Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
VP Exam 3
| Question | Answer |
|---|---|
| Jost Paradigm - Female | Chromosomal Level: 2X chromosomes (no SRY gene) Gonadal level (no SRY, undifferentiated gonads -> ovaries = LOW testosterone/MIH) Phenotype: internal-loss of Wolffian/no MIH-Mullerian develops, external-no testosterone=no fusion |
| Stages of Estrus | Proestrus Estrus Metestrus Diestrus |
| Proestrus | Egg starts to develop |
| Estrus | Ovulation, receptive to male |
| Metestrus | Avoidance of males (short transitional phase) |
| Diestrus | Pregnancy, or pausing phase (may remain here for the season) |
| Endogenous Cycle | Internally generated cycle, but may still be PARTIALLY regulated by external cues |
| Exogenous Cycle | Cycle triggered by external cues, such as temperature, day length, and food availability |
| Spontaneous Ovulation | Ovulation occurs as part of a regulated time-course at the end of a cycle |
| Induced (Triggered) Ovulation | Ovulation occurs either as potential mate is observed or is induced by copulation |
| Ovulation | ovary must “break through” the wall of the ovary to enter the reproductive tract |
| Uterus Anatomy | Outer layer: myometrium (smooth muscle) Inner layer: endometrium (tissue grows and dies off) |
| Myometrium | smooth muscle (outer layer) portion of the uterus |
| Endometrium | inner layer of the uterus that grows and dies off |
| Cervix | transition from uterus to vagina (birth canal) |
| Ovary: cells | Granulosa cells (nurse cells) Theca cells (interstitial cells) |
| Granulosa Cells | Nurse cells (supply nutrients for developing egg) -1 egg cell surrounded by hundreds of granulosa cells -When egg is released, granulosa cells (corpus luteum/yellow body)->progesterone -release inhibin (short-loop feedback against FSH) |
| Theca Cells | Interstitial cells -Produce testosterone, which moves into granulosa cells, where it is converted to estrogen |
| Gonadotropin-Releasing Hormone (GnRH) | Hormone from hypothalamus that stimulates the anterior pituitary to release FSH and LH |
| Follicle-Stimulating Hormone (FSH) | Signaled by GnRH to be released from the anterior pituitary -Stimulates granulosa cells to convert testosterone to estrogen and produce nutrients |
| Lutenizing Hormone (LH) | Signaled by GnRH to be released from the anterior pituitary -Stimulates Testosterone release (Theca cells) -Causes growth of endometrium |
| Follicle | Egg + ALL surrounding granulosa cells |
| Menstrual Cycle | |
| Menstrual Phase | -Cells of corpus luteum die-> No progesterone produced -Endometrium dies off (LOW progesterone levels), blood appears |
| Early Follicular Phase | Estrogen -Neg. fdbck @ low levels -FSH, LH, GnRH levels constant -Positive fdbck @ high levels -More GnRH-> More LH-> more testosterone-> more estrogen -More GnRH->more FSH->?? Progesterone -Strong inhibitor of GnRH, LH & FSH |
| Late Follicular Phase | -GnRH levels rise, LH increases, theca cells make testosterone -GnRH->FSH stimulates granulosa cells to convert testosterone to estrogen =Neg. fdbck from estrogen=relatively constant LH and FSH =Endometrium grows back under the influence of estrogen |
| Ovulation | Endpoint of LH surge (from positive feedback of estrogen) |
| Luteal Phase | |
| Premotor Cortex | Responds to ex/int stim., coordinates muscle groups Memorized sequences Mirror neurons |
| Mirror Neurons | -The same neurons that are activated in picking something up are also activated in seeing someone else picking something up. -Only activated when there is a deliberate movement -Important in learning, empathy |
| Primary Motor Cortex | Activates muscle groups (axons down the spinal chord), plasticity |
| Cerebral Cortex | -Premotor Cortex + Primary Motor Cortex -involved in movement |
| Carebellum | Error correction signals (muscle coordination/feedback), vestibulocer., spinocer. (balance: eye movements, central muscles for large movement, comm. w/spine), cerebrocer. (comm. w/cerebral cortex, regulates fine controlled movement: speech, face, fingers) |
| Basal Ganglia | Caudate nucleus Putamen Globus pallidus -Controls timing/coordination of voluntary movements -Activity can be measured seconds before a movement (an enormous period of time, physiologically) -chain of inhibitions |
| Chain of Inhibitions | Inhibit the inhibitor, allows excitation of others |
| Cat Experiment | Remove premotor/motor cortexes, but leave brainstem intact. The cat can walk on a treadmill due to Central Pattern Generator (CPG) |
| Central Pattern Generator (CPG) | Neural circuit that develops a rhythmic pattern that underlies a complex behavior and is independent of sensory input -Infants (able to support head): if you allow them to hold onto your hands and move your hands away, they take steps |
| Reflex | -Rapid, predictable motor response to stimulus -Purposeful -Unlearned, involuntary, but can be modified / overridden |
| Components of Reflex Arc | -Stimulus -Sensory receptor -Sensory neuron -[Interneuron] -Motor neuron -Target -Response |
| Spinal Reflex | Refers to synapses located only in the spinal chord. The brain is not part of this reflex, but overrides it (ex: urination). Includes: stretch, deep tendon, flexion, and crossed extension reflexes |
| Stretch Reflex | Prevents muscle over-stratch, aids in balance and posture. -Stim: muscle stretch, resp: contraction -agonistic muscle resp: stretch |
| Flexion Reflex | -Protective response to a noxious stimulus -Coordination of flexors and extensors for withdrawal of limb |
| Crossed Extension Reflex | -Occurs along with flexion reflex -Extension of opposite limb to compensate for withdrawal |
| Skeletal Muscle Fibers | Long, narrow, cylindrical, multi-nucleated cells that travel the length of the muscle and give it a striated appearance |
| Motor Units | Somatic motor neuron + all the muscle fibers it innervates that creates an all-or-nothing contraction Eyes: 3 motor units (small, detailed) -Calf (gastrocnemius): up to 1,000 motor units controlled by one neuron |
| Sarcomere | |
| Myosin | -Thick filament -Dark band: myosin +/- actin -Head: ATPase, makes contact with actin |
| Actin | -Thin filament -Light band: actin only -Tropomyosin - winds around the actin (like a rope), located on the surface of the groove -Troponin – binds calcium, changes shape, moves tropomyosin into the groove |
| Dark Band | Myosin (thick filament) with or w/o actin |
| Light Band | Actin (thin filament) only |
| Tropomyosin | Protein that winds around actin like a rope and sits on the surface of the groove, blocking myosin binding. |
| Troponin | Calcium-binding protein that causes tropomyosin to move into the groove of an active filament in order for myosin to bind |
| Excitation | Action pot. that occurs at neuromuscular junction, where Na+/K+ ligand-gated channels lie. Depolarizes the membrane to trigger an action potential in the muscle fiber. T-tubules allow the action potential to travel closer to the center of muscle fiber |
| Contraction | Calcium binds troponin, which knocks tropomyosin into the groove, myosin binds actin -Rest: ADP+Pi -Attach/Power Stroke: -Release (recovery stroke): ATP |
| Coupling | Action pot. from excitation travels to SR. When voltage-gated Ca++ channels open due to the action potential, Ca++ rushes out of the SR. |
| Muscle Contraction | Excitation (action potential), coupling (SR), contraction (myosin/actin) -Cross-bridge cycling |
| No Calcium (Muscle Contraction) | No attachment (troponin doesn't move tropomyosin into the groove)- no contraction -Limp muscles |
| No ATP (muscle contraction) | No detachment of myosin head from actin filament - rigor mortis -rigid muscles |
| Muscle Energetics | Creatine Phosphate + ADP <-> Creatine + ATP Anaerobic glycolysis <-> Aerobic catabolism |
| Twitch Muscle Fibers | Slow oxidative, fast glycolytic, Fast oxidative |
| Slow oxidative twitch muscle fibers | -Postural muscles (very strong) -Slow ATPase (myosin head) -Many mitochondria, myoglobin (stores oxygen in muscle) -Rich blood supply (dark meat) |
| Fast glycolytic twitch muscle fibers | -Fast ATPase (Quick response, not necessarily strong) -Few mitochondria, myoglobin -Poor blood supply -Become anaerobic very quickly |
| Fast oxidative twitch muscle fibers | -Decently fast, decently strong |
| Stimulus vs. Frequency | High frequency (contraction) -Summation -Increased contractions (stronger) -Fusion (Sustained contractions) ->Tetanus (Smooth, sustained contraction) |
| Tetanus | Smooth, sustained muscle contraction |
| Force vs. Length | Short sarcomeres:Crowded actin fils, myosin heads can’t access the actin -No binding for power stroke=no force Long sarcomeres:Myosin barely overlaps actin=TINY force (actin&myosin can’t make contact) Ideal:max myosin bound to actin, but not too cr |
| Velocity vs. Force | -Light load = fast contraction -Large load = slow contraction -Velocity CAN be negative |
| Universal Gas Law | PV=nRT Increased T increases volume or pressure of the gas |
| Law of Partial Pressures | Total pressure exerted by a gas mixture is the sum total of pressures exerted by individual gases -At high elevations, partial pressure of O2 decreases because the overall pressure decreases (same relative concentration of O2) |
| Gas Solubility | Pressure: increases solubility (soda can) Temperature: decreases solubility (boiling water) Salt: liberates gas (decreases solubility) -Marine organisms have less O2 available than freshwater -plasma |
| Gas Solubility (numbers to know) | O2: 2.2 mmol/L N2: 1.1 mmol/L CO2: 77 mmol/L -All creatures initially lived in the ocean (before evolution to land) -It’s harder for air-breathing animals to get rid of CO2 waste, so we have extra CO2 in our body (Bicarbonate buffer) |
| Convection | Mass (bulk) flow of a gas mixture or aqueous solution Ex: respiration, blood flow, water currents (used by fish) -may be unidirectional or tidal flow |
| Diffusion | Movement of atoms/molecules down their concentration gradient due to random motion -occurs between lungs&blood/blood&tissues |
| Hemoglobin | Oxygen-binding protein (4 subunits, O2 binds to iron) carries O2 from lungs to blood and tissues When not bound to O2, is dark red (bluish), when bound to O2, is bright red. |
| CO2 and O2 Equilibria | =O2+ Hb <-> Hb-O2 =CO2+ H2O <-> H2CO3 <-> H+ + HCO3- (CO2 <-> carbonic acid <-> bicarbonate) -Reaction is driven in a particular direction to maximize CO2 pickup or dropoff at a particular location |
| Gas Exchange Membrane | Thin layer of tissue that separates the external environment and internal tissues. Respiratory structures increase surface area: Lungs/gills |
| Lungs | Invaginated respiratory structure |
| Gills | Exvaginated respiratory structure -may be internal (has a cavity for protection but still projects out) or external |
| Concurrent Gas Exchange | Blood and current in same direction -Fish |
| Countercurrent Gas Exchange | -Advantage: gradient is maintained (no equilibrium) -Blood has been depleted of oxygen, and encounters transfer of oxygen into blood even at the point where water oxygen concentration is low. Potential for higher metabolism (more oxygen extracted) |
| Cross-current Gas Exchange | Blood is at an angle with the current -Not quite as effective as counter-current -When traveling at high speed, it won’t make a difference |
| Ventilation | The convective (mass flow of fluid) movement of air into and out of the lungs (inhalation/exhalation). |
| External Respiration | The diffusion of gases across the gas exchange membrane |
| Gas Transport | The convective movement of gases via the blood |
| Internal Respiration | The diffusion of gases across the gas exchange membrane (blood <-> tissues). |
| Active Ventilation | An animal uses metabolic energy to generate its own ventilator currents -Ram ventilation – constantly moving into an area of higher [oxygen] |
| Passive Ventilation | An animal takes advantage of already existing air or water currents -Often in marine species |
| Breathing in Fish (gills) | Water enters the buccal cavity (mouth), passes over the gills, and exits |
| Breathing in Amphibians | 1.Inspiration:Nares O,glottis C,buccal floor cavity moves down (vol inc, air enters) 2.Inspiration:Nares C, glottis O,Buccal cavity floor moves up(vol dec, pressure inc, air moves to lungs) Expiration:Nares&glottis open,abs contract Gas exch thru skin |
| Breathing in Reptiles | Suction using thoracic and ab muscles -Buccal cavity (digestion) can evolve without ventilator constraints -Lung compression (Elastic lungs passively enlarge) OR Lung expansion (Elastic lungs pass. become smaller) -Energy is only invested one direction |
| Breathing in mammals: summary | Active inspiration, passive expiration, (active expiration) |
| Active inspiration | -External intercostals (between ribs on the outside of the rib cage) contract -Ribs are elevated and sternum flares -Diaphragm moves inferiorly (flattens) |
| Passive Expiration | -External intercostals relax -Ribs and sternum are depressed -Diaphragm moves superiorly (domes up) |
| Active Expiration | -Forceful decrease in the size of thoracic cavity -Abdominal muscles contract (push organs onto the diaphragm, which then moves up) -Internal intercostal muscles contract -allows for a greater inspiratory vol -Occurs during/after exercise |
| External intercostals | muscles between ribs on the exterior |
| Internal intercostals | muscles between ribs in the interior |
| Pre-botzinger complex | Portion of the medulla that interacts with Pons. -Series of stimulatory/inhibitory signals lead to a cycle of breathing -Involuntary, but not autonomic (can be overridden by conscious effort) -Sensitive to CO2 |
| Aortic Arch | Aortic bodies have chemoreceptors (measure pH, etc.) that aid in control of ventilation |
| Carotid Body | Chemoreceptor (measures CO2, pH, etc.) |
| Hyperpnea | Increased ventilation in response to increased O2 need -ncreasing ventilation (depth of breathing) because the body needs it ->After exercise |
| Hyperventilation | Pathological (deliberate or stress-induced) increase in ventilation that is not triggered by the need for O2 -Shallow breathing, decreases the ability to obtain O2 -Expels CO2, which is the signal for oxygen intake |
| Alveoli | Open, rounded space -Thin cell walls – diffusion -Increased surface area -Hydrogen bonds can be a problem, so we have a detergent (surfactant) so that alveoli can expand |
| Surfactant | Detergent made in the last trimester of fetal life that prevents hydrogen bonding of alveoli to each other |
| Bronchioles | Smooth muscle, controlled by ANS -Sympathetic–dilation -Parasympathetic–constriction (to block irritants) |
| Asthma | -Inappropriate constriction of bronchioles ->Inflammation ->Tissue swelling (edema) even at rest ->Pain/sensitivity (Exposure to allergen/temperature trigger) ->Narrow passageway makes it hard to inhale -Parasympathetic stimulation |
| Emphysema | Loss of alveoli that results in reduced surface area for gas exchange -Reduced lung elasticity -Desire to get smaller decreases -Ability to get rid of old air is decreased ->Requires active expiration |
| O2 Partial Pressures at sea level, low humidity (numbers to know!) | -Atmospheric = 152 mmHg -Alveolar (lungs) = 104 mmHg (tidal respiration-mixing old air & new air) -Venous = 40 mmHg (blood coming back to the lungs to pick up oxygen-lowest levels of oxygen) |
| Oxygen levels in plasma | 0.3 ml O2/100 ml |
| Oxygen levels in whole blood | 20 ml O2/100 ml -(Hemoglobin allows for huge metabolism) |
| Hemoglobin Ripple Effect | Binding O2 causes conformational change in one unit, which causes conformational changes in all the other units -Causes sigmoidal curve |
| Fetal Hemoglobin | Contains alpha and gamma forms -stronger affinity for O2 (transfer from mother to fetus) |
| Oxygen Binding Curve | STEEP-Ripple effect:binding oxygen causes other groups to bind more oxygen=Quick transfer (pick-up&drop off in rvrs) PLATEAU:Saturation-At slightly higher elev., dec PP in the air around you&in lungs. Body PO2 sat. No metab change at elev. Edema-sat. |
| Myoglobin Binding Curve | Not sigmoidal due to single protein (no snowball effect) |
| Bohr Effect | A decrease in the O2 affinity of a respiratory pigment -Right or Left shift -Root Effect:some fish ->decrease in the amount of O2 a respiratory pigment can bind at saturation. ->Shift right and down (affects saturation) ->Air bladder (buoyancy |
| Bohr Effect Right Shift | Dec affinity -Dec O2 loading -Inc O2 unloading -Advantageous during higher metabolism -Inc in temperature -Inc CO2, H+ /\ conf of Hb such that it drops off more O2 -O2 is harder to pick up in the lungs -Doesn’t affect plateau (only steep part of c |
| Bohr Effect Left Shift | Increased affinity -Increased O2 loading -Decreased O2 unloading Advantageous in the lungs -We want to drop off only enough oxygen needed -When metabolism is reduced |
| Partial Pressures at sea level, low humidity (numbers to know!) | -Atmospheric = 30 mmHg -Alveolar = 40 mmHg -Venous = 45 mmHg |
| Carbon Dioxide levels in Plasma | 3 ml CO2/100 ml plasma (10x as much can go into plasma than oxygen) -Some also converted to bicarbonate |
| Chloride Shift | The exchange of a Cl- for bicarbonate across the red blood cell membrane. -Enables RBC to pick up or drop off high levels of CO2. -Red blood cells: CO2 -> bicarbonate ion (kicked out into plasma) -Replaced with Cl- (ensures no net charge difference) |
| Chloride Shift in Tissue | -Gets rid of H+ and bicarbonate -Drives the rxn toward CO2 pickup -Prevents accumulation of bicarbonate in the cell -Increases CO2 pick-up |
| Chloride Shift in Lungs | -Cl- shifted out of RBC -Brings bicarbonate back into cell to increase CO2 levels -Increases CO2 drop off |
| Carbon Monoxide | Can bind heme strongly and irreversibly. -Produced by incomplete combustion -Competes with O2 binding to heme group -People with CO poisoning will still look red and alive |
| Gill-breathing fish circulatory system | Sinus venous -> atrium -> ventricle -> bulbous arteriosus -> gills -> systemic tissues ->return to heart (decreasing oxygen content in blood until reaching gills again) -SLOW delivery of oxygen |
| Atrium | Entryway to the heart |
| Ventricle | Pump of the heart |
| Amphibian circulatory system | Arteries -> atrium -> ventricle (pumps simultaneously to body/lungs) -> returns to heart mixed (oxygenated + deoxygenated) -NOT EFFICIENT, but they can absorb O2 through skin |
| Reptilian (non-crocodilian) heart | Body -> atrium -> Right side of ventricle (One ventricle with partial wall) -> pump to lungs -> Left side of ventricle (some mixing, but partial separation of oxygenated/deoxygenated blood)->body |
| Crocodilian Heart | 2 atria, 2 ventricles R-L Shunting (waiting for prey under water for long periods of time) heart -> body (bypasses lungs) |
| Avian/Mammalian Heart | 2 circuits (pulmonary/systemic) to maintain blood pressure. Both ventricles pump the same vol of blood. Most muscle is on the left (L ventricle is stronger=more pressure) -Valves |
| Valve | One-way door, Cup-shaped -Pressure from above-atrium or weight (blood accumulation)=valves open -Pressure from below–closing of valve |
| Pulmonary Circuit | To and from lungs R ventricle -> L atrium (R ventricle -> pulmonary artery -> lungs -> pulmonary veins -> left atrium -> L atrioventricular valve->systemic) |
| Systemic Circuit | To and from body L ventricle -> R atrium (L ventricle -> aorta -> body -> inferior/superior vena cava -> R atrium) -Higher pressure (L ventricle is strong) -Further distance, body upright = fighting gravity to return blood through the heart |
| Circulatory Pathway | Sup vena cava/inf vena cava-> R Atr-> tricuspid valve (R atroventricular valve) [syst circ]-> [pulm circ]: pulm vent-> pulm valve-> pulm artery-> lung-> pulm vein-> L atrium (last pulm circ)-> bicuspid valve-> L vent (syst circuit)-> aortic valve->aorta |
| Superior Vena Cava | Blood from top part of the body |
| Inferior Vena Cava | Blood from the lower part of the body |
| Pacemaker Action Potential (Sinoatrial Node) | Muscle fiber cells: leaky K+ chan, w/time, close (rel perm dec, so K+ current influence dec) -Drifting rest pot Threshold: open Ca2+ chan(most Ca is outside heart) -Depol V-gate K+ channels open -Repol |
| PNS and SNS on Pacemaker Action Potential | PNS:acetylcholine causes leaky K+ channels to close SLOWER SNS:norepinephrine increases the rate of closing of K+ leaky channels (threshold is reached faster) |
| Action potential in contractile muscle fibers | Pace. act pot->open Na+ activ gates -de.Na+ channels inact, V-gate Ca2+ chan open->plateau (Ca2+ influx).Contr (Ca2+ not from SR, but same function).K V-gates open->re. Long act pot:1 per contr(must relax-no sust contr).Prevents tetanus->pump act in hear |
| Sinoatrial Node (SA node) | Beginning of R atrium, shares current to cause both atria to contract simultaneously so blood->ventricles. |
| Atroventricular Node (AV node) | (secondary pacemaker) gets the electrical signal and delays transfer of the signal to the ventricles |
| Electrical Current | SA node shares current w/both atria to cause simultaneous contraction. AV node sends the message between the 2 ventricles (the AV bundle)->Purkinje fibers-> sides of ventricles (creates pressure upward) |
| Purkinje fibers | Myocardial fibers that conduct electrical stimuli to cause heart contraction |
| Electrocardiogram | 3 leads: L/R arm, L leg P wave, ventricular depolarization, T wave |
| P wave | atrial depolarization (SA node generates electric potential, wave spreads, initial charge difference) -You can NOT measure atrial contraction |
| QRS Wave (Ventricular Depolarization) | -Electrical wave causes heart movement -Entire ventricle is in the middle of the cardiac action potential -Doesn’t show atrial repolarization (P wave is much smaller than QRS, like throwing a pebble into a big wave) |
| T Wave | End of the cardiac action potential (relaxation) |
| Heart | Valves C: blood->atria Blood weight press.->AV valves O -Blood->vent, contr to maint press. -Electr sig->bottom of vent&up -AV valves C, semilunar valves O from press. -Ventr relax, press. in ventr dec, aortic/pulm arterial press. inc, semilunar valv |
| Artery | Carries blood from the heart Smooth Muscle -Vasodilation (locally-more blood flow, over body-low bp)/constriction (locally less blood flow, over body-high bp) -Elastic: propels blood forward and helps maintain blood pressure |
| Vein | Carry blood to heart -Distensible for pooling blood -Valves (particularly in lower veins) ->Prevent back-flow ->Help the blood move against gravity |
| Capillary | Site of gas exchange; diffusion of nutrients and wastes. Thin (1-cell thick) walls. -Arteriole -> venoule (Metarteriol) -Precapillary sphincters (no blood flow) -Helps maintain bp: Default=Closed=no “side roads” open=No local diffusion |
| Capillary beds | High metabolism: With CO2 and H+, sphincters relax, capillary beds open, blood moves through, brings in new O2, take out CO2 and H+ -In high temperatures: preferential relaxation of sphincters |
| Cardiac Output Equation | CO (L/m) = HR (b/m) x SV (L/b) |
| Cardiac Output Regulation of Heart Rate | -Sympathetic Nervous System: Epinephrine: increases HR -Parasympathetic Nervous System: Acetylcholine = Slower HR |
| Cardiac Output Regulation of Stroke Volume | -EDV = End Diastolic Volume (Preload): Relaxation of ventricles (maximum ventricle vol) -ESV = End Systolic Volume: Contraction of ventricles (minimum ventricle vol) |
| End Diastolic Volume (EDV) | Depends on length of filling time -Longer = more blood to start with. Depends on venous return (payload) -Blood volume -Vasoconstriction = more blood back to heart -HR -may directly affect stroke volume |
| End Systolic Volume (ESV) | -Stretch of ventricle -Contractility ->Sympathetic causes stronger contraction ->Large afterload (high blood pressure) = hypertension -Heart has to work hard to get blood in |
| Stroke Volume (SV) | |
| Afterload | Pressure that the heart has to pump against |
| Preload | Force/pressure exerted by blood returning to the heart (venous return/EDV) |
| Venous Return | Amount of blood returned by the veins to the heart -Preload -EDV (amount of blood in ventricle at the end of diastole) |
| Increasing Venous Return | -Exercise -Increased sympathetic tone on veins -Slower heart rate (More pooling = more efficient return of blood) |
| Decreasing venous return | faster HR (less pooling = less efficient blood return) |
| Frank-Starling Relation | Stretching of cardiac muscle increases vigor of contraction -Increased preload (EDV) will stretch cardiac muscle -Increased contraction will decrease ESV |
| Changes in End Diastolic Volume | Contractility -Frank-Starling (due to elasticity) -Sympathetic input (stress hormones) Afterload -Force/pressure produced by blood w/in the post-ventricle artery -Inverse relationship between afterload and SV (valves) |
| EDV and SV | Increased EDV may directly increase SV Decreased EDV may directly decrease SV |
| EDV and HR | As HR increases, CO increases -If HR increases too far, we lose filling time ->SV plummets (EDV significantly decreases) ->CO decreases (pass out) |
| Heart Failure | condition in which the heart fails to pump an adequate amount of blood |
| Causes of Heart Failure | Defective valves (incompetence OR stenosis) •Blood goes in the wrong direction-Murmur Arteriosclerosis Chronic hypertension Myocardial Infarct (heart attack) |
| Incompetence | damage of valves so they hyper- extend when closed |
| Stenosis | stiffening of valves due to cholesterol buildup |
| Myocardial Infarct | Heart attack-damaged muscle makes it harder to pump blood into the body |
| Left Heart Failure | Systemic circuit fails -Blood backs up in the pulmonary circuit (capillaries) Pulmonary edema -Fluid in the blood moves into the lungs (diffusion distance decreases) -Effective pO2 decreases -Congestive heart failure |
| Right Heart Failure | Pulmonary circuit fails (not pumping as effectively to lungs) -Blood backs up in the systemic circuit Congestion and edema in the periphery (Lower legs-gravity) |
| Hyperosmotic | Describes a solution that has a higher solute concentration relative to another solution, and therefore gains osmotic pressure as water flows down its concentration gradient |
| Hypertonic | Describes an extracellular environment that has a higher solute concentration than inside the cell, causing the cell to crenate |
| Hyposmotic | Describes a solution that has a lower solute concentration relative to another solution, and therefore loses osmotic pressure as water flows down its concentration gradient |
| Hypotonic | Describes an extracellular environment that has a lower solute concentration than inside the cell, causing the cell to swell and lyse |
| Isosmotic | Describes a solution that has a similar solute concentration relative to another solution, resulting in no net movement of water between the solutions |
| Isotonic | Describes an extracellular environment that has a similar solute concentration as inside the cell, resulting in no net movement of water in or out of the cell |
| Body fluid composition | Extracellular: 1/3 -interstitial (in tissues) -plasma (in blood) Intracellular: 2/3 |
| Body fluid regulation | Input vs. output -volume, ions, (osmolarity) Organs -kidneys, gills, salt glands, lungs |
| Drinking/Environmental Water | MARINE:hypertonic/osmotic, excessive ion absorption, inadequate water FRESHWATER:hypotonic/osmotic, inadequate ions, excessive water absorption TERRESTRIAL: need drinking water |
| Sources of water and salt | Drinking/environmental water Air-dried food metabolic water |
| Air dried foods | Always have some water content -H2O content in seeds, nuts, and grains depends on humidity -Stored underground ( @night, rel humidity inc, water comes out of the air) |
| Metabolic Water | Animals that survive on metabolic water DO NOT produce more metabolic water than other organisms (amt. of water produced by oxid. is fixed by chem) -Better at CONSERVING the water |
| Obligatory Water Loss (types) | Respiratory, Urinary, Fecal |
| Respiratory water loss | Depends on external humidity/breathing method (ex:kangaroo rat) |
| Kangaroo Rat (respiratory water loss) | Water in air -H2O leaves the surface of the mouth & moves into the lungs, temp on the mouth’s surface dec (evap) -air moves past the cool mouth (exhalation), H2O condenses on the mouth MOST OF THE WATER STAYS IN THE RESPIRATORY PASSAGES – NOT LOST TO E |
| Dogs | Panting=deliberately poor at conserving water (evaporative cooling) |
| Urinary Water Loss | Nitrogenous wastes (amino acids and nucleic acids) require water in order to reduce toxicity -Ammonia (toxic) -Urea -Uric acid (non-toxic) |
| Fecal Water Loss | Depends on vol/types of food consumed and type of feces -Pellets: highly dehydrated (conserves water) -Stools: loose, humans have 50% of stools composed of water in a healthy digestive tract |
| Kangaroo rat vs. Lab rat | Metabolic water: no change Urinary: -kangaroo rat-VERY solid pellets (net gain in metabolic water). -lab rat-pellets, but smushy (net loss of metabolic water) |
| U/P | (Urine/Plasma) -Comparison of osmotic pressure of urine to osmotic pressure of blood plasma -Concentration of particles in urine and plasma -Not necessarily the same TYPE of particles -Ratio indicates osmolarity of urine |
| U/P=1 | Isosmotic -Water excreted in same relation to solutes as prevails in blood plasma -Solute excreted in same relation to water as prevails in blood plasma -Plasma osmotic pressure unchanged |
| U/P<1 | Hyposmotic -Water is preferentially excreted -Solutes are preferentially held back from excretion -Plasma osmotic pressure is raised (Higher particle concentration) -Freshwater fish, frogs, etc. |
| U/P>1 | Hyperosmotic -Water is preferentially held back from excretion -Solutes are preferentially excreted -Plasma osmotic pressure is lowered -Keeps water in the body, deliberately gets rid of solutes -Marine organisms, desert and most terrestrial organism |
| Human Osmotic U/P Range | .1-4 Both hyposmotic and hyperosmotic, but usually hyperosmotic |
Created by:
Medgbert
Popular Biology sets