into fibrin


What is factor XIIIa?

The enzyme that strengthens and cross-links the newly "carved" fibrin


How is factor XIIIa made?

Formed from plasma protein factor XIII by thrombin


What kind of feedback is thrombin involved in?

Positive feedback


Why are activated platelets essential to clotting, even if the main component of clots is fibrin?

Because the cascade of enzymatic reactions occurs on the surface of platelets, and because once activated, they display "Platelet factor" (PF) phospholipids that act as cofactors in clotting


What are the two pathways that make up the early half of the clotting cascade?

Intrinsic pathway and extrinsic pathway


What are the steps in the intrinsic pathway of early clotting?

XII is converted to XIIa due to collagen contact; this catalyes the conversion of XI to XIa, then IX to IXa (which activates VIII into VIIIa as a cofactor for next step), then X to Xa, then prothrombin to thrombin


What problem in the clotting cascade causes the majority of hemophilia cases?

Problems with VIII's conversion to VIIIa, which is a cofactor for converting X to Xa


What are the steps in the extrinsic pathway of early clotting?

Tissue factor protein (in outer plasma membrane of tissue cells, exposed after damage) binds to VII, into VIIa. Then catalyzes X into Xa (and also IX into IXa as a cofactor for more X to Xa conversion at intersection with intrinsic pathway)


Do intrinsic and extrinsic pathways occur simultaneously or serially?

Serially: usually always starts with activation of tissue factor from damage, no by XII into XIIa


How are large amounts of thrombin created if only the extrinsic pathway really produces it?

Positive feedback on factors V, VIII, and XI in the intrinsic pathway: independently triggers intrinsic pathway without XII into XIIa


Why is the liver important to clotting?

Produces many clotting factors, and produces bile salts that are necessary for absorption of Vitamin K to make prothrombin and clotting factors


What two substances inhibit platelet aggregation?

Prostacyclin (PGI2) and NO


What are the three main anticlotting mechanisms?

With TFPI, with thrombin, and with antithrombin III


How does TFPI inhibit clotting?

Secreted by endothelial cells: binds to VII-VIIa to inhibit X-Xa


How does thrombin inhibit clotting?

Thrombin binds to endothelial cell receptors (thrombomodulin) to cause thrombin to bind to protein C to inactivate VIIIa and Va; interesting because thrombin activates VIII and V if endothelium is damaged, but inhibits them if intact


How does antithrombin III inhibit clotting?

Inactivates thrombin and clotting factors when it binds to heparin on endothelial cells


What is the fibrinolytic system?

Removes clots: plasminogen activated into plasmin by plasminogen activating factors: the plasmin enzyme breaks down clots


What is t-PA?

Tissue plasminogen activator: secreted by endothelial cells; binds to fibrin during clot formation; this allows tPA to generate plasmin from plasminogen


How does aspirin affect clotting?

Inhibits platelet COX (generates prostaglandins and thromboxanes), but not endothelial: no impairment of PGI2