A&P II Exam 2

Identify at least two each of the transport, protective, and regulatory functions of the circulatory system.
-TRANSPORT: O2, CO2, nutrients, waste, hormones, stem cells

-PROTECTIVE: WBCs, inflammation, antibodies, platelets

-REGULATORY: stabilize fluid distribution, balance pH of ECF, body temp

What are the 2 principal components of the blood?
-PLASMA: ECM (clear, light yellow fluid)

-FORMED ELEMENTS: cells & cell fragments (RBC, WBC, platelets)

List the 3 major classes of plasma proteins. Which one is absent from blood serum?
-albumin: smallest & most abundant; transport various solutes and buffer the pH of plasma

-globulins: various roles in solute transport, clotting, & immunity

-fibrinogen: clotting protein *absent from serum*

Define the viscosity and the osmolarity of blood. Explain why each of these is important for human survival.
-VISCOSITY: thickness – the resistance of a fluid to flow, resulting from the cohesion of its particles
>important in circulatory function because it partially governs the flow of blood through the vessels

-OSMOLARITY: amount of dissolved particles
>governs the rate of reabsorption of fluids between blood & tissue fluid

What does hemopoiesis mean? After birth, what one cell type is the starting point for all hemopoiesis?
>the production of blood, especially its formed elements

-stem cells: pluripotent or hemopoietic

Describe the size, shape, and contents of an eythrocyte, and explain how it acquires its unusual shape.
>NO NUCLEUS – loses it and other organelles during maturation

-discoidal cell with a thick rim and thin center

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What is the function of hemoglobin? What are its protein and no protein moieties called?
-hemoglobin is the red pigment – role in O2 & CO2 transport

-globins (protein)

-heme (nonprotien)

Define hematocrit, hemoglobin concentration, and RBC count, and give the units of measurement in which each is expressed.
-hematocrit: packed cell volume (%)

-hemoglobin concentration: concentration in whole blood (g/dL)

-RBC count: #/volume of whole blood (mil/uL)

List the stages in the production of an RBC and describe how each stage differs from the previous one.
(1) decrease in cell size
(2)increase in cell #
(3)synthesize hemoglobin
(4)nucleus shrivels and is discharged from cell

>>pluripotent stem > erythrocyte CFU > erythroblast > reticulocyte > mature cell

What is the role of erythropoietin in the regulation of RBC count? What is the role of gastroferritin?
-ERYTHROPOIETIN: hormone that stimulates the ECFU to transform into an erythroblast

-GASTROFERRITIN: binds Fe2+ in the stomach and transports it to the small intestine

What happens to each component of an RBC and its hemoglobin when it dies and disintegrates?
-fragments are digested by macrophages in the liver and spleen

-Hb > heme >iron (storage use) AND >biliverdin > bile > feces
>globin > free amino acids

What are the 3 primary causes or categories of anemia? What are its 3 primary consequences?
-CAUSES:
(1) inadequate erythropoiesis or hemoglobin synthesis
(2) hemorrhagic anemia from bleeding (blood loss)
(3) hemolytic anemia from RBC destruction

-CONSEQUENCES:
(1) tissues suffer hypoxia
(2) blood osmolarity is reduced (more blood is transferred from bloodstream to the intracellular spaces > edema)
(3) decrease in blood viscosity – decrease in BP because of decrease in volume & viscosity

What are antibodies and antigens? How do they interact to cause a transfusion reaction?
-ANTIGENS: complex molecules (proteins, glycoproteins, glycolipids) that are unique to each individual – they occur on the surfaces of all cells and enable the body to distinguish its own cells from foreign matter

-ANTIBODIES: body’s response to foreign antigen
>>secrete proteins that bind the antigen, causing AGGLUTINATION (which marks them for destruction)

What antibodies and antigens are present in people with each of the four ABO blood types?
-O: (universal donor) – Anti-A & Anti-B; NO ANTIGEN

-A: Anti-B, Antigen A

-B: Anti-A, Antigen B

-AB: (universal recipient, rarest) – NO ANTIBODIES; Antigen A & B

Describe the cause, prevention, and treatment of HDN.
-caused by maternal antibodies attacking fetal blood

-prevented by RhoGAM shot

-treated with phototherapy

Why might someone be interested in determining a person’s blood type other than ABO/Rh?
paternity, criminal cases
What is the overall function of leukocytes?
protect against infection and other diseases
List the 5 kinds of leukocytes in order of abundance. Identify whether each is a granulocyte or agranulocyte, and describe how to identify each one.
(1) NEUTROPHILS -(gran) – most abundant, lavendar granules

(2) LYMPHOCYTES – (agran) – little cytoplasm

(3) MONOCYTES – (agran) – more cytoplasm

(4) EOSINOPHILS – (gran) – red granules

(5) BASOPHILS – (gran) – blue granules

What does leukopoiesis have in common with erythropoietin? How does it differ?
-same: begins with the same hemopoietic stem cells (HSC)

-different: leukopoiesis > WBC

What can cause an abnormally high or low WBC?
>normal: 5000-10000

-LOW: leukopenia; lead, arsenic, mercury poisoning, radiation, sickness, infectious diseases > presents an elevated risk of infection and cancer

-HIGH: leukocytosis; indicates infection, allergy, dehydration, leukemia

WBCs fight infection, and leukemia is an abnormally high WBC count. Yet leukemia patients are very vulnerable to infection. Explain this seeming as a paradox.
they are immature cells
What are the 3 basic mechanisms of hemostasis?
-cessation of bleeding

(1) vascular spasm – prompt constriction of broken vessel

(2) platelet plug formation – platelets adhere to exposed collagen fibers of vessel wall

(3) coagulation – clotting (platelets become enmeshed in fibrin threads)

How do the extrinsic and intrinsic mechanisms of coagulation differ? What do they have in common?
-extrinsic – initiated by clotting factors released by the damaged blood vessels and perivascular tissues

-intrinsic – uses only clotting factors found in the blood itself

>>in most cases, both work simultaneously to contribute to hemostasis

In what way does blood clotting represent a negative feedback loop? What part of it is a positive feedback loop?
-once clot begins to form Thrombin & Factor V > prothrombin activator > thrombin

-everything else is negative

Describe some of the mechanisms that prevent blood clotting in undamaged vessels?
-platelet repulsion – platelets do not adhere to healthy blood vessels

-dilution – at normal rates of blood flow, thrombin (chops fibrinogen into shorter strands of fibrin) is diluted so quickly that a clot has little chance to form

-anticoagulants – antithrombin, heparin

Describe a common source and effect of pulmonary embolism.
clots most often form in the leg vein of most inactive people then travel to small arteries to block the flow >> kidney, heart, brain, lung >> causing tissue death “infarction” pulmonary embolism >> lung clot
circulatory system
consists of the heart, blood vessels, and blood
cardiovascular system
refers ONLY to the heart and vessels
serum
remaining fluid when blood clots and the solids are removed

>identical to plasma EXCEPT for the absence of fibrinogen

plasma protiens:
ALBUMINS: -smallest and most abundant
-contributes to viscosity and osmolarity
-influences blood pressure, flow and fluid balance

GLOBULINS: antibodies
-provide immune system functions
-alpha, beta and gamma

FIBRINOGEN:
-precursor of fibrin threads that help form blood clots

>>formed by liver EXCEPT globulins (produced by plasma cells)

nonprotein components of plasma
-nitrogenous compounds: free amino acids, nitrogenous wastes (urea)

-nutrients: glucose, vitamins, fats, cholesterol, phospholipids, minerals

-dissolved O2, CO2, and nitrogen

-electrolytes: Na makes up 90% of plasma cations

properties of blood
-VISCOSITY: resistance of a fluid to flow > how THICK – resulting from the cohesion of its particles
-plasma is 2x as viscous as water (important in circulatory function)

-OSMOLARITY: the total molarity of those dissolved particles that cannot pass through the blood vessel wall
>too high – blood absorbs too much water, increasing BP
>too low – too much water stays in tissue, BP decreases and edema occurs

>optimum osmolarity is achieved by bodies regulation of sodium ions, proteins, and RBCs

starvation and plasma proteins
-hypoproteinemia: deficiency of plasma proteins >>extreme starvation, liver or kidney disease, severe burns

-kwashiorkor: children with severe protein deficiency > fed on cereals once weaned >>thin arms and legs, swollen abdomen

hemopoiesis
-the production of blood, expecially its formed elements
hemopoietic tissues
-produce blood cells

>yolk sac produces stem cells for first blood cells >> colonize fetal bone marrow, liver, spleen and thymus

-liver stops producing blood cells at birth
-spleen remains involved with lymphocyte production
-red bone marrow produces all 7 formed elements

pluripotent stem cells
hemopoietic stem cells
colony forming units
specialized stem cells only producing one class of formed element of blood
myeloid hemopoiesis
blood formation in the bone marrow
lymphoid hemopoiesis
blood formation in the lymphatic organs
adult vs. fetal hemoglobin
fetal hemoglobin binds to O2 tighter
nutritional needs for erythropoiesis
-IRON: key requirement, lost daily

-VITAMIN B12 and FOLIC ACID: rapid cell division & DNA synthesis

-VITAMIN C & COPPER: cofactors for enzymes synthesizing hemoglobin

erythrocyte homeostasis
-negative feedback control
>drop in RBC causes kidney hypoxemia
>kidney production of erythropoietin stimulates bone marrow
>RBC count increases in 3-4 days
anemia
-inadequate erythropoiesis or hemoglobin synthesis

-hemorrhagic anemia from bleeding

-hemolytic anemia from RBC destruction

blood types
blood types and transfusion compatibility are a matter of interactions between plasma proteins and erythrocytes
antigens
complex molecules on surface of cell membrane that are unique to the individual
agglutinogens
antigens on the surface of the RBC that is the basis for blood typing
antibodies
protiens (gamma globulins) secreted by plasma cells

-part of immune response to foreign matter
-bind antigens and mark them for destruction
-forms antigen-antibody complexes

-agglutinins – antibodies in the plasma that bring about transfusion mismatch

agglutination
-antibody molecule binding to antigens

-causes clumping of red blood cells

-each antibody can attach to several foreign antigens on several different RBCs at the same time

ABO group
-ABO bloodtype is determined by presence or absence of antigens (agglutinogens) on RBCs
O
-most common

-neither antigen

-universal donor

AB
-rarest

-both A & B antigens
-no antibodies

-universal recipient

Rh group
-Anti-D agglutinins not normally present

-can cause hemolytic disease of newborn if not prevented

leukocytes
-least abundant formed element

-conspicuous nucleus

-spend only a few hours in bloodstream before migrating to connective tissue

-retain organelles for protein synthesis

granules
-all WBCs have LYSOSOMES called nonspecific granules – inconspicuous so cytoplasm looks clear

-granulocytes have specific granules that contain enzymes and other chemicals employed in defense against pathogens

granulocytes
-NEUTROPHILS: barely visible granules; 3-5 nucleus
>first to injury site; increased numbers in bacterial infections; phagocytosis of bacteria; release antimicrobial chemicals

-EOSINOPHILS: large rosy-orange gran; bilobed nucleus
>increased #s in parasitic infections, allergies, diseases of spleen and CNS; phagocytosis of antigen-antibody complexes, allergens, and inflammatory chemicals
>not much for them to do so they create wars to wage (ALLERGIES)

-BASOPHILS: large, abundant violet gran.; obscure large S-shaped nucleus
>increased #s in chicken pox, sinusitis, diabetes;
>secrete HISTAMINE – vasodilator – speeds blood flow to injured area
>secrete HEPARIN – anticoagulant – promotes mobility of other WBCs in the area

agranulocytes
-LYMPHOCYTES: bluish cytoplasm; ovoid/round, uniform dark violet nucleus
>destroy cells (cancer, foreign, virally infected cells); “present” antigens to activate other immune cells; coordinate actions of other immune cells; secrete antibodies and provide immune memory

-MONOCYTES: largest WBC; ovoid, kidney or horseshoe -shaped nucleus
>increased numbers in viral infections and inflammation; leave blood stream and transform into macrophages (phagocytize pathogens and debris) >>APCs (ANTIGEN PRESENTING CELLS)

leukocyte disorders
-LEUKOPENIA: low WBC; caused from radiation, poisons, infectious disease; effects – elevated risk of infection

-LEUKOCYTOSIS: high WBC count; caused by infection, allergy and disease

-LEUKEMIA: cancer of hemopoietic tissue that usually produces an extraordinary high number of circulating leukocytes and their precursors

hemostasis
-the cessation of bleeding

-3 mechanisms: vascular spasm, platelet plug formation, coagulation >>platelets play in important role in all three

platelets
-small fragments of megakaryocyte cells

-secrete vasoconstrictors that help reduce blood loss
-stick together to form platelet plugs to seal small breaks
-secrete procoagulants or clotting factors
-initiate formation of clot-dissolving enzyme
-chemically attract neutrophils and monocytes to sites of inflammation
-phagocytize and destroy bacteria
-secrete growth factors that stimulate mitosis to repair blood vessels

vascular spasm
-prompt constriction of a broken vessel > most immediate protection against blood loss

-causes: pain receptors, smooth muscle injury, platelets release serotonin (vasoconstrictor)

-effects: prompt constriction of a broken vessel; provides time for other 2 clotting pathways

platelet plug formation
-endothelium smooth, coated with prostacyclin (platelet repellant)

>broken vessel exposes collagen >platelet pseudopods stick to damaged vessel and other platelets > pseudopods contract and draw walls of vessel together forming a plug

-platelets degranulate releasing a variety of substances
-positive feedback cycle is active until break in small vessel in sealed

coagulation
-most effective defense against bleeding

-conversion of plasma protein FIBRINOGEN into insoluble FIBRIN THREADS to form framework of clot

-procoagulants – clotting factors, usually produced by the liver, are present in plasma

enzyme amplification in clotting
-rapid clotting – each activated cofactor activates many more molecules in the next step of sequence
completion of coagulation
>activation of factor X (leads to production of prothrombin activator) > prothrombin activator (converts prothrombin to thrombin) > thrombin (converts fibrinogen into fibrin)

>>POSITIVE FEEDBACK – thrombin speeds up formation of prothrombin activator

fate of blood clots
-clot retraction occurs within 30 minutes
-platelet-derived growth factor secreted by platelets and endothelial cells > mitotic stimulant for fibroblasts and smooth muscle to multiply and repair damaged vessel

-FIBRINOLYSIS – dissolution of a clot > positive feedback occurs; plasmin (fibrin-dissolving enzyme) promotes formation of fibrin

hemophilia
-clotting disorder > deficiency of any clotting factor can shut down the coagulation cascade

-physical exertion causes bleeding and excruciating pain

hematoma
-masses of clotted blood in tissues
coagulation disorders
-thrombosis – abnormal clotting in unbroken vessel
>thrombus – clot (most likely to occur in leg veins of inactive people)

-pulmonary embolism – clot may break free, travel from veins to lungs
>embolus – anything that can travel in the blood and block blood vessels

-infarction – tissue death – may occur if clot blocks blood supply to an organ (MI or stroke)

distinguish between the pulmonary and systemic circuits and state which part of the heart supplies each one
-PULMONARY:supplied by RIGHT side of heart; carries blood TO the lungs for gas exchange and returns it to the heart

-SYSTEMIC: supplied by LEFT side of heart; supplies blood to every organ (incl. other parts of the lungs and the heart itself)

name 3 layers of the heart and describe their structural differences
-EPICARDIUM: serous membrane of the EXTERNAL heart surface

-ENDOCARDIUM: lines INTERIOR; covers valve surface and is continuous with the endothelium of blood vessels

-MYOCARDIUM: MIDDLE; cardiac muscle; thickest layer and performs the work of the heart

what are the functions of the fibrous skeleton?
-provides structural support for the heart

-anchors cardiocytes and gives them something to pull against

-electrical insulation between atria and ventricles

-provide elastic recoil to aid in filling heart chamber

trace the flow of blood through the heart, naming each chamber and valve in order
RT atrium > R AV (triscupid) > R ventricle > pulmonary valve > pulmonary trunk > pulmonary arteries > lung > pulmonary veins > L atrium > L AV (bicuspid) > L ventricle > aortic valve
what are the 3 principal branches of the left coronary artery? where are they located on the heart surface? what are the branches of the right coronary artery and where are the located?
-LEFT:
(1)anterior ventricular
(2)circumflex branch
(3)left marginal branch

-RIGHT:
(1)right marginal branch
(2)posterior interventricular branch

what is the medical significance of anastomoses in the coronary arterial system?
provides a backup pathway to supply blood if way is blocked
why do the coronary arteries carry a greater blood flow during ventricular diastole that they do during ventricular systole?
-SYSTOLE compresses arteries and aortic valves are open covering opening to coronary arteries

-DIASTOLE blood rushes backward against closed valves rushing into coronary arteries

what are the 3 major veins that empty into the coronary sinus?
(the coronary sinus empties blood into the R atrium)

1-great cardiac vein

2-posterior interventricular vein (middle cardiac)

3-left marginal vein

what organelles are less developed in cardiac muscle than in skeletal muscle? which are more developed? what is the functional significance of the differences between muscle types?
-LESS: SR, lacks terminal cisternae, no satellite cells ( so repair of damaged muscle is almost entirely fibrosis)

-MORE: mitochondria (because the heart relies exclusively on aerobic respiration)

what exactly is an intercalated disc and what function is served by each of its components?
-thick connections that join cardiocytes end to end

>interdigitating folds – cells interlock
>mechanical junctions – prevent cells from pulling apart
>electrical junctions (gap) – enable cardiocytes to electrically stimulate each other >> creates unified action

cardiac muscle rarely uses anaerobic fermentation to generate ATP. what benefit do we gain from this fact?
it is not prone to faigue
where is the pacemaker of the heart located? trace the path of electrical excitation from there to a cardiocyte of the L ventricle naming each component of the conduction system along the way.
-the SA node in the RIGHT atrium

>SA node > AV node > AV bundle (bundle of His) > R & L bundle branches > Purkinje fibers

why does the heart have a nerve supply, since in continues to beat even without one?
to modify the heart rate and contraction strength
define systole and diastole
SYSTOLE – contraction

DIASTOLE – relaxation

how does the pacemaker potential of the SA node differ from the resting membrane potential of a neuron? why is this important in creating the heart rhythm?
cells of the SA node do not have a stable membrane potential > it drifts up, showing a gradual depolarization >> creating a regular beat
how does excitation-contraction coupling in cardiac muscle resemble that of skeletal muscle? how is it different?
SAME: both have signal that causes depolarization

DIFFERENT: SM waits for signal and has a stable resting potential whereas CM doesn’t

what produces the plateau in the action potentials of cardiocytes? why is this important to the pumping ability of the heart?
-Ca2+ entering through slow Ca+ channels prolonging depolarization of membrane and myocardial contraction >>more sustained contraction for expulsion of blood from the heart chambers; as long as the AP is in its plateau, the cardiocytes contract
identify the portion of theECG that coincides with each of the following events: atrial depolarization, atrial systole, atrial repolarization, ventricular depolarization, ventricular systole, ventricular depolarization, and ventricular diastole
-P wave – atrial depolarization

-PQ segment – atrial systole

-QRS – atrial repolarization/ ventricular depolarization

-ST segment – ventricular systole

-T wave – vent. repolarization

-T-P – vent. diastole

explain how a pressure gradient across a heart valve determines whether a ventricle ejects blood?
the heart valve opens when pressure on one side of a valve is greater than pressure on the other, forcing the blood through
what factors are thought to cause the first and second heart sounds? when do these sounds occur?
S1 – lubb – louder > AV valves CLOSE

S2 – dupp – softer > aortic valve closes

what phases of the cardiac cycle are isovolumetric? explain what this means
> volume remains constant, no blood is ejected

>>occurs during the contraction and relaxation phases

-the semilunar valves are closed, the AV valves have not yet opened & the ventricles are taking in no blood

define cardiac output in words and with a simple formula
> the amount of blood ejected by each ventricle in 1 minute

CO = HR X SV

>typical resting values: CO = (75bpm)(70mL/beat)= 5250mL/beat >>the bodies total volume of blood (4-6L) passes through the heart every minute

describe the cardiac center and innervation of the heart
-CARDIAC CENTER – initiates autonomic output to heart (reticular formation of medulla oblongata)

-CARDIOSTIMULATORY EFFECT – sympathetic pathway

-CARDIOINHIBITORY – communicated by way of VAGUS nerves

explain what is meant by positive and negative chronotropic and isotropic agents
-CHRONOTROPIC agents: affect HR
>positive – increase HR (epinephrine, norepi., sympathetic stim)
>negative – decrease HR (too much K, ACH, parasym)

-ISOTROPIC agents: contractility
>positive – increase contractility (too much Ca, epi., norepi., caffeine)
>negative – decrease contractility (decrease Ca & increase in K, myocardial hypoxia, acidosis)

how do preload, contractility, and after load influence stroke volume and cardiac output?
-INCREASE preload > increase contractility > increase SV > increase CO

-INCREASE afterload > decrease SV > decrease CO

explain the principle behind Frank-Starling law of the heart. How does this mechanism normally prevent pulmonary or systemic congestion?
-the ventricles tend to eject as much blood as they receive

-SV is proportional to the EDV

-w/in limits, the more the ventricles are stretched, the harder they contract on the next beat

pulmonary circuit
RIGHT side of heart

-carries blood to lungs for gas exchange and back to heart

systemic circuit
LEFT side of heart

-supplies oxygenated blood to all tissues of the body and returns it to the heart

pericardium
-double waled sac that encloses the heart > allows heart to beat without friction, provides room to expand, yet resists excessive expansion
epicardium
-visceral pericardium

-heart covering (serous membrane)

endocardium
smooth inner lining of heart and blood vessels
myocardium
layer of cardiac muscle proportional to work load

-muscle spirals around heart which produces wringing motion

fibrous skeleton
-framework of collagenous and elastic fibers

-provides structural support and attachment for cardiac muscle and anchor for valve tissue

-electrical insulation between atria and ventricles > important in timing and coordination of contractile activity

right and left atria
-2 superior chambers

-receive blood returning to heart

-auricles enlarge chamber

right and left ventricles
-2 inferior chambers

>pump blood into arteries

heart valves
ensure a ONE-WAY flow of blood through the heart
atrioventricular (AV) valves
-controls blood flow between atria and ventricles

-right > tricuspid
-left > bicuspid

chordae tendineae
-cords connect AV valves to papillary muscles on floor of ventricles

-prevent AV valves from flipping inside out or bulging into the atria when the ventricles contract

semilunar valves
-control flow into great arteries >> open and close because of blood flow and pressure
AV valve mechanics > ventricles relax
-pressure drops inside ventricles > semilunar valves close as blood attempts to back up into the ventricles from the vessels > AV valves open > blood flows from atria to ventricles
AV valve mechanics > ventricles contract
-AV valves close as blood attempts to back up into the atria > pressure rises inside of the ventricles > semilunar valves open and blood flows into great vessels
coronary circulation
-5% of blood pumped by heart is pumped to the heart itself through the coronary circulation to sustain its strenuous workload

-LCA > anterior interventricular branch & circumflex branch

-RCA > *supplies right atrium & sinoatrial node (pacemaker)* >>right marginal branch & posterior interventricular branch

coronary blood flow: myocardial infarction
=heart attach: interruption of blood supply to the heart from a blood clot or fatty deposit can cause death of cardiac cells within minutes
>>sudden death of a patch of myocardium resulting from long-term obstruction of coronary circulation

-some protection from MI is provided by arterial anastomoses which provides an alternative route of blood flow (collateral circulation) within the myocardium

coronary blood flow: ventricular contraction
-blood flow to the heart muscle during vent. contraction is slowed, unlike the rest of the body (only when relaxed)

-reasons:
(1)contraction of the myocardium compresses the coronary arteries and obstructs blood flow

(2)opening of the aortic valve flap during ventricular systole covers the openings to the coronary arteries blocking blood flow into them

(3)during ventricular diastole, blood in the aorta surges back toward the heart and into the openings of the coronary arteries

venous drainage of heart
-5-10% drains directly into heart chambers, right atrium and right ventricle by way of the thebesian veins

-the rest returns to the right atrium by the: great cardiac vein, middle cardiac vein, left marginal vein, and coronary sinus

cardiocytes
striated, short, thick, branched cells, one central nucleus surrounded by light staining mass of glycogen
intercalated discs
-join cardiocytes end to end

-interdigitating folds – interlock with each other and increase surface area of contact

-mechanical junctions – tightly join cardiocytes

-electrical junctions – gap junctions allow ions to flow between cells allowing cells to stimulate each other

>>ventricles act like a single unified cell

cardiac conduction system
-generates and conducts rhythmic electrical signals in the following order:

>SA node: initiates HB and determines HR; pacemaker in right atrium near base of superior vena cava

>AV node: electrical gateway to the ventricles; fibrous skeleton acts as an insulator to prevent currents from getting to the ventricles from any other route

>AV bundle (bundle of His): forks into R & L branches, pass through the interventricular septum toward apex

>Purkinje fibers: nervelike processes spread throughout ventricular myocardium

sinus rhythm
-normal heartbeat triggered by the SA node
ectopic focus
-another part of heart fires BEFORE SA node

-caused by hypoxia, electrolyte imbalance, caffeine, nicotine, or other drugs

abnormal rhythm: nodal rhythm
if SA node is damaged, heart rate is set by AV node

> slower but can survive

abnormal rhythm: intrinsic ventriular rhythm
if both SA and AV nodes are not functioning, rate set at 20-40bpm

>requires pacemaker to sustain life

arrhythmia
any abnormal cardiac rhythm > failure of conduction system to transmit signals (heart block)
ventricular fibrillation
serious arrhythmia caused by electrical signals reaching different regions at widely different times > heart can’t pump blood

-kills quickly if not stopped

>>defibrillation: strong electrical shock whose intent is to depolarize the entire myocardium, stop the fibrillation, and reset SA nodes to sinus rhythm

pacemaker physiology
-SA node does NOT have a stable resting membrane potential > starts at -60mV and drifts upward from a SLOW inflow of Na+

-gradual depolarization is called pacemaker potential >> slow inflow of Na+ WITHOUT compensating outflow of K+

-when reaches threshold of -40mV, voltage-gated FAST Ca+ AND Na+ channels open

>>each depolarization of the SA node sets off one heartbeat

action potential of a cardiocyte
Na+ gates open > RAPID depolarization > Na+ gates close > SLOW Ca+ channels close > Ca+ channels close, K+ channels open (repolarization)
cardiac cycle
one complete contraction and relaxation of all four chambers of the heart
2 main variables that govern fluid movement
(1)PRESSURE: causes a fluid to flow

(2)RESISTANCE: opposes fluid flow
> great vessels have positive blood pressure so ventricular pressure must rise above this resistance for blood to flow into great vessels

pressure gradients and flow
-fluid flows ONLY if it is subjected to more pressure at one point than another which creates a pressure gradient
> fluid flows DOWN its pressure gradient from high pressure to low

>>pressure controls when valves open and close

auscultation
listening to sounds made by body
heart sounds
-S1: “lubb” – louder and longer > occurs with closures of AV valves

-S2: “dupp” – softer and sharper > occurs with closure of semilunar valves

phases of cardiac cycle
ventricular filling > isovolumetric contraction > ventricular ejection > isovolumetric relaxation
end-diastolic volume
amount of blood contained in each ventricle at the end of ventricular filling (130mL of blood)
stroke volume
about 70mL of blood is ejected of the 130mL in each ventricle
end-systolic volume
the 60mL left behind
total duration of cardiac cycle
0.8sec in a heart beating 75bpm
congestive heart failure
results from the failure of either ventricle to eject blood effectively

>usually due to a weakened heart

left ventricular failure
blood backs up into the lungs causing pulmonary edema
> shortness of breath or sense of suffocation
right ventricular failure
blood backs up in the vena cava causing systemic or generalized edema

>enlargement of liver, pooling of fluid in abdominal cavity, swelling of feet, fingers, ankles

cardiac reserve
the difference between a person’s max and resting CO

> increases with fitness, decreases with disease

heart rate
-PULSE: surge of pressure produced by each heart beat that can be felt with fingertips

-tachycardia: resting HR above 100

-bradycardia: resting HR below 60

chronotropic effects of the autonomic nervous system
-autonomic nervous system does not initiate the heartbeat, it MODULATES rhythm and force

-cardiac centers in the reticular formation of the medulla oblongata initiate autonomic output to the heart

-cardiostimulatory: sympathetic > adrenergic, cAMP second messenger system >accelerates uptake of Ca+ by SR allowing the cardiocytes to relax more quickly; diastole becomes too brief for adequate filling so both SV and CO are reduced

-cardioinhibitory: parasympathetic by way of VAGUS nerve >cholinergic effects on SA and AV nodes > ACh binds to receptors > opens K gates in nodal cells, as K leaves the cells, they become hyperpolarized and fire less frequently so the heart slows down
**works FASTER than sympathetics because they do not need a second messenger system

>without influence from the cardiac centers, the heart has an intrinsic firing rate of 100 bpm

vagal tone
holds down the heart rate to 70-80bpm at rest > steady background firing rate of the vagus nerves
inputs to cardiac center
-cardiac centers in the medulla receive input from many sources and integrate it into the “decision” to speed or slow the heart

-higher brain center affect HR: cerebral cortex, limbic system, hypothalamus

-medulla also receives input from muscles, joints, and brainstem: proprioceptors, baroreceptors, chemoreceptors
>>chemoreflexes and baroreflexes, responses to fluctuation in blood chemistry, are both NEGATIVE feedback loops

chronotropic chemicals
-catecholamines (NE and einephrine)

-drugs: nicotine, TH, caffeine (inhibits cAMP breakdown)

-electrolytes:
>**K+ has the greatest chronotropic effect
>>hyperkalemia – excess K+ in cardiocytes; myocardium less excitable, HR slows and becomes irregular
>>hypokalemia – deficiency K+ in cardiocytes; cells hyperpolarized, require increased stimulation

>calcium: hypercalcemia – excess of Ca+ (decreases HR and contraction strength)
>>hypocalcemia – deficiency of Ca+ (increases HR and contraction strength)

stroke volume
amount of blood coming out

-3 variables govern SV:
(1)preload
(2)contractility
(3)afterload

preload
amt. of tension in ventricular myocardium immediately BEFORE it begins to contract (how full is the heart?)

-Frank-Starling law of heart: SV is proportional to EDV – ventricles eject as much blood as they receive, the more they are streched the harder they contract

contractility (& inotropic agents)
how hard the myocardium contracts for a given preload

-positive inotropic agents: TOO MUCH Ca+ (hypercalcemia) can cause prolonged contractions; catecholamines, glucagon

-negative inotropic agents: NOT ENOUGH Ca+ (hypocalcemia) can cause weak, irregular heartbeat; hyperkalemia,

afterload
the BP in the aorta and pulmonary trunk immediately DISTAL to the semilunar valves >>opposes the opening of these valves, limits SV

-hypertension increases after load and opposes ventricular ejection

exercise and cardiac output
-exercise increases cardiac output
-proprioceptors signal cardiac center
-increased muscular activity increases venous return
-increase in HR and SV cause an increase in cardiac output
-increased SV allows heart to beat more slowly at rest
coronary artery disease (CAD)
a constriction of the coronary arteries > usually a result of atherosclerosis (accumulation of lipid deposits that degrade the arterial wall and obstruct the lumen)

-monocytes penetrate walls of damaged vessels and transform into macrophages > absorb cholesterol and fats to be call foam cells >> can grow into atherosclerotic plaques (ATHEROMAS)

ATHEROSCLEROSIS
>accumulation of lipid deposits that degrade the arterial wall and obstruct the lumen

-major risk factor is excess of LDL in the blood combined with defective LDL receptors in the arterial walls

-unavoidable risk factors: heredity, age, male

name the 3 tunics of a typical blood vessel and explain how they differ from each other
(1) tunica interna: endothelium (lines inside of vessel and is exposed to blood)

(2) tunica media: smooth muscle (thickest)

(3) tunica externa: connective tissue, often merges with that of neighboring blood vessels

contrast the tunica media of a conducting artery, arteriole, and venule and explain how the histological differences are related to the functional differences
-conducting artery: large, 40-70 layers of elastic sheets alternating with thin layers of smooth muscle

-arteriole: up to 25 layers smooth muscle, little elastic

-venule: 1-2 layers smooth muscle

describe the differences between a continuous capillary, a fenestrated capillary and a sinusoid
-continuous capillary: continuous tube of endothelium

-fenestrated: filtration pores in endothelium (allow for rapid passage of small molecules; important in organs that engage in rapid absorption or filtration)

-sinusoid: wide gaps in endothelium with no basal lamina (large pores allow proteins and blood cells to pass through)

describe 2 routes by which substances can escape the blood stream and pass through the capillary wall into the tissue fluid
fenestration pores, sinusoids, diffusion of gasses
describe the differences between a medium vein and a medium (muscular) artery. state the functional reasons for the differences
-muscular artery: smaller branches that distribute blood to specific organs

-medium vein: discontinuous SM layer with valves to help with blood return

contrast anastomosis and a portal system with the typical pathway of blood flow
-NORMAL – 1 capillary network (heart > artery > capillary > vein > heart)

-portal system – blood flows through 2 consecutive capillary networks

-anastomosis – 2 paths to the same point (point where 2 blood vessels merge)

for a healthy 15 year old girl at rest, what would be typical readings for systole pressure, diastole pressure, pulse pressure, and mean arterial pressure?
-SP: 112 mm Hg
-DP: 76mm Hg
-PP (diff btwn S & D): 36mm Hg
-MAP: 76 + (36/3)=88mm Hg
explain why arterial blood flow is pulsatile and venous flow is not
because it is effected by the cardiac cycle and veins are not
what 3 variables affect peripheral resistance to blood flow? which of these is most able to change from one minute to the next?
-viscosity

-vessel length (pressure and flow decrease with distance)

-vessel radius – changes quickly

what are the 3 primary mechanisms for controlling vessel radius? briefly explain each
(1) local control – autoregulation (ability of tissues to regulate their own blood supply)

(2) neural control – vasomotor center (of medulla oblongata)

(3) hormonal control –

explain how the baroreflex serves as an example of homeostasis and negative feedback
increases BP changes are detected in carotid sinuses > signal sent to brainstem > decrease HR and CO, maintaining a balanced BP
explain how the body can shift the flow of blood from one organ system to another
-through vasoconstriction > path of least resistance

>if a specific artery constricts, pressure downstream from the constriction decreases and pressure upstream from it rises

list the 3 mechanisms of capillary exchange and relate each one to the structure of the capillary wall
(1) diffusion – endothelial cell cytoplasm

(2) filtration and reabsorption – fenestrations

(3) transcytosis – intercellular clefts between endothelial cells

what forces favor capillary filtration? reabsorption?
-filtration – hydrostatic pressure

-reabsorption – colloid osmotic pressure

how can a capillary shift from a predominantly filtering role at one time to a reabsorbing role at another
through a change in capillary BP
state 3 fundamental causes of edema and explain why it can be dangerous
(1) increase in capillary filtration
(2) decrease in capillary reabsorption
(3) obstructed lymphatic drainage

>>O2 delivery and waste removal are impaired and tissues may begin to die >>pulmonary edema, circulatory shock

explain how respiration aids venous return
inhale > expansion of thoracic cavity and its internal pressure drops > downward movement of diaphragm increases pressure in abdominal cavity > if abdominal pressure on the IVC rises while thoracic pressure on it drops, then blood is squeezed upward toward the heart

>> blood flows faster when you inhale

explain how muscular activity and venous valves aid venous return
-skeletal muscle pump – contracting muscles squeeze the blood out of the compressed part of a vein and the valves ensure that this blood can go ONLY TOWARD the heart >> no backflow
define circulatory shock. what are some causes of low venous return shock?
> any state in which CO is insufficient to meet the body’s metabolic needs

-decreased blood volume (hypovolemic shock)
-obstructed venous return
-venous pooling (normal TBV but too much in lower body)

in what conspicuous way does perfusion of the brain differ from perfusion of the skeletal muscle
-skeletal muscles receive a highly variable blood flow depending on their state of exertion

-cerebral perfusion remains constant

how does a stroke differ from a transient ischemic attack? which of these bears a closer resemblance to a myocardial infarction?
-TIA – brief episodes of cerebral ischemia, like a mini stroke

-stroke – sudden death (infarction) of brain tissue caused by ischemia; lasts longer, severe damage

how does the low hydrostatic blood pressure in the pulmonary circuit affect the fluid dynamics of the capillaries there?
blood flows more slowly and therefore has more time for gas exchange
contrast the vasomotor response of the lungs with that of the skeletal muscles to hypoxia
-pul. arteries CONSTRICT > blood flow is redirected to better ventilated regions

-SM – dilate in response

trace the flow of a RBC from right ventricle to left atrium and name the vessels along the way
R ventricle > pulmonary trunk > R & L pulmonary arteries > superior, middle, inferior lobar arteries > capillary beds > pulmonary veins > L atrium (receives 2 pulmonary veins on each side)
the lungs have 2 separate arterial supplies. explain their function
-one is for gas exchange

-the other is for general cell needs

concisely contrast the destinations of the external and internal carotid arteries
-EXTERNAL – provides blood to external head structure EXCEPT the orbits

-INTERNAL – brain and orbits

briefly state the organs or parts of organs that are supplied with blood by the cerebral arterial circle, the celiac truck, the superior mesentary artery and the internal iliac artery
-CEREBRAL ARTERIAL CIRCLE – (Circle of Willis) – cerebrum

-CELIAC TRUNK – stomach, liver, spleen, pancreas

-SUPERIOR MESENTERIC ARTERY – small intestines, some of large

-INTERNAL ILIAC ARTERY – urinary bladder, prostate gland, uterus, vagina

if you were dissecting a cadaver, where would you look for the internal and external jugular veins? What muscle would help you distinguish one from the other?
> the neck

-internal: DEEP to sternocleidomastoid
-external: SUPERFICIAL to sternocleidomastoid

state 2 ways in which the great saphenous vein has special clinical significance. where is this vein located?
> located in the LEG (arises from medial side of arch, up through the leg and thigh, into the inguinal region)

(1) long-term IV administration
(2) used as grafts in coronary bypass surgery

arteries/veins/capillaries
-ARTERIES: (efferent) carry blood AWAY from heart

-VEINS: (afferent) carry blood TO heart

-CAPILLARIES: microscopic, thin-walled vessels that connect the smallest arteries to the smallest veins

tunica interna
-lines blood vessels and is exposed to blood

-endothelium – acts as a selectively permeable barrier; secrete chemicals that stimulate dilation or constriction of the vessel; normally repels blood cells and platelets that may adhere to it and form a clot; when tissue around vessel is inflamed, the endothelial cells produce cell-adhesion molecules that induce leukocytes to adhere to the surface

tunica media
-smooth muscle, collagen, elastic tissue

-strengthens vessel and prevents blood pressure from rupturing them

-vasomotion – changes in diameter of the blood vessel brought about by smooth muscle

tunica externa
-loose connective tissue that often merges with that of neighboring blood vessels, nerves, or other organs

-vasa vasorum – small vessels that supply blood to at least the outer half of the larger vessels

arteries
-large vessels > RESISTANCE VESSELS – have a strong, resilient tissue structure that resists high blood pressure
conducting arteries
-elastic or large; biggest

>aorta, common carotid, suvclavian, pulmonary trunk, common iliac arteries

-expand during systole, recoil during diastole which lessens fluctuations in blood pressure

distributing arteries
-muscular or smooth

-distributes blood to SPECIFIC organs

> brachial, femoral, renal, splenic arteries

resistance arteries (arterioles)
-smallest arteries > control the amount of blood to various organs
metarterioles
short vessels that link arterioles and capillaries, they contain precapillary sphincters

>constriction of these sphincters reduces or shuts off blood flow through their respective capillaries > diverts blood to other tissues

aneurysm
weak point in an artery or the heart wall

-forms a thin-walled, bulging sac that pulsates with each heartbeat and may rupture at any time

-most common sites – abdominal aorta, renal arteries, arterial circle at the base of the brain

-can cause pain by putting pressure on other structures

-most common cause – atherosclerosis and hypertension

arterial sense organs
sensory structures in the walls of certain vessels that monitor blood pressure and chemistry

> transmit information to brainstem that serves to regulate heart rate, vasomotion, and respiration

-carotid sinuses
-carotid bodies
-aortic bodies

carotid sinuses
-baroreceptors

-in walls of internal carotid artery
-monitors blood pressure > signaling brainstem > decreased HR and vessels dilation in response to high blood pressure

carotid bodies
-chemoreceptors – monitor blood chemistry

-mainly transmit signals to the brainstem respiratory centers

-adjust respiratory rate to stabilize pH, CO2, and O2

capillaries
-site where nutrients, wastes, and hormones pass between the blood and tissue fluid through the walls of the vessels (exchange vessels)

>>”business end” of the cardiovascular system

-3 capillary types: distinguished by ease with which substances pass through their walls and by structural differences that account for their greater or lesser permeability

continuous capillaries
-occur in most tissues

-tight junctions forming a continuous tube with intercellular clefts > allow passage of solutes such as glucose

-pericytes wrap around the capillaries and contain the same contractile protein as muscle > contract and regulate blood flow

fenestrated capillaries
-kidneys, small intestine

-organs that require rapid absorption or filtration

-allow for passage of only small molecules

sinusoids
-discontinued capillaries

-liver, bone marrow, spleen

-irregular blood-filled spaces with large fenestrations > allow proteins (albumin), clotting factors, and new blood cells to enter the circulation

capillary beds
-organized networks of capillaries > usually supplied by a single metarteriole
3/4
the amount of the body’s capillaries that are shut down at a given time
veins
-greater capacity for blood containment than arteries

-thinner walls, flaccid, less muscular and elastic tissue

-collapse when empty, expand easily

-have steady blood flow

-merge to form larger veins

-subjected to relatively low blood pressure

varicose veins
-blood pools in the lower legs in people who stand for long periods, stretching the veins

-cusps of the valves pull apart in enlarged superficial veins further weakening vessels > blood backflows and further distends the vessels, their walls grow weak and develop into varicose veins

>heredity weakness, obesity, pregnancy

-hemorrhoids are varicose veins of the anal canal

circulatory routes – most common
heart > arteries > arterioles > capillaries > venules > veins

-passes through only ONE network of capillary networks before returning to heart

portal system
-blood flows through 2 consecutive capillary networks before returning to the heart

>between hypothalamus and anterior pituitary
>in kidneys
>between intestines to liver

anastomoses
-the point where 2 blood vessels merge
arteriovenous anastomosis
-shunt

-artery flows directly into vein bypassing capillaries

venous anastomosis
(ex: CR > freeway)

-most common – one vein empties directly into another

-reason vein blockage less serious than an arterial blockage

arterial anastomosis
-2 arteries merge

-provides collateral (alternative) routes of blood supply to a tissue

-coronary circulation and around joints

blood flow
the amount of blood flowing through an organ, tissue, or blood vessel in a give time (mL/min)

-at rest, total flow is quite constant and is equal to the cardiac output

perfusion
the flow per given volume or mass of tissue in a given time
blood pressure
-the force that blood exerts against a vessel wall

-measured at brachial artery

-one of the body’s chief mechanisms in preventing excessive blood pressure is the ability of the arteries to stretch and recoil during the cardiac cycle
>expansion and recoil maintains steady flow of blood throughout cardiac cycle, smooths out pressure fluctuation and decreases stress on small arteries

>>determined by: CO, BV and peripheral resistance

systolic pressure
-highest

-taken during ventricular contraction (left ventricle)

diastolic pressure
-lowest

-taken during ventricular relaxation (chambers of heart refill with blood)

pulse pressure
-DIFFERENCE between S and D pressure

-important measure of stress exerted on small arteries by pressure surges generated by the heart

mean arterial pressure (MAP)
-mean pressure one would obtain by taking measurements at several intervals throughout the cardiac cycle

-DP + (1/3 of PP)

-average BP that most influences risk level for edema, fainting, atherosclerosis, kidney failure, and aneurysm

hypertension
high BP > can weaken small arteries and cause aneurysms
hypotension
chronic LOW BP > caused by blood loss, dehydration, anemia
peripheral resistance
opposition to blood flow caused by friction of the blood vessel walls

-depends on:
(1) viscosity – thickness – RBC and albumin concentration elevate this the most

(2) vessel length – the farther liquid travels through a tube, the more cumulative friction it encounters; pressure and flow decline with distance

(3) vessel radius – MOST POWERFUL INFLUENCE over flow (wide hallway vs. small hallway)
>>markedly affects blood velocity

laminar flow
flows in layers, faster in center

>blood flow (F) proportional to the fourth power of radius (r)
-arterioles can constrict to 1/3 of fully relaxed radius

>>an increase of 3X in the radius of a vessel results in 81X the flow

blood flow from aorta to capillaries
blood velocity (speed) decreases for 3 reasons:

(1) greater distance, more friction to reduce speed

(2) smaller radii of arterioles and capillaries offers more resistance

(3) farther from heart, the number of vessels and their total cross-sectional area becomes greater and greater

blood flow from capillaries to vena cava
flow increases again

-decreased resistance going from capillaries to veins

-large amount of blood forced into smaller channels (many capillaries > fewer veins)

-never regains velocity of large arteries

control by arterioles
arterioles are the most significant point of control over peripheral resistance and flow

-outnumber any other type of artery, providing the most numerous control points

-more muscular in proportion to their diameter – highly capable of vasomotion

regulation of BP & flow: vasomotion
-quick and powerful way of altering blood pressure and flow

(1) local control
(2) neural control
(3) hormonal control

change in vessel radius

-vasoconstriction: by muscular effort that results in smooth muscle contraction

-vasodilation: by relaxation of the smooth muscle

local control
-autoregulation

-vasoactive chemicals – substances secreted by platelets, endothelial cells, and perivascular tissue stimulate vasomotion

– reactive hyperemia – if blood supply is cut off then restored, flow increases above normal (EX: crossing legs > need to get tissue “caught up”)

-angiogenesis – growth of new blood vessels

neural control
-vasomotor center of medulla oblongata exerts sympathetic control over blood vessels throughout the body > stimulates most vessels to constrict, but dilates vessels in skeletal and cardiac muscle to meet demands of exercise

>baroreflex – auto., negative feedback response to changes in BP > need constant BP so enough gets to brain

>chemoreflex – auto response to changes in blood chemistry
>>primary role: adjust respiration to changes in blood chemistry
>>secondary role: vasomotion; also stimulate breathing

>medullary ischemic reflex – auto response to a drop in perfusion of the brain (not enough blood in brain)
>>medulla oblongata monitors its own blood supply

hormonal control
-some have vasoactive effects
-some regulate water balance

>angiotensin – vasoconstrictor (raises BP)
>aldosterone – promotes Na and water retention by kidneys (not as much urination so increases BV and BP)
>ADH – promotes water retention and raises BP
>epi & norepi – most blood vessels: vasoconstriction; SM & CM: vasodilation

2 purposes of vasomotion
(1) general method of raising or lowering BP throughout the whole body

(2) method of rerouting blood from one region to another for perfusion of individual organs

localized vasoconstriction
if a specific artery constricts, the pressure downstream drops, pressure upstream rises > enables routing blood to different organs as needed

>EX: vigorous exercise dilates arteries in lungs, heart and muscles; dozing in armchair after big meal > vasoconstriction in lower limbs raises BP above the limbs redirecting blood to intestinal arteries

capillary exchange
>2-way movement of fluid across capillary walls (water, oxygen, glucose, amino acids, lipids, minerals, antibodies, hormones, wastes, CO2, ammonia)

-the most important blood in the body is in the capillaries
-only through capillary walls are exchanges made between the blood and surrounding tissues

3 routes: endothelial cell cytoplasm, intercellular clefts between endothelial cells, filtration pores of the fenestrated capillaries

mechanisms involved: diffusion, transcytosis, filtration, reabsorption

diffusion
-most important

>glucose and O2 more concentrated IN blood > diffuse out
>CO2 and other waste more concentrated in tissue > diffuse INTO blood

-can only occur if: the solute can permeate the plasma membranes of the endothelial cell OR find passages large enough to pass through

-lipid soluble substances: steroid hormones, O2 and CO2 diffuse easily through plasma membranes

-water soluble substances: glucose and electrolytes must pass through filtration pores and intercellular clefts

>large particles: proteins are held back (just like RBCs, they stay in circulation)

transcytosis
-endothelial cells pick up material on one side of plasma membrane by pinocytosis or receptor mediated endocytosis (requires energy for ATP), transport vesicles across cell, discharge material on other side by exocytosis

>important for fatty acids, albumin, and some hormones (insulin)

filtration and reabsorption
-fluid filters OUT of the arterial end of the capillary and osmotically reenters at the venous end > delivers materials to the cell and removes metabolic wastes

-capillaries reabsorb about 85% of the fluid they filter (the other 15% is absorbed by the lymphatic system and returned to the blood)
>>exception: kidney capillaries; alveolar capillaries (in lung) absorb completely to keep fluid out of air spaces

hydrostatic pressure
physical force exerted against a surface by a liquid

EX: blood pressure

blood hydrostatic pressure
the force generated by the pumping action of the heart which helps push fluid and solutes OUT of capillaries

>high on arterial end, low on venous end

colloid osmotic pressure
a pulling force exerted by colloids that help maintain the water content of blood > draws fluid INTO capillary

>results from plasma proteins (albumin) – more in blood

>oncotic pressure = net COP (blood COP – tissue COP)

edema
the accumulation of excess fluid in a tissue > occurs when fluid filters into a tissue faster than it is absorbed

-3 primary causes:
(1) increased capillary filtration – kidney failure, histamine release, old age, poor venous return

(2) reduced capillary absorption – hypoproteinemia, liver disease, dietary protein deficiency

(3) obstructed lymphatic drainage – surgical removal of lymph nodes

consequences of edema
– tissue necrosis – oxygen delivery and waste removal impaired

-pulmonary edema – suffocation threat

-cerebral edema – headaches, nausea, seizures, coma

– severe edema or circulatory shock – excess fluid in tissue
spaces causes low blood volume and low blood pressure

mechanisms of venous return
> the flow of blood back to the heart

-pressure gradient – BP is the most important force in venous return

-gravity – drains blood from head and neck

-skeletal muscle pump in limbs

-thoracic (respiratory) pump – inhalation > thoracic cavity expands and thoracic pressure decreases, abdominal pressure increases forcing blood upward >> blood flows faster w/inhalation

-cardiac suction of expanding atrial space

circulatory shock
any state in which CO is insufficient to meet the body’s metabolic needs

-cardiogenic shock – inadequate pumping of heart (MI)
-low venous return – cardiac output is low because too little blood is returning to the heart

3 principle forms of circulatory shock
(1) hypovolemic shock – most common; loss of blood volume: trauma, burns, dehydration

(2) obstructed venous return shock – tumor or aneurysm compresses a vein

(3) venous pooling (vascular) shock – long periods of standing, sitting or widespread vasodilation
>neurogenic shock – loss of vasomotor tone, vasodilation causes from emotional shock to brainstem injury

other forms of circulatory shock
-septic shock – bacterial toxins trigger vasodilation and increased capillary permeability

-anaphylactic shock – severe immune reaction to antigen, histamine release, generalized vasodilation, increased capillary permeability

compensated shock
-several homeostatic mechanisms bring about spontaneous recovery

-decreased BP triggers baroreflex and production of angiotensin II, both counteract shock by stimulating vasoconstriction

-if person faints and falls to horizontal position, gravity restores blood flow to brain > quicker if feet are raised

decompensated shock
-if compensating mechanisms inadequate, several life-threatening positive feedback loops occur:

>poor cardiac output results in myocardial ischemia and infarction

> slow circulation can lead to disseminated intravascular coagulation

> ischemia and acidosis of brainstem depresses vasomotor and cardiac centers

circulatory routes to brain
-total blood flow to brain fluctuates LESS than that of any other organ
> blood flow can be shifted from one active brain region to another

-brain regulates its own blood flow to match changes in BP and chemistry
> cerebral arteries dilate as systemic BP drops, constrict as BP rises
>main chemical stimulant: pH

transient ischemic attacks
-brief episodes of cerebral ischemia

-often precedes a stroke

stroke (cerebral vascular accident)
-sudden death of brain tissue caused by ischemia
circulatory routes: lungs
-LOW pulmonary blood pressure > flow slower so more time for gas exchange

-engaged in capillary fluid absorption > prevents fluid accumulation in alveolar walls and lumens

-unique response to hypoxia – pulmonary arteries constrict in diseased area & redirects flow to better ventilated region

pulmonary circulation
-pulmonary trunk > pulmonary arteries > lungs > pulmonary veins > return to L atrium
hypertension
-most common cardiovascular disease

-the “silent killer”
> major cause of heart failure, stroke, kidney failure
>> damages heart by increasing afterload
>> renal arterioles thicken in response to stress > drop in renal BP leads to salt retention (aldosterone) and worsens the overall hypertension

-primary hypertension: obesity, sedentary behavior, diet, nicotine

-secondary hypertension: (secondary to other disease) – kidney disease, hyperthyroidism

list the primary functions of the lymphatic system. what do you think would be the most noticeable effect of clamping the right lymphatic duct closed?
-immunity: immune cells stand guard in lymph nodes against foreign matter

-fluid recovery: reabsorb excess fluid and return it to blood

-lipid absorption: in the small intestine, lacteal absorb dietary lipids that are not absorbed by the blood capillaries

>>swelling of the right arm

how does fluid get into the lymphatic system? what prevents it from draining back out?
>by draining out of tissues due to pressure

>endothelial cells prevent flow back into tissue as well as valves

what to NK, T, and B cells have in common? how do their functions differ?
>all 3 are lymphcytes

-NK – immune survalence

-T cells – some direct acquired immune response

-B cells – antibodies

predict the relative seriousness of removing the following organs from a 2-year old:
a) lymph node – nothing

b) spleen – OK but somewhat more vulnerable to infections

c) thymus – never develop immunity – die

d) tonsils – nothing

what are macrophages? give 4 examples and state where they are found
> any cell, other than a leukocyte, that is specialized for phagocytosis – nonspecific second line of defense > they start out as monocytes in the blood then migrate into tissue to phagocytize invaders or debris

1) microglia – CNS
2) alveolar macrophages – lungs (dust cells)
3) hepatic macro. – liver
4) dendritic cells

how do interferons and the complement system protect against disease?
-interferons – proteins secreted by cells when they are infected by viruses > alert neighboring cells and protect them from becoming infected
> bind to surface receptor on those cells & activate 2nd messenger systems within > induces synthesis of antiviral proteins

-complement system – completes the action of antibody – inactive form circulates in blood until activated by the presence of pathogens > contributes to pathogen destruction by: inflammation, immune clearance, phagocytosis, cytolysis

summarize the benefits of fever and the limits of these benefits
1) promotes interferon activity
2) increases MR and accelerates tissue repair
3) inhibits reproduction of bacteria and viruses

-problem: metabolism gets out of balance, delirious, convulsions, coma, brain damage, death

list the cardinal signs of inflammation and state the cause of each
1) redness – hyperemia or extravasated erythrocytes (cells that have left the bloodstream; sunburn)

2) swelling – increase fluid filtration from capillaries

3) heat – hyperemia (increased blood flow by vasodilation)

4) pain – from direct injury to the nerves, pressure on the nerves from the edema, stimulation of pain receptors by prostaglandins

how does specific immunity differ from nonspecific defense
1) specificity – immunity is directed against a particular pathogen

2) memory

how does humoral immunity differ from cellular immunity?
-HUMORAL – (antibody mediated) – employs antibodies, effective against extracellular invaders

-CELLULAR – (cell mediated) – cells directly attack, works against intracellular invaders

contrast active and passive immunity. give a natural and an artificial example of each
-ACTIVE – body makes own antibodies or T cells against a pathogen

> natural – production of antibodies or T cells as a result of natural exposure to pathogen
> artificial – prod. of T cells or antibodies as a result of vaccination against a disease

-PASSIVE – body acquires them from another person or animal that has developed immunity to the pathogen

> natural – fetus acquiring them from mother, baby from breast milk
> artificial – injection of an immune serum (snake bites)

what structural properties distinguish antigenic molecules from those that are not antigenic?
LARGE – over 10,000 amu complex
what is an immunocompetent lymphocyte? what does a lymphocyte have to produce in order to become immunocompetent?
> capable of recognizing antigens presented to them by APC

> have surface antigen receptors

what role does the thymus play in the life history of a T cell?
it is the “school” where the T cell is educated to learn self and foreign antigens – also where it is killed if it fails to learn lessons
what role does an antigen-presenting cell play in the activation of a T cell?
process antigens so it can be recognized by T cells
name 3 types of lymphocytes that are involved in cellular immunity. which of these is also essential to humoral immunity?
1) cytotoxic – carry out attack

2) helper – promote action of Tc cells *play key roles in humoral immunity*

3) regulatory – limit immune response by inhibiting multiplication and cytokine secretion

what are the 3 phases of an immune response
1) recognition
2) attack
3) memory

OR > recognize, react, remember

explain why cytotoxic T cells are activated by a broader range of host cells than are helper T cells
Tc respond to any nucleated cell in body

Th cells respond only to MHC-II proteins, which occur only on APCs

describe some ways in which cytotoxic T cells destroy target cells
– use chemicals > perforins and granzymes > trigger apoptosis

-interferons stop viral replication, activate macrophages

what is the difference between a B cell and a plasma cell
plasma cells are B cells that make antibodies
describe 4 ways in which antibody acts against an antigen
1) neutralization – neutralize part of a toxin

2) complement fixation – bind to complement – changes enemies shape and exposes their complement-binding sites

3) agglutination –

4) precipitation – attract phagocytitic cells for clearance

why does the secondary immune response prevent a pathogen from causing disease, while the primary immune response does not?
the primary response only leaves an immune memory of the antigen

-the secondary response is quicker and stronger so it is gone before you get sick

how does subacute hypersensitivity differ from acute hypersensitivity? give an example of each
-ACUTE – immediate, response is rapid
> bee sting

– SUBACUTE – slower onset, longer lasting
> lupus

aside from the time required for a reaction to appear, how does delayed hypersensitivity differ from acute and subacute types?
it involves Tc not antibodies
state some reasons why antibodies may begin attacking self-antigens that they did not previously respond to. what are these self-reactive antibodies called?
-reasons: cross reactivity, abnormal exposure of self-antigens to the blood, change in structure of self-antigens

> autoantibodies

what is the distinction between a person who has an HIV infection and a person who has AIDS
AIDS – have HIV but their Th count in below 200uL
how does a reverse transcriptase inhibitor such as AZT slow the progress of AIDS
a reverse transcriptase uses the viral RNA as a template to synthesize DNA >> opposite of usual genetic transcription
> prevents virus from reproducing
amount of bacterial cells in the body
the body harbors about 10,000 times as many bacterial cells as human cells
immune system
not an organ system but a population of cells that inhabit all of our organs and defend the body from agents of disease
lymphatic system
network of organs and vein-like vessels that recover fluid

> inspect it for disease agents
> activate immune responses
> return the fluid to the bloodstream

functions of the lymphatic system
1) fluid recovery – fluid continually filters from the blood capillaries into the tissue spaces

2) immunity – excess filtered fluid picks up foreign cells and chemicals from the tissues > passes through lymph nodes where immune cells stand guard against foreign matter > activate a protective immune response

3) lipid absorption – lacteals in small intestine absorb dietary lipids that are not absorbed by the blood capillaries

components of the lymphatic system
-lymph – recovered fluid

-lymphatic vessels – transport the lymph

-lymphatic tissues – composed of aggregate of lymphocytes and macrophages that populate many organs in the body

-lymphatic organs – defense cells are especially concentrated in the organs; separated from surrounding organs by connective tissue capsules

lymph
-clear, colorless fluid, similar to plasma, but much less protein

– extracellular fluid drawn into lymphatic capillaries

lymphatic capillaries
-penetrate nearly every tissue of the body (absent from CNS, cartilage, cornea, bone and bone marrow)
lymphatic vessels
large vessels with valves, which collect and carry lymph to lymph nodes
route of lymph flow
lymphatic capillaries, collecting vessels (course through many nodes), six lymphatic trunks (drain major portions of body) , two collecting ducts: right & thoracic, subclavian veins
mechanisms of lymph flow
lymph flows at low pressure and slower speed than venous blood
natural killer cells (NK)
large lymphocytes that attack and destroy bacteria, transplanted tissue, host cells infected with viruses or have tuned cancerous

-responsible for immune surveillance

T cells
mature in thymus
B cells
activation causes proliferation and differentiation into plasma cells that produce antibodies
macrophages
large, phagocytic cells of the connective tissue

-phagocytize tissue debris, dead neutrophils, bacteria, and other foreign matter

-process foreign matter and display antigenic fragments to certain T cells alerting the immune system to the presence of the enemy

> APCs

dendritic cells
branched, mobile APCs

-alert immune system to pathogens that have breached their surface

reticular cells
act as APCs in the thymus
diffuse lymphatic tissue
-simplest form

-lymphocytes are scattered, rather than densely clustered

-prevalent in body passages open to the exterior – respiratory, digestive, urinary, reproductive tracts

lymphatic nodules (follicles)
-dense masses of lymphocytes and macrophages that congregate in response to pathogens

-constant feature of the lymph nodes, tonsils, and appendix

lymphatic organs
-have well defined anatomical sites

-primary lymphatic organs – red bone marrow, thymus
> site where T and B cells become immunocompetent (able to recognize and respond to antigens)

-secondary lymphatic organs – lymph nodes, tonsils, and spleen > immunocompetent cells populate these tissues

red bone marrow
-involved in hemopoiesis and immunity

-highly vascular material
-separated from osseous tissue by endosteum of bone
-as blood cells mature, they push their way through the reticular and endothelial cells to enter the sinus and flow away in the blood stream

thymus
-member of the endocrine, lymphatic, and immune systems
-houses developing lymphocytes
-secretes hormones regulating their activity

-reticular epithelial cells seal off cortex from medulla forming blood-thymus barrier

lymph node
-the most numerous lymphatic organs
-about 450 in young adult

-cleanse the lymph
-act as a site of T and B cell activation

-parenchyma divided into cortex and medulla
> germinal centers where B cells multiply and differentiate into plasma cells

lymph node locations
-cervical – monitor lymph coming from head and neck

-axillary – receive lymph from upper limb and female breast

-thoracic – receive lymph from mediastinum, lungs, and airway

-abdominal – monitor from urinary and reproductive systems

-intestinal and mesenteric – monitor from digestive tract

-inguinal – receive lymph from entire lower limb

-popliteal – receive from the leg proper

lymphadenopathy
collective term for all lymph node diseases
metastasis
phenomenon in which cancerous cells break free from the original, primary tumor, travel to other sites in the body, and establish new tumors

-tend to lodge in the first lymph node they encounter > multiply there and eventually destroy the node > tend to spread to the next node downstream

>>treatment of breast cancer is lumpectomy – mastectomy along with removal of nearby axillary nodes

tonsils
patches of lymphatic tissue located at the entrance to the pharynx

-guard against ingested or inhaled pathogens
-each covered with epithelium
-have deep pits lined with lymphatic nodules

3 main sets of tonsils
1) palatine – most often infected

2) lingual – at root of tongue

3)pharyngeal (adenoid) – single tonsil on wall of nasopharynx

spleen
-body’s largest lymphatic organ

-2 types of tissue:
1) red pulp – sinuses filled with erythrocytes
2) white pulp – lymphocytes, macrophages surrounding small branches of splenic artery

-FUNCTIONS: blood production in fetus, blood reservoir, erythrocyte “graveyard”, white pulp monitors blood for foreign antigens

-highly vascular and vulnerable to trauma and infection

pathogens
environmental agents capable of producing disease

-infectious organisms, toxic chemicals, radiation

3 lines of defense against pathogens
1) 1st line – external barriers, skin, mucous membranes

2) 2nd line – several nonspecific defense mechanisms
> leukocytes and macrophages, antimicrobial proteins, immune surveillance, inflammation, fever
> effective against a broad range of pathogens

3) 3rd line – IMMUNE SYSTEM > defeats a pathogen and leaves the body a “memory” so it can defeat it faster in the future

nonspecific resistance
guards equally against a broad range of pathogens

-their effectiveness does NOT depend on prior exposure
-skin and mucous membranes
-leukocytes and macrophages, antimicrobial proteins, immune surveillance, inflammation, fever

immunity
-specific defense because it results from prior exposure to a pathogen

-usually provides future protection only against that particular one

antimicrobial proteins
proteins that inhibit microbial reproduction and provide short-term, nonspecific resistance to pathogenic bacteria and viruses

-interferons
-complement system

interferons
secreted by certain cells infected by viruses

-of no benefit to the cell that secretes them

-alert neighboring cells and protect them from becoming infected

complement systems
proteins in the blood that help antibodies and T cells kill their target

-synthesized mainly by the liver
-circulate blood in inactive form
-activated by presence of pathogen

4 methods of pathogen destruction
1) inflammation – mast cells and basophils secrete histamine and other inflammatory chemicals > activates and attracts neutrophils and macrophages > speed pathogen destruction in inflammation

2) immune clearance – principal means of clearing foreign antigens from the bloodstream

3) phagocytosis – bacteria, viruses and pathogens are opsonized – microbial cell coated and serves as binding sites for phagocyte attachment

4) cytolysis – complement proteins are split, bind to enemy cell > attract more complement proteins > membrane attack complex forms (forms a hole in target cell > electrolytes leak out, water flows in rapidly and cell ruptures

3 routes of complement activation
1)classical pathway – requires antibody to get started; part of specific immunity; antibody binds to antigen on surface of the pathogenic organism (forms antigen-antibody complex), changing shape of antibody & exposing a pair of complement-binding sites

2) alternative pathway – nonspecific, does not require antibody

3)lectin pathway – lectins: plasma proteins that bind to carbohydrates

immune surveillance
-NK cells continually patrol the body on the lookout for pathogens and diseased host cells

-NK cells attack and destroy > bacteria, cells of transplanted organs, cells infected with viruses, and cancer cells
>>NK binds to enemy cell > release perforins (create a hole in plasma membrane) and secrete granzymes (protein degrading enzyme > induce apoptosis)

Reye syndrome
serious disorder in children younger than 15 following an acute viral infection such as chicken pox or influenza

>swelling of brain neurons
>fatty infiltration of liver and other viscera
>pressure of swelling brain
>nausea, vomiting, disorientation, seizures, coma

>> can be triggered by the use of aspirin to control fever

inflammation
local defensive response to tissue injury of any kind, including trauma and infection

>general purposes:
-limit spread of pathogens, then destroys them
-remove debris from damaged tissue
-initiate tissue repair

>4 cardinal signs: redness, swelling, heat, pain

cytokines
class of chemicals that regulate inflammation and immunity

-secreted mainly by leukocytes
-alter physiology/ behavior of receiving cell

process of inflammation
1)mobilization of body defenses – most immediate requirement for dealing with tissue injury is to get the defensive leukocytes to the site quickly
>local hyperemia – increase bloodflow beyond normal
>vasoactive chemicals dilate local blood vessels
>selectins – cell-adhesion molecules aid in recruitment of leukocytes

2)containment and destruction of pathogens – prevent the pathogens from spreading throughout the body
>fibrinogen filters into tissue fluid clots, forms sticky mesh that walls off microbes
>heparin prevents clotting
>neutrophils (chief enemy of bacteria) accumulate at injury site w/in the hour (exhibit chemotaxis after leaving bloodstream)

3)tissue cleanup and repair – monocytes (macrophages once enter tissue)
>edema – swelling compresses veins and reduces venous drainage, forces open valves of lymphatic capillaries promoting lymphatic drainage
>pus – accumulation of dead neutrophils, bacteria, cellular debris

tissue repair
-platelet-derived growth factor – secreted by blood platelets

-hyperemia delivers oxygen, amino acids, other necessities for protein synthesis

-increased heat increases metabolic rate

-fibrin clot forms scaffold for tissue reconstruction

-pain makes us limit the use of a body part so it has a chance to rest and heal

antigen
any molecule that triggers an immune response

-large molecular weights of over 10,000 amu

-complex molecules with structures unique to the individual
>can distinguish “self” from foreign

epitopes
antigenic determinants – certain regions of an antigen molecule that stimulate immune responses
haptens
too small to be antigenic in themselves

-must combine with a host macromolecule
-create a unique complex that the body recognizes as foreign

>cosmetics, detergents, industrial chemicals, poison ivy, animal dander
>penicillin

life cycle of T cells
1) BORN in red bone marrow > released into the blood as still undifferentiated stem cells that colonize the thymus

2) MATURE in thymus
>negative selection – T cells that fail tests must be eliminated >> 2% of T cells leave thymus

3) DEPLOYMENT – naive T cells leave thymus and colonize lymphatic tissues and organs everywhere in the body

B cells
-group fetal stem cells remain in bone marrow and develop into B cells

-leave bone marrow and colonize same lymphatic tissues and organs as T cells

antigen-presenting cells (APCs)
-T cells cannot recognize their antigens on their own so APCs help

-function depends on major histocompatibility complex proteins > act as ID tags that label every cell of your body as belonging to you

antigen processing
APC encounters antigen > internalizes it by endocytosis > digests it into molecular fragments > displays relevant fragments (epitopes) in the grooves of the MHC protein
cellular immunity
CELL-MEDIATED – a form of specific defense in which the T lymphocytes directly attack and destroy diseased or foreign cells, and the immune system REMEMBERS the antigens and prevents them from causing disease in the future

-involves 4 classes of T cells: cytotoxic, helper, regulatory, memory

cytotoxic (Tc) cells
-killer T cells

-carry out attack on enemy cells

helper T (Th) cells
GENERALS – makes decisions/ plan of attack
regulatory T (Tr) cells
-calms things down after battle so things don’t get killed that are supposed to be there

-limit immune response
-inhibit multiplication and cytokine secretion by other T cells

>>important in pregnancy – “hangs out” around placenta so body does not attack baby

memory T (Tm) cells
responsible for memory in cellular immunity

-descend from Tc cells

immunity – recognition
-antigen presentation
>APC encounters and processes an antigen > migrates to nearest lymph node > displays it to the T cells > when T cell encounters its displayed antigen on the MHC protein, the initiate the immune response:
> MHC-I proteins – “this is what I am making” – occur on every nucleated cell in the body

>MHC-II proteins – “this is what we are killing” – occur only on APC and display only foreign antigens

-T cell activation
>begins when Tc or Th binds to a MHCP displaying an epitope that the T cell is programmed to recognize
>T cell must check twice to see if is is really bound to a foreign antigen > COSTIMULATION >> successful costimulation will trigger clonal selection

immunity – attack
-Tc cells are the only T cells that directly attack other cells

-when Tc cell recognizes a complex of antigen and MHC-I protein on a diseased or foreign cell it “docks” on that cell > delivers a lethal hit of toxic chemicals > goes off and searches for another enemy cell while chemicals do their work

immunity – memory
-immune memory follows primary response

-following clonal selection, some Tc and Th cells become memory cells

-T cell recall response

humoral immunity
-more indirect method of defense that cellular immunity

-B lymphocytes produce antibodies that bind to antigens and tag them for destruction by other means

>recognition: activation begins when an antigen binds to several surface receptors > links them together > taken into cell by receptor-mediated endocytosis > B cell processes the antigen > links some of the epitopes to its MHC-II proteins > displays these on the cell surface

>attack: antibodies bind to antigen, render it harmless or tag it for destruction

>memory: some B cells differentiate into memory cells

immunoglobulin
an antibody is a defensive gamma globulin found in the blood plasma, tissue fluids, body secretions, and some leukocyte membranes