Koofers

Human Physiology Final - Flashcards

Flashcard Deck Information

Class:KINE 304 - Human Physiology
Subject:Kinesiology & Hlth Sciences
University:William and Mary
Term:Spring 2010
- of -
INCORRECT CORRECT
- INCORRECT     - CORRECT     - SKIPPED
Shuffle Remaining Cards Show Definitions First Take Quiz (NEW)
Hide Keyboard shortcuts
Next card
Previous card
Mark correct
Mark incorrect
Flip card
Start Over
Shuffle
      Mode:   CARDS LIST       ? pages   PRINT EXIT
Heart contraction of cardiac muscle
Myocardium heart muscle; shares similarities w/ both skeletal and smooth muscle; appearance is striated (I & A bands, Z & M lines, H zones); cross bridge formation initiated by binding of Ca++ w/ troponin; myocardiocites are smaller than sk. muscle cells (mononucleated)
Manner in which Ca++ increase different from skeletal muscle SR less developed than in sk. muscle; T-tubular network more developed than in sk. muscle; AP spreads thu T-tubules & releases Ca++ from SR (most Ca++ from SR); influx of extracellular Ca++ also binds w/ troponin (force of contraction dependent upon influx of extracellular Ca++); during re-polarization Ca++ channels close and pumps move Ca++ back into SR and extracellular fluid
Excitation of Myocardium caused by depol. of cell membrane; resting membrane potential of most myocardial cells: -85 to -95 mV; depol. of membrane potential results in AP; in myocardium, depol. caused by two types of voltage gated channels: 1. fast Na+ channels 2. slow channels (Ca++ and Na+ channels), *slow channels important in that they cause "plateau effect: of AP, and also bc Ca++ influx can directly participate in contractile processes, plateau important bc it prevents summation of twitches (duration of AP = that of twitch); repol. caused by closing of slow channels & opening of K+ channels
Generated by Koofers.com
What causes AP in myocardium? certain regions of heart contain specialized myocardial cells capable of spontaneously & rhythmically depol. (pacemaker pot.--self excitation); How: "resting" membrane pot. of cells at SA node is -55 to -60 mV (at this pot. fast Na+ channels inactivated); membranes of these cells more permeable to Na+ & Ca++; membrane pot. grad. depol. to threshold pot. of -40; slow channels open for ~150ms; repol caused by closing of slow channels & opening of K+ channels; repol. about efflux; ryanodine receptors open Ca++ channels on SR (activated by increased Ca++ in cytosol (from extracellular)
what causes AP in myocardium (2) when membrane potential goes back down to -55 to -60mV, K+ channels close; natural "leakiness" of membrane allows pot. to gradually depol. until once again threshold potential is reached; natural rhythmicity of pp occurs at rate of 100/min; typically SA node is pacemaker for rest of heart;
how does electrical excitation generated at SA node spread throughout heart? pp spreads to other cell membranes to cause regular AP via intercalated disks (gap junctions); electrical resistance at junctions is much lower than that of rest of cell membrane; gap junctions w/in intercalated disks allow diffusion of ions from membrane of one myocardial cell to membrane of adjacent one; results in functional syncytium; yet all myocardial cells of heart do not contract simultaneously; have 2 functional syncytiums: 1. atrial, 2. ventricular; contractions of atria & ventricles are staggered (enables ventricles to properly fill w/ blood b4 they contract, allows heart as effective pump)
how does the delay in spreading of electrical excitation from atria to ventricles occur? fibrous tissue separating the two; electrical excitation spread from atria to ventricles via AV node; AV node is specialized cluster of conducting cells at base of right atrium that crosses fibrous tissues; as AP passes thru AV node, it is delayed b4 it passes thru AV bundle & on to bundle of His & purkinje fibers to excite ventricular myocardium
Generated by Koofers.com
The heart as a pump heart actually functions as two separate pumps
cardiac output (Q): amount of blood ejected by each ventricle per min; Q = HR x SV(stroke volume); at rest, ~5 liters/min (72bpm x .07 liters/beat); have 5-6 liters of blood; during exercise, Q can increase to 35 liters/min
How does heart increase cardiac output(Q)? 2 primary methods by which Q is regulated: 1. intrinsic regulation (change in end diastolic vol.), 2. regulation by autonomic nervous system (HR) + (SV), (also by hormones--epi); heart rate: pacemaker of SA node is 100bpm, but heart receives sympathetic (norepi) & parasympathetic (or vagal) input (Ach); sympathetic increases heart rate, parasympathetic decreases heart rate; neural input also affects rate of conduction of AP thru AV junction; chronotropic (influencing heart rate); stroke volume
stroke volume 1. same neurotransmitters (Ach & norepi) affect force of contraction of myocardium, 2. starling's law--as end diastolic vol. increases, so does SV (force contraction increases b/c of change in length of sarcomere; regulated by venous return; 3. hormones (epi) increase contractility of myocardium; ejection fraction used to measure effectiveness of pump; inotropic (influencing contractility)
Generated by Koofers.com
Blood flow through vessel determined by: 1. pressure difference b/t 2 ends of vessel; 2. resistance to blood flow (a. diameter of vessel, b. length of vessel, c. viscosity of fluid); BF=diff in press./resistance
3 basic principles to control blood flow 1. blood flow to each tissue accurately controlled in relation to tissue needs (needs can increase 20-30x, but Q can only increase ~7x); 2. Q regulated by sum total of local tissue flow (as EDV increases, so does Q); 3. arterial pressure can be regulated independently of local blood flow control or Q control (if pressure decreases it can be restored by constricting arterioles and contracting large venous reserves)
Vascular system determines where blood is needed; functional components: a)arteries (big pipes), b) aterioles (smaller pipes), c) capillaries (smaller), d) venules (getting bigger), e)veins (big again); (pressure progressively decreases)
Arteries transport blood under increased pressure to tissues; strong walls w/ elastic qualities (compliant); large vessels w/ decreased resistance; increased pressure vessels (changes during cardiac cycle): pulse pressure=diff b/t systolic & diastolic pressure, Mean Arterial Pressure considered average (MAP=DP+1/3PP) ~93mm Hg
Generated by Koofers.com
Arterioles small branches of Arterial system; strong muscular walls (allow constriction/relaxation); act as control valves to regulate BF to capillaries; increased pressure vessels, but less than arteries; MAP ~35mm Hg; resistance to BF regulated by smooth muscle,
How is resistance to BF regulated by smooth muscle? a) local control--decreased O2, increased CO2, increased H+ cause vasodilation & decreased resistance (relationship b/t activity of tissue & BF), b) extrinsic control--1. neural effects-sympathetic nervous system (norepi) can cause vasodilation/vasoconstriction, 2. hormonal effects-epi can cause vasoconstriction/vasodilation
Capillaries exchange of gases, nutrients & metabolic byproducts (1 arteriole splits into many caps); thin walls w/ no elastic qualities & no smooth muscle; smaller diameter vessels; walls are very permeable; flow rate decreases when passing thru caps (increased transit time--a good thing, gets more O2 out of red blood cells); most substances (O2, CO2) pass across cap walls via passive diffusion, w/ interstitial fluid, but hydrophilic substances cross membrane either thru water filled channels or by carrier mediated transport; can increase rate of passive diffusion by increasing [] gradient of by hyperemia
hyperemia greater blood flow
Generated by Koofers.com
Venules diameters greater than those of capillaries and arterioles; walls are thinner and have much weaker muscular coat than those in arterioles; but pressure also much less, so venules still significantly contract
Veins return blood to heart; decreased resistance due to increased diameter & compliance of walls; avg pressure ~10mm Hg; act as blood reservoirs; walls have little smooth muscle yet venous pressure & rate of return of blood to heart can be regulated: 1. smooth muscle innervated by sympathetic nervous system (decreased diameter & compliance), 2. venous (muscle) pump (pulmonary pump); rate of venous return greatly affects Q; as total BF demand by tissues increases so must venous return
blood avg human has ~5.5 liters; composed of liquid & several different types of cells; plasma-liquid component (~55% of total volume); plasma also contains several diff types of proteins;
proteins in plasma a) albumins--most abundant, formed in liver, act as binding/carrier proteins, b) globulins--several functions (clotting factors, enzymes, antibodies), c) fibrinogen--blood clotting (hormones, metabolites)
Generated by Koofers.com
blood cells A) leukocytes (WBC)--involved w/ the immune response (monocytes, neutrophils), B) platelets--cell fragments, involved in blood clotting (coagulation), C) erythrocytes (RBC)--specialized to transport O2 from lungs to tissues
Erythrocytes HCT (hematocrit value) ~45% in males & 42% in females; very small and easily deformed; shaped as biconcave disk (can fold to squeeze thru cap); contain hemoglobin (Hb), carries O2; Hb molecule consists of 4 subunits (allosteric binding); each subunit contains a heme (Fe containing-binds O2) & polypeptide chain (globin-binds CO2); Hb content is 16g/dl in men & 14g/dl in women; blood about 20% saturated with O2; each gram Hb combines w/ 1.4 ml of O2, so 1dl (100ml) carries ~20ml of O2
Growth and formation of Erythrocytes pluripotent stem cells produced in b marrow; become "committed stem cells;" differentiate into "proerythroblast;" continues to differentiate-produces Hb, nucleus shrinks & extruded (live 4 mos), lose other organelles; differentiated (adult) RBC leaves marrow/enters circulation; RBC prod. reg. by tissues oxygenation; tissue ox. affects erythroprotein prod. (mainly synth in kidneys- stimulates proliferation & differentiation); have enzymes that make ATP; become fragile and rupture passing thru caps; Hb released broken down (bilirubin); Fe released intact/carried by transferrin to marrow to liver where stored as ferritin
Anemia 1. decreased HCT (low % of RBC in whole blood); 2. decreased Hb content of RBCs; 3. combination
Generated by Koofers.com
Respiration exchange of gases b/t organism & its environment; in large organism, 2 sites of respiration: 1. b/t blood and alveolar air (external), 2. between blood and cells of body (internal); lungs surrounded by pleural sac (pressure b/t pleural sac & lung is -4mm Hg--intrapleural or intrathoracic pressure; 756mmHg, -4 is relative to air); alveolar pressure (press w/in alveoli) is 0mmHg b/t breaths
airway leading to alveoli pharynx-->larynx-->trachea-->bronchi-->bronchioles-->alveoli (lungs)
pleural sac space between lungs & pleura filled with fluid
transpulmonary pressure difference between intrapleural pressure and alveolar pressure; prevents lung from collapsing (walls would stick if collapsed b/c of surfactant lining inner walls of clusters)
Generated by Koofers.com
ventilation exchange of air between atmosphere & alveoli; air moves from increase pressure to decreased pressure; flow=pressure diff/ resistance; Boyle's law: P1 x V1 = P2 x V2 (inverse relationship b/t volume and pressure)
inspiration contraction of diaphragm (drops down) & external intercostal muscles (expands ribcage); increase intrathoracic volume causing decrease in alveolar pressure; air moves from environment to lungs; continues until alveolar pressure = atmospheric pressure
expiration elastic recoil of muscles & connective tissue of thorax; thoracic cavity decreases to original dimensions; decreased volume of lungs, increased alveolar pressure; air moves out of lungs until alveolar pressure = atmospheric pressure; normally expiration is passive
Lung volumes and capacities tidal volume, expiratory reserve volume, residual volume, inspiratory reserve volume, vital capacity, total lung capacity, minute ventilation, anatomic dead space, alveolar ventilation, physiological dead space
Generated by Koofers.com
tidal volume normal resting breathing (~500ml)
expiratory reserve volume amount of air forcibly expired after normal expiration
residual volume amount of air that always remains in the lungs (1000ml)
inspiratory reserve volume amount of air that can be forcibly inspired after normal inspiration (300ml)
Generated by Koofers.com
vital capacity amount of air maximally expired following maximal inspiration (5000ml)
total lung capacity vital capacity (5000ml) + Residual volume (1000ml) = 6000ml
minute ventilation amount of air moved in and out of lungs per minute; tidal volume x respiratory rate = minute ventilation;
Anatomic dead space segment of airways that do not allow gaseous exchange; of 500ml expired from alveoli, ~ 150ml remains in airway passages (deadspace); when inhalation occurs, 150ml left from previous exhalation, only 350ml of fresh air inspired
Generated by Koofers.com
alveolar ventilation volume of "fresh" air entering alveoli per minute; 350ml x 12 breaths/min = 4200ml; (alveolar dead space: alveoli w/ inadequate blood supply)
exchanges of gases in alveoli & tissues during tissue metabolism, O2 consumed and CO2 produced; at cap. of tissues blood loses O2 and gains CO2; relative amounts of O2 consumed and CO2 produced called respiratory quotient (RQ = CO2/O2); RQ depends upon food substrate used to produce ATP (CHO=1, protein=.8, fat=.7); O2 added to pulmonary circulation=O2 consumed by tissues; CO2 leaving pulmonary circulation=CO2 produced by tissue
exchange of gases partial pressures-->Dalton's law: in mixture of gases, pressure of each gas independent of others, total pressure is sum of partial pressures of individual gases; mvmnt of gases dictated by differences in partial pressure, exchange occurs until eqbm reached; atmospheric gas pressures at sea level = 760mmHg; PO2=160mmHg, PCO2=.3mmHg
Gas exchange in Lungs alveolar gas pressures will determine pressures in arterial blood (PO2=105mmHg, PCO2=40mmHg); venous systemic blood gas pressures: (PO2=40mmHg, PCO2=46mmHg--CO2 leave blood to alveoli); differences in partial pressures cause diffusion so that arterial PO2 & PCO2 = alveolar partial pressures (eqbm); to ensure proper gaseous exchange b/t pulmonary cap & alveoli, air supply = blood supply (ventilation=perfusion); w/ internal resp, diffusion of gases occurs b/t cap blood & interstitial fluid
Generated by Koofers.com
Oxygen transport in blood each liter of arterial blood contains ~200ml of O2: 1. dissolved in plasma: ~3ml, 2. reversibly combined w/ Hb (oxyhemoglobin): ~197ml; PO2 in blood determines saturation of Hb w/ O2; metabolic factors can affect O2/Hb dissociation curve (increased temp (Bohr affect) and acidity lower affinity);
CO2 transport in blood each liter of venous blood carries ~40ml of CO2; CO2 much more soluble in H2O than O2 (1. dissolved in plasma & RBC:~10%, 2. combined w/ Hb/other proteins (carbamino compounds): ~30%, 3. carried in form of HCO3-:~60%); (H2O + CO2<-->H2CO3-<-->HCO3- + H+); HCO3- then enters plasma via "chloride shift;" in pulmonary cap. process reversed & plasma CO2 diffuses into alveoli [CO poisoning-->CO has greater affinity for Hb than O2 does, CO crowds out O2)
Regulation of Ventilation breathing pattern controlled by medulla (medullary inspiratory neurons); peripheral (carotid/aortic) & central (medulla) chemoreceptors sensitive to arterial O2, CO2 & [H+]; normally ventilation not controlled by arterial dissolved PO2 (only if PO2 decreases below 60mmHg); only peripheral chemoreceptors sensitive to arterial PO2; PCO2 in arterial blood is major stim. for vent. (2-5mmHg increase in arterial PCO2 doubles ventilation); lung disease causes increase in PCO2 & stimulates ventilation; decreased arterial PCO2, decreased vent. & allows metabolically produced CO2 to build up to normal
Relationship of CO2 to H+ H2O + CO2 <--> H2CO3 <--> HCO3- + H+; ability of CO2 to regulate ventilation mainly due to H+; both at peripheral & central chemoreceptors, but at central receptors play bigger role (70%); other effects increase ventilation during exercise: increased epi, increased temp, increased neural impulses from mvmnt
Generated by Koofers.com
Kidneys & Regulation of water and inorganic ions kidneys comprised of ~2mill independently functioning nephrons; each nephron comprised of glomerulus & long tubule; glomerulus is tuft of capilaries; blood enters glom via afferent arteriole & exits via efferent arteriole; glom surrounded by bowman's capsule (bowmans capsule-->proximal tubule-->loop of henle-->distal tubule-->cortical collecting duct-->medullary collecting duct-->renal pelvis); peritubular cap network (supplied from efferent arterioles)
Major functions of kidneys 1. regulate water content, mineral comp. & pH; 2. excrete endproducts of metabolism; 3. excretion of foreign chemicals (pesticides, preservatives); 4. secrete hormones (erythropoietin, vit D, renin); 5. gluconeogenisis
Three basic processes of Renal system a) filtration (as blood goes thru glomerulus, pushes in bulk thru bowmans capsule), b) reabsorption, c) secretion (things that are to large to filter)
Filtration ~21% of Q passes thru kidneys (1.2 liters/min); glom receives blood from afferent arterioles (high caliber), efferent arterioles are high resistance (high pressure in glom--60mmHg); force resisted by colloid osmotic pressure (27mmHg) & hydrostatic pressure of bowmans space (15mmHg); sum of forces called glomerular filtration pressure; permeability of glom up to 500x greater than other cap. (b/c: endothelial cells perforated by "fenestrae," basement membrane is meshlike, epithelial cells contain "slit pores"); ~20% of plasma in glom filtered to BC; normal GFR ~125 ml/min
Generated by Koofers.com
Mechanism of autoregulation of GFR despite changes in renal blood flow, GFR essentially unchanged: juxtoglomerular complex responsible; mechanism: a)afferent arteriolar vasodilator feedback, b)efferent arteriolar vasoconstrictor feedback; macala densa--specialized region where epithelial cells of tubule contact arterioles
Filtration 2 with decreased ionic conc in filtrate ascending limb (decreased GFR) there is a signal from macula densa causing dilation of afferent arteriole (increased renal blood flow, increased GFR); with decreased ionic conc in filtrate in ascending limb (decreased GFR) macula densa releases renin which indirectly constricts efferent arteriole (Increased GFR)
Reabsorption peritubular capillaries reabsorb >99% of H2O & most electrolytes from filtrate; what causes mvmnt from tubule across epithelial cells into interstitium?: mvmnt of H2O dependent on Na+ transport (most reabsorption occurs at proximal tubule-descending); reabsorption of Na+ is active process (H2O by diffusion); Na+ diffuses from tubular lumen into epithelial cell, then actively transported into interstitium by Na+/K+ pump (secretion of K+ into lumen); Na+/K+ pumps found thruout tubular network; luminal membrane most permeable at proximal tubules (not so tight junctions)
Reabsorption 2 diff segments of tubular network have diff permeabilities to H2O; H2O Reabsorption Network: [descending]: proximal tubule:65%, loops of Henle:15%, [ascending]: distal tubules: 10%, collecting ducts:9.3%, passing into urine: .7%; H2O reabsorption at collecting ducts regulated by ADH;ADH controls # of H2O channels in luminal membrane (increased ADH-increased permeability-increased reabsorption-less peed out); ADH secretion controlled by baroreceptors in aorta & carotid artery (increased pressure decreased ADH) & by osmoreceptors in hypothalamus (dec. osm. dec. ADH)
Generated by Koofers.com
Na+ Reabsorption under hormonal regulation; 1. aldosterone: mineralocorticoid secreted by adrenal cortex (stimulates Na+ reabsorption from collecting ducts, high genetic expression of Na+/K+ pumps (long term)); 2. Renin-Angiotensin system: renins released by juxtaglomerular apparatus. forms antiogensin I, then converted to angiotension II (angiotensin II stimulates aldosterone production). Na+ also undergoes secondary active transport that is responsible for reabsorption of most other substances in filtrate (cotransport: substances pulled along w/ Na+ from lumen into epithelial cell)
Secretion certain substances are transported from interstitium into lumen of tubular network to be excreted in urine; ex: a) K+ via Na+/K+ pumps: as Na+ reabsorbed from filtrate into interstitium, K+ secreted into filtrate from interstitium, b) H+ via countertransport w/ Na+: as Na+ reabsorbed from filtrate into interstitium, H+ secreted into filtrate from interstitium, c) urate via similar exchange mech., d) toxins, additives, etc
Digestion and Absorption occurs w/in gastrointestinal (GI), aka alimentary, tract; tract consists of mouth, pharynx, esophagus, stomach, s. intestine, l. intestine, rectum; accessory glands include: liver, gallbladder, pancreas (secrete into GI to help w/ digestion [exocrine glands])
Digestion processing of ingested foods into molecular forms that can be transferred (absorbed), along w/ H2O & electrolytes, from external envnmnt to body's internal envnmnt, then moved via circulatory system to all cells; mouth to anus: ~15ft; breakdown of complex foodstuffs into smaller, absorbable molecules
Generated by Koofers.com
4 major processes in GI tract motility, secretion, digestion, absorption
Motility muscular contractions (skeletal and smooth) mix & advance contents of GI tract [tone-constant low level contraction of smooth muscle, steady pressure, returns walls to normal size following distension; propulsion-push contents thru tract, speed varies according to function of that segment (esophagus fast, SI slow); mixing-mix foods with digestive juices allowing breakdown, helps absorption by maintaining contact of contents w/in SI w/ walls of SI (rich blood supply allowing absorption)]
Secretion (of GI) exocrine glands secrete digestive juices at specific locations throughout tract; consist of H2O (taken from plasma), electrolytes, specific organic component (enzymes, bile salts, mucus), normally H2O returned back into plasma (o.w. diarrhea)
Digestion of CHOs mainly consume polysaccharides like starch (plants) or glycogen (meats), & cellulose (plants--nondigestible), & some disaccharides (sucrose, lactose); must be broken down into monosaccharides (glucose, fructose, galactose); occurs in mouth and mainly in SI
Generated by Koofers.com
Digestion of Proteins long chains of individual AAs held together by peptide bonds. peptidases breakdown proteins in stomach (highly acidic-pepsin) & SI (other peptidases)
Digestion of Fats (not water soluble); 95% of dietary fats are triglycerides (glycerol backbone w/ 3 FAs); almost all (up to 99%) of digestion of fats occurs in SI (small amounts in stomach); first step is breakdown of fats into small globules (micells); this emulsification requires bile salts (produced in liver, released from gallbladder); after emulsification, most fates broken down into monoglycerides & FAs by lipases (pancreatic, enteric) which can then be absorbed into blood stream; digestion and absorption of fats takes much longer than that of CHOs or proteins
Absorption
Generated by Koofers.com

List View: Terms & Definitions

  Hide All 71 Print
 
Front
Back
 Heartcontraction of cardiac muscle
 Myocardiumheart muscle; shares similarities w/ both skeletal and smooth muscle; appearance is striated (I & A bands, Z & M lines, H zones); cross bridge formation initiated by binding of Ca++ w/ troponin; myocardiocites are smaller than sk. muscle cells (mononucleated)
 Manner in which Ca++ increase different from skeletal muscleSR less developed than in sk. muscle; T-tubular network more developed than in sk. muscle; AP spreads thu T-tubules & releases Ca++ from SR (most Ca++ from SR); influx of extracellular Ca++ also binds w/ troponin (force of contraction dependent upon influx of extracellular Ca++); during re-polarization Ca++ channels close and pumps move Ca++ back into SR and extracellular fluid
 Excitation of Myocardiumcaused by depol. of cell membrane; resting membrane potential of most myocardial cells: -85 to -95 mV; depol. of membrane potential results in AP; in myocardium, depol. caused by two types of voltage gated channels: 1. fast Na+ channels 2. slow channels (Ca++ and Na+ channels), *slow channels important in that they cause "plateau effect: of AP, and also bc Ca++ influx can directly participate in contractile processes, plateau important bc it prevents summation of twitches (duration of AP = that of twitch); repol. caused by closing of slow channels & opening of K+ channels
 What causes AP in myocardium?certain regions of heart contain specialized myocardial cells capable of spontaneously & rhythmically depol. (pacemaker pot.--self excitation); How: "resting" membrane pot. of cells at SA node is -55 to -60 mV (at this pot. fast Na+ channels inactivated); membranes of these cells more permeable to Na+ & Ca++; membrane pot. grad. depol. to threshold pot. of -40; slow channels open for ~150ms; repol caused by closing of slow channels & opening of K+ channels; repol. about efflux; ryanodine receptors open Ca++ channels on SR (activated by increased Ca++ in cytosol (from extracellular)
 what causes AP in myocardium (2)when membrane potential goes back down to -55 to -60mV, K+ channels close; natural "leakiness" of membrane allows pot. to gradually depol. until once again threshold potential is reached; natural rhythmicity of pp occurs at rate of 100/min; typically SA node is pacemaker for rest of heart;
 how does electrical excitation generated at SA node spread throughout heart?pp spreads to other cell membranes to cause regular AP via intercalated disks (gap junctions); electrical resistance at junctions is much lower than that of rest of cell membrane; gap junctions w/in intercalated disks allow diffusion of ions from membrane of one myocardial cell to membrane of adjacent one; results in functional syncytium; yet all myocardial cells of heart do not contract simultaneously; have 2 functional syncytiums: 1. atrial, 2. ventricular; contractions of atria & ventricles are staggered (enables ventricles to properly fill w/ blood b4 they contract, allows heart as effective pump)
 how does the delay in spreading of electrical excitation from atria to ventricles occur?fibrous tissue separating the two; electrical excitation spread from atria to ventricles via AV node; AV node is specialized cluster of conducting cells at base of right atrium that crosses fibrous tissues; as AP passes thru AV node, it is delayed b4 it passes thru AV bundle & on to bundle of His & purkinje fibers to excite ventricular myocardium
 The heart as a pumpheart actually functions as two separate pumps
 cardiac output(Q): amount of blood ejected by each ventricle per min; Q = HR x SV(stroke volume); at rest, ~5 liters/min (72bpm x .07 liters/beat); have 5-6 liters of blood; during exercise, Q can increase to 35 liters/min
 How does heart increase cardiac output(Q)?2 primary methods by which Q is regulated: 1. intrinsic regulation (change in end diastolic vol.), 2. regulation by autonomic nervous system (HR) + (SV), (also by hormones--epi); heart rate: pacemaker of SA node is 100bpm, but heart receives sympathetic (norepi) & parasympathetic (or vagal) input (Ach); sympathetic increases heart rate, parasympathetic decreases heart rate; neural input also affects rate of conduction of AP thru AV junction; chronotropic (influencing heart rate); stroke volume
 stroke volume1. same neurotransmitters (Ach & norepi) affect force of contraction of myocardium, 2. starling's law--as end diastolic vol. increases, so does SV (force contraction increases b/c of change in length of sarcomere; regulated by venous return; 3. hormones (epi) increase contractility of myocardium; ejection fraction used to measure effectiveness of pump; inotropic (influencing contractility)
 Blood flow through vessel determined by:1. pressure difference b/t 2 ends of vessel; 2. resistance to blood flow (a. diameter of vessel, b. length of vessel, c. viscosity of fluid); BF=diff in press./resistance
 3 basic principles to control blood flow1. blood flow to each tissue accurately controlled in relation to tissue needs (needs can increase 20-30x, but Q can only increase ~7x); 2. Q regulated by sum total of local tissue flow (as EDV increases, so does Q); 3. arterial pressure can be regulated independently of local blood flow control or Q control (if pressure decreases it can be restored by constricting arterioles and contracting large venous reserves)
 Vascular systemdetermines where blood is needed; functional components: a)arteries (big pipes), b) aterioles (smaller pipes), c) capillaries (smaller), d) venules (getting bigger), e)veins (big again); (pressure progressively decreases)
 Arteriestransport blood under increased pressure to tissues; strong walls w/ elastic qualities (compliant); large vessels w/ decreased resistance; increased pressure vessels (changes during cardiac cycle): pulse pressure=diff b/t systolic & diastolic pressure, Mean Arterial Pressure considered average (MAP=DP+1/3PP) ~93mm Hg
 Arteriolessmall branches of Arterial system; strong muscular walls (allow constriction/relaxation); act as control valves to regulate BF to capillaries; increased pressure vessels, but less than arteries; MAP ~35mm Hg; resistance to BF regulated by smooth muscle,
 How is resistance to BF regulated by smooth muscle?a) local control--decreased O2, increased CO2, increased H+ cause vasodilation & decreased resistance (relationship b/t activity of tissue & BF), b) extrinsic control--1. neural effects-sympathetic nervous system (norepi) can cause vasodilation/vasoconstriction, 2. hormonal effects-epi can cause vasoconstriction/vasodilation
 Capillariesexchange of gases, nutrients & metabolic byproducts (1 arteriole splits into many caps); thin walls w/ no elastic qualities & no smooth muscle; smaller diameter vessels; walls are very permeable; flow rate decreases when passing thru caps (increased transit time--a good thing, gets more O2 out of red blood cells); most substances (O2, CO2) pass across cap walls via passive diffusion, w/ interstitial fluid, but hydrophilic substances cross membrane either thru water filled channels or by carrier mediated transport; can increase rate of passive diffusion by increasing [] gradient of by hyperemia
 hyperemiagreater blood flow
 Venulesdiameters greater than those of capillaries and arterioles; walls are thinner and have much weaker muscular coat than those in arterioles; but pressure also much less, so venules still significantly contract
 Veinsreturn blood to heart; decreased resistance due to increased diameter & compliance of walls; avg pressure ~10mm Hg; act as blood reservoirs; walls have little smooth muscle yet venous pressure & rate of return of blood to heart can be regulated: 1. smooth muscle innervated by sympathetic nervous system (decreased diameter & compliance), 2. venous (muscle) pump (pulmonary pump); rate of venous return greatly affects Q; as total BF demand by tissues increases so must venous return
 bloodavg human has ~5.5 liters; composed of liquid & several different types of cells; plasma-liquid component (~55% of total volume); plasma also contains several diff types of proteins;
 proteins in plasmaa) albumins--most abundant, formed in liver, act as binding/carrier proteins, b) globulins--several functions (clotting factors, enzymes, antibodies), c) fibrinogen--blood clotting (hormones, metabolites)
 blood cellsA) leukocytes (WBC)--involved w/ the immune response (monocytes, neutrophils), B) platelets--cell fragments, involved in blood clotting (coagulation), C) erythrocytes (RBC)--specialized to transport O2 from lungs to tissues
 ErythrocytesHCT (hematocrit value) ~45% in males & 42% in females; very small and easily deformed; shaped as biconcave disk (can fold to squeeze thru cap); contain hemoglobin (Hb), carries O2; Hb molecule consists of 4 subunits (allosteric binding); each subunit contains a heme (Fe containing-binds O2) & polypeptide chain (globin-binds CO2); Hb content is 16g/dl in men & 14g/dl in women; blood about 20% saturated with O2; each gram Hb combines w/ 1.4 ml of O2, so 1dl (100ml) carries ~20ml of O2
 Growth and formation of Erythrocytespluripotent stem cells produced in b marrow; become "committed stem cells;" differentiate into "proerythroblast;" continues to differentiate-produces Hb, nucleus shrinks & extruded (live 4 mos), lose other organelles; differentiated (adult) RBC leaves marrow/enters circulation; RBC prod. reg. by tissues oxygenation; tissue ox. affects erythroprotein prod. (mainly synth in kidneys- stimulates proliferation & differentiation); have enzymes that make ATP; become fragile and rupture passing thru caps; Hb released broken down (bilirubin); Fe released intact/carried by transferrin to marrow to liver where stored as ferritin
 Anemia1. decreased HCT (low % of RBC in whole blood); 2. decreased Hb content of RBCs; 3. combination
 Respirationexchange of gases b/t organism & its environment; in large organism, 2 sites of respiration: 1. b/t blood and alveolar air (external), 2. between blood and cells of body (internal); lungs surrounded by pleural sac (pressure b/t pleural sac & lung is -4mm Hg--intrapleural or intrathoracic pressure; 756mmHg, -4 is relative to air); alveolar pressure (press w/in alveoli) is 0mmHg b/t breaths
 airway leading to alveolipharynx-->larynx-->trachea-->bronchi-->bronchioles-->alveoli (lungs)
 pleural sacspace between lungs & pleura filled with fluid
 transpulmonary pressuredifference between intrapleural pressure and alveolar pressure; prevents lung from collapsing (walls would stick if collapsed b/c of surfactant lining inner walls of clusters)
 ventilationexchange of air between atmosphere & alveoli; air moves from increase pressure to decreased pressure; flow=pressure diff/ resistance; Boyle's law: P1 x V1 = P2 x V2 (inverse relationship b/t volume and pressure)
 inspirationcontraction of diaphragm (drops down) & external intercostal muscles (expands ribcage); increase intrathoracic volume causing decrease in alveolar pressure; air moves from environment to lungs; continues until alveolar pressure = atmospheric pressure
 expirationelastic recoil of muscles & connective tissue of thorax; thoracic cavity decreases to original dimensions; decreased volume of lungs, increased alveolar pressure; air moves out of lungs until alveolar pressure = atmospheric pressure; normally expiration is passive
 Lung volumes and capacitiestidal volume, expiratory reserve volume, residual volume, inspiratory reserve volume, vital capacity, total lung capacity, minute ventilation, anatomic dead space, alveolar ventilation, physiological dead space
 tidal volumenormal resting breathing (~500ml)
 expiratory reserve volumeamount of air forcibly expired after normal expiration
 residual volumeamount of air that always remains in the lungs (1000ml)
 inspiratory reserve volumeamount of air that can be forcibly inspired after normal inspiration (300ml)
 vital capacityamount of air maximally expired following maximal inspiration (5000ml)
 total lung capacityvital capacity (5000ml) + Residual volume (1000ml) = 6000ml
 minute ventilationamount of air moved in and out of lungs per minute; tidal volume x respiratory rate = minute ventilation;
 Anatomic dead spacesegment of airways that do not allow gaseous exchange; of 500ml expired from alveoli, ~ 150ml remains in airway passages (deadspace); when inhalation occurs, 150ml left from previous exhalation, only 350ml of fresh air inspired
 alveolar ventilationvolume of "fresh" air entering alveoli per minute; 350ml x 12 breaths/min = 4200ml; (alveolar dead space: alveoli w/ inadequate blood supply)
 exchanges of gases in alveoli & tissuesduring tissue metabolism, O2 consumed and CO2 produced; at cap. of tissues blood loses O2 and gains CO2; relative amounts of O2 consumed and CO2 produced called respiratory quotient (RQ = CO2/O2); RQ depends upon food substrate used to produce ATP (CHO=1, protein=.8, fat=.7); O2 added to pulmonary circulation=O2 consumed by tissues; CO2 leaving pulmonary circulation=CO2 produced by tissue
 exchange of gasespartial pressures-->Dalton's law: in mixture of gases, pressure of each gas independent of others, total pressure is sum of partial pressures of individual gases; mvmnt of gases dictated by differences in partial pressure, exchange occurs until eqbm reached; atmospheric gas pressures at sea level = 760mmHg; PO2=160mmHg, PCO2=.3mmHg
 Gas exchange in Lungsalveolar gas pressures will determine pressures in arterial blood (PO2=105mmHg, PCO2=40mmHg); venous systemic blood gas pressures: (PO2=40mmHg, PCO2=46mmHg--CO2 leave blood to alveoli); differences in partial pressures cause diffusion so that arterial PO2 & PCO2 = alveolar partial pressures (eqbm); to ensure proper gaseous exchange b/t pulmonary cap & alveoli, air supply = blood supply (ventilation=perfusion); w/ internal resp, diffusion of gases occurs b/t cap blood & interstitial fluid
 Oxygen transport in bloodeach liter of arterial blood contains ~200ml of O2: 1. dissolved in plasma: ~3ml, 2. reversibly combined w/ Hb (oxyhemoglobin): ~197ml; PO2 in blood determines saturation of Hb w/ O2; metabolic factors can affect O2/Hb dissociation curve (increased temp (Bohr affect) and acidity lower affinity);
 CO2 transport in bloodeach liter of venous blood carries ~40ml of CO2; CO2 much more soluble in H2O than O2 (1. dissolved in plasma & RBC:~10%, 2. combined w/ Hb/other proteins (carbamino compounds): ~30%, 3. carried in form of HCO3-:~60%); (H2O + CO2<-->H2CO3-<-->HCO3- + H+); HCO3- then enters plasma via "chloride shift;" in pulmonary cap. process reversed & plasma CO2 diffuses into alveoli [CO poisoning-->CO has greater affinity for Hb than O2 does, CO crowds out O2)
 Regulation of Ventilationbreathing pattern controlled by medulla (medullary inspiratory neurons); peripheral (carotid/aortic) & central (medulla) chemoreceptors sensitive to arterial O2, CO2 & [H+]; normally ventilation not controlled by arterial dissolved PO2 (only if PO2 decreases below 60mmHg); only peripheral chemoreceptors sensitive to arterial PO2; PCO2 in arterial blood is major stim. for vent. (2-5mmHg increase in arterial PCO2 doubles ventilation); lung disease causes increase in PCO2 & stimulates ventilation; decreased arterial PCO2, decreased vent. & allows metabolically produced CO2 to build up to normal
 Relationship of CO2 to H+H2O + CO2 <--> H2CO3 <--> HCO3- + H+; ability of CO2 to regulate ventilation mainly due to H+; both at peripheral & central chemoreceptors, but at central receptors play bigger role (70%); other effects increase ventilation during exercise: increased epi, increased temp, increased neural impulses from mvmnt
 Kidneys & Regulation of water and inorganic ionskidneys comprised of ~2mill independently functioning nephrons; each nephron comprised of glomerulus & long tubule; glomerulus is tuft of capilaries; blood enters glom via afferent arteriole & exits via efferent arteriole; glom surrounded by bowman's capsule (bowmans capsule-->proximal tubule-->loop of henle-->distal tubule-->cortical collecting duct-->medullary collecting duct-->renal pelvis); peritubular cap network (supplied from efferent arterioles)
 Major functions of kidneys1. regulate water content, mineral comp. & pH; 2. excrete endproducts of metabolism; 3. excretion of foreign chemicals (pesticides, preservatives); 4. secrete hormones (erythropoietin, vit D, renin); 5. gluconeogenisis
 Three basic processes of Renal systema) filtration (as blood goes thru glomerulus, pushes in bulk thru bowmans capsule), b) reabsorption, c) secretion (things that are to large to filter)
 Filtration~21% of Q passes thru kidneys (1.2 liters/min); glom receives blood from afferent arterioles (high caliber), efferent arterioles are high resistance (high pressure in glom--60mmHg); force resisted by colloid osmotic pressure (27mmHg) & hydrostatic pressure of bowmans space (15mmHg); sum of forces called glomerular filtration pressure; permeability of glom up to 500x greater than other cap. (b/c: endothelial cells perforated by "fenestrae," basement membrane is meshlike, epithelial cells contain "slit pores"); ~20% of plasma in glom filtered to BC; normal GFR ~125 ml/min
 Mechanism of autoregulation of GFRdespite changes in renal blood flow, GFR essentially unchanged: juxtoglomerular complex responsible; mechanism: a)afferent arteriolar vasodilator feedback, b)efferent arteriolar vasoconstrictor feedback; macala densa--specialized region where epithelial cells of tubule contact arterioles
 Filtration 2with decreased ionic conc in filtrate ascending limb (decreased GFR) there is a signal from macula densa causing dilation of afferent arteriole (increased renal blood flow, increased GFR); with decreased ionic conc in filtrate in ascending limb (decreased GFR) macula densa releases renin which indirectly constricts efferent arteriole (Increased GFR)
 Reabsorptionperitubular capillaries reabsorb >99% of H2O & most electrolytes from filtrate; what causes mvmnt from tubule across epithelial cells into interstitium?: mvmnt of H2O dependent on Na+ transport (most reabsorption occurs at proximal tubule-descending); reabsorption of Na+ is active process (H2O by diffusion); Na+ diffuses from tubular lumen into epithelial cell, then actively transported into interstitium by Na+/K+ pump (secretion of K+ into lumen); Na+/K+ pumps found thruout tubular network; luminal membrane most permeable at proximal tubules (not so tight junctions)
 Reabsorption 2diff segments of tubular network have diff permeabilities to H2O; H2O Reabsorption Network: [descending]: proximal tubule:65%, loops of Henle:15%, [ascending]: distal tubules: 10%, collecting ducts:9.3%, passing into urine: .7%; H2O reabsorption at collecting ducts regulated by ADH;ADH controls # of H2O channels in luminal membrane (increased ADH-increased permeability-increased reabsorption-less peed out); ADH secretion controlled by baroreceptors in aorta & carotid artery (increased pressure decreased ADH) & by osmoreceptors in hypothalamus (dec. osm. dec. ADH)
 Na+ Reabsorptionunder hormonal regulation; 1. aldosterone: mineralocorticoid secreted by adrenal cortex (stimulates Na+ reabsorption from collecting ducts, high genetic expression of Na+/K+ pumps (long term)); 2. Renin-Angiotensin system: renins released by juxtaglomerular apparatus. forms antiogensin I, then converted to angiotension II (angiotensin II stimulates aldosterone production). Na+ also undergoes secondary active transport that is responsible for reabsorption of most other substances in filtrate (cotransport: substances pulled along w/ Na+ from lumen into epithelial cell)
 Secretioncertain substances are transported from interstitium into lumen of tubular network to be excreted in urine; ex: a) K+ via Na+/K+ pumps: as Na+ reabsorbed from filtrate into interstitium, K+ secreted into filtrate from interstitium, b) H+ via countertransport w/ Na+: as Na+ reabsorbed from filtrate into interstitium, H+ secreted into filtrate from interstitium, c) urate via similar exchange mech., d) toxins, additives, etc
 Digestion and Absorptionoccurs w/in gastrointestinal (GI), aka alimentary, tract; tract consists of mouth, pharynx, esophagus, stomach, s. intestine, l. intestine, rectum; accessory glands include: liver, gallbladder, pancreas (secrete into GI to help w/ digestion [exocrine glands])
 Digestionprocessing of ingested foods into molecular forms that can be transferred (absorbed), along w/ H2O & electrolytes, from external envnmnt to body's internal envnmnt, then moved via circulatory system to all cells; mouth to anus: ~15ft; breakdown of complex foodstuffs into smaller, absorbable molecules
 4 major processes in GI tractmotility, secretion, digestion, absorption
 Motilitymuscular contractions (skeletal and smooth) mix & advance contents of GI tract [tone-constant low level contraction of smooth muscle, steady pressure, returns walls to normal size following distension; propulsion-push contents thru tract, speed varies according to function of that segment (esophagus fast, SI slow); mixing-mix foods with digestive juices allowing breakdown, helps absorption by maintaining contact of contents w/in SI w/ walls of SI (rich blood supply allowing absorption)]
 Secretion (of GI)exocrine glands secrete digestive juices at specific locations throughout tract; consist of H2O (taken from plasma), electrolytes, specific organic component (enzymes, bile salts, mucus), normally H2O returned back into plasma (o.w. diarrhea)
 Digestion of CHOsmainly consume polysaccharides like starch (plants) or glycogen (meats), & cellulose (plants--nondigestible), & some disaccharides (sucrose, lactose); must be broken down into monosaccharides (glucose, fructose, galactose); occurs in mouth and mainly in SI
 Digestion of Proteinslong chains of individual AAs held together by peptide bonds. peptidases breakdown proteins in stomach (highly acidic-pepsin) & SI (other peptidases)
 Digestion of Fats(not water soluble); 95% of dietary fats are triglycerides (glycerol backbone w/ 3 FAs); almost all (up to 99%) of digestion of fats occurs in SI (small amounts in stomach); first step is breakdown of fats into small globules (micells); this emulsification requires bile salts (produced in liver, released from gallbladder); after emulsification, most fates broken down into monoglycerides & FAs by lipases (pancreatic, enteric) which can then be absorbed into blood stream; digestion and absorption of fats takes much longer than that of CHOs or proteins
 Absorption 
36, "/var/app/current/tmp/"