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Physiology Exam 3 Study Guide

by: Sierra Mongeon

Physiology Exam 3 Study Guide BIOS 213

Marketplace > University of Nebraska Lincoln > Biology > BIOS 213 > Physiology Exam 3 Study Guide
Sierra Mongeon
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Hello! Here is the study guide for exam 3! It includes everything except what will be covered on Monday. Enjoy! Pro Study Tip: Wear the same perfume/cologne to class that you wear to exams. Smell...
Human Physiology
Dr. Tony Zera
Study Guide
Physiology, University of Nebraska
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This 11 page Study Guide was uploaded by Sierra Mongeon on Friday April 15, 2016. The Study Guide belongs to BIOS 213 at University of Nebraska Lincoln taught by Dr. Tony Zera in Winter 2016. Since its upload, it has received 153 views. For similar materials see Human Physiology in Biology at University of Nebraska Lincoln.


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Date Created: 04/15/16
BIOS 213 – Exam 3 Study Guide Muscular system Function = contraction, force generation Myo- and Sarco- Types • Skeletal o Striated, multinucleate o Connected to bones via tendons o Voluntary o Paired; antagonistic (extensor/flexor) o Controlled by neural input (NMJ) o Most major muscles of body • Cardiac o Striated, uninucleate, branched o Involuntary o Muscle cells are self-stimulating (spontaneous depolarization), contract as a unit o Only in heart • Smooth o Not striated o Involuntary o Surround organs and tubes (like digestives system, uterus) § Can contract strongly even when stretched!! Structure (skeletal muscle) • Myofiber/muscle fiber = muscle cell • Myofibril = bundle of contractile proteins (actin and myosin; these are myofilaments) • Sarcolemma = muscle cell membrane • Motor unit (MU) = neuron and all muscle fibers (cells) it innervates. o Collateral branches of axon o Large MU= power, large control (thigh) o Small MU = precision (eyeball) • Graded contraction d/t varying numbers motor units activated (recruitment) • Neuromuscular junction = NMJ; where axon and muscle meet o Motor end plate: special region of sarcolemma. Nicotonic ACh receptors here (always excitatory) o Where nerve impulse à muscle contraction The Sarcomere (striated muscle only; it make the striations!) • Basic functional (contractile) unit. • Actin and myosin arrangement = linear, overlapping o Actin = thin o Myosin = thick • I band, H zone, A band, Z disc (draw diagram) How do these change during contraction? Sliding Filament Theory • Filaments themselves don’t shorten. They just overlap/slide past each other. • Powered by ATP • Actin has binding sites for myosin; myosin has heads + tails. o Heads attach to actin = crossbridges • Heads pull on actin = power stroke Muscle Contraction of ONE MYOFIBER: sequence of events -Excitation Contraction Coupling (AP in neuron to cross bridge formation) 1. AP in motor neuron reaches NMJ, causes release of ACh from neuron (synaptic vesicles) 2. ACh binds to receptors (nicotinic; always excitatory) on motor end plate (part of sarcolemma) causing an end plate potential a. EPP = opening of Na+/K+ channels. b. Eventually causes AP in sarcolemma 3. AP conducted across sarcolemma à T-tubules (parts of sarcolemma that dip into muscle fiber, take AP inside) 4. T-tubules act on terminal cisternae of sarcoplasmic reticulum (sacs containing Ca++) and cause them to release Ca++ 5. Ca++ binds to troponin 6. Troponin changes shape à tropomyosin changes shapeàactin binding site exposed a. Allows myosin to form cross bridge 7. ATP attached to myosin hydrolyzed (ADP + P) à cross bridge formed 8. Release of P à power stroke a. ADP falls off after myosin moves 9. Binding of new ATP causes myosin to detach à relaxation a. No new ATP to bind = rigor mortis 10.Ca++ removed by Ca++ ATPase (pump) à back into terminal cisternae *NOTE: one AP only causes small amt. of contraction (twitch). Multiple APs needed for complete contraction This is where recruitment comes in. WHOLE MUSCLE contraction • Muscle twitch = basic unit of contraction o Response of single muscle fiber to single AP o All or none, no change in force (blink of an eye) o Studied in lab = isometric twitch (Fig A) • Differences in types of contractions needed o Differences in force (picking up small object vs. large weight) o Difference in speed/explosiveness (throwing vs. picking up light box) • Differences in contraction achieved by: o Summation of twitches § Frequency of stimulation • High freq= peak tension rises until constant level reached • Step-wise increase in force = treppe • Maximum plateau = tetanus o Differences in muscle fiber type § Diameter: greater = more force (can be trained to increase w/ exercise; why weightlifters have large muscles) § Fast vs. slow twitch o Recruitment of motor units § More MU = more fibers contracting = greater force • As more force is required, bigger motor units recruited § Conscious control! § Responsible for smooth movement § Different sizes of motor units à larger/smaller number of muscle fiber • Small = fine control • Large = gross/coarse control • Neural control of skeletal muscles o Motor neurons: upper and lower § Upper: interneurons in the brain, synapse with lower § Lower: somatic motor neurons. • Cell bodies in brain stem/spinal cord • Synapse directly with muscle cells • Destroyed by ALS o Muscle spindle apparatus § Sensory organ--Muscle length o Golgi tendon organ § Sensory organ--Tension muscle exerts on tendon Exercise Physiology Muscle fiber types: • Slow: aerobic, endurance; slow contraction speed, high myoglobin/mitochondria (red color), thin (so O2 can penetrate) o Myoglobin = oxygen carrying molecule, similar to hemoglobin in blood • Fast: anaerobic, force and speed, fast fatigue, thick, low myoglobin/mitochondria • Genetic – born with a set amount of each, can’t change fast to slow etc. o Many muscles are mixture of both o Marathon runner vs. sprinter • Intermediate fibers: can become more slow/fast-like, trained by exercise Metabolism (catabolism = release of energy) • Aerobic and anaerobic o Aerobic = more efficient (more ATP), requires O2, mitochondria § Low intensity exercise (walking) o Anaerobic; less ATP, no O2 required, in cytoplasm § High intensity (sprinting) • Energy sources: Fat and carbohydrates o Fat = Triglycerides § aerobic only! More energy; preferred. o Carbs= glucose + other sugars, glycogen (complex carb) § both types, but usually used during anaerobic, less energy o Fuel use by muscles during exercise § Low intensity uses fats (aerobic), moderate intensity uses 50/50 combination fats and carbs (combo aerobic/anaerobic), high intensity uses carbs (anaerobic) § Remember: fat is the preferred molecule! (more energy) Measuring exercise intensity 1. VO2 max = “aerobic capacity” a. Limit of aerobic ability; max rate of oxygen use (how much can you do before you’re “winded”?) b. Exercise intensity measured by % of VO2 max c. Training increases VO2 max (cardio system and lungs more efficient at O2 delivery) 2. Lactate Threshold a. % of VO2 max where you start making shift from aerobic to anaerobic (start producing lactic acid) b. usually 50-70% VO2 max i. exercise increases this **Monday’s lecture: study Glycogen depletion Oxygen Debt Other points from handout. Cardiovascular system Function: transport (oxy, nutrients, heat, waste) The heart • Provides force for moving blood through vessels • 4 chambers: right and left atria and ventricles o Atria à blood from veins, pump blood to ventricles o Ventriclesà blood from atria, pump blood into arteries o Veins = back to heart, Arteries = Away • Understand diagram in notes 2 circuits for blood flow 1. Pulmonary – to lungs and back a. Picks up O2, releases CO2 2. Systemic – to rest of body and back a. Provides nutrients, O2 to all organs. b. Picks up CO2 to be taken back to lungs **Know pathways listed in notes Heart Valves Function: Prevent backflow/regurgitation of blood • Atrioventricular (AV): btwn atria and ventricles o Tricuspid –right side o Bicuspid - left side o Open when arial pressure exceeds Vent. pressure • Semilunar (SL); btwn ventricles and major arteries o Pulmonary- rt. Ventricle à pulmonary artery o Aortic- lt. Ventricle à aorta o When Vent. Pressure exceeds artery pressure Heart sounds are produced by the closing of these valves 1 sound = AV valves closing 2 ’ = SL closing 1. Systole: Ventricles CONTRACT a. Blood pumped out 2. Diastole: Ventricles RELAX a. Vent. Fill b. 80% filling take place before atria contract Electrical Activity of the Heart • Heart muscle joined by gap junctions o Allows it to function as 2 separate pumps (atria and ventricle) § insulating region; allows for separation of A/V contraction • Pacemaker cells = modified myocardial cells, spontaneous depolarization • Located in sinoatrial node (SA node) o Main pacemaker of the heart • Pacemaker potential = cells depolarize spontaneously o HCN channel (special ion channel) o Bring cell to threshold, opens Ca++ channel o Causes CAP (cardiac action potential) § Ca++ channel: This is a slow channel! Causes sustained depolarization (plateau) like long twitch § Long dep = long refractory period. Prevents summation, maintains rhythmic beating • Contraction using sarcomeres (troponin, actin, myosin etc.) • Repolarization = open K+ channels (just like in neuron) • Movement of CAP through heart o SA nodeà atriaàAV nodeàBundle of HisàPurkinje fibers o Apex of heart contract slightly before top of ventricles (makes vent work like a pump) o All cells of either atria/vent contract in unison (joined by gap junctions) • The ECG/EKG o Measures electrical activity, 3 distinct waves o P, QRS, T § P = atrial depolarize § QRS = vent depolarize § T = vent repolarize Mechanical activity of heart • Diastole o Filling with blood o 80% V filling before atria contract o AV valves open, A and V relaxed • Systole o Emptying of blood o Contraction; SL valves open The Heartbeat (Cycle in reference to ventricles) 1. Diastole a. AV valves open, atrial/vent filling 2. End diastole a. SA node fires, “P wave” b. atria contract, “top off” vent 3. Systole a. AV node fires, vent depolarize b. “QRS” complex c. Ventricles contract, AV valves closed (1 heart sound) d. SL valves open 4. End systole a. Vent relax, repolarize; “T” wave b. SL valves close (2 heart sound) 5. Early Diastole a. Atria filling, ventricles relax b. AV valves open, 80% vent filling Heart Disorders 1. Ischemic heart disease a. Deficient oxygen supply to heart cells b. Anaerobic metabolism; heart muscle not adapted for this c. Cells die after few minutes, irreversible damage + scarring d. Causes heart attack (MI) i. MI detected by change in EKG, increased levels of troponin (special kind found in heart muscle) and other compounds in blood 2. Arrhythmias a. Irregular heartbeat d/t irregular rate of electric excitation/contraction; usually faster than normal i. Flutter: function as pump (coordination), just faster than normal ii. Fibrillation: disorganized, uncoordinated, don’t function as a pump. 1. Less bad if in atria 2. V-fib = death in minutes; blood isn’t being pumped to body/brain iii. Can be caused by problems with SA node… 1. Sinus brady/tachycardia (slow/fast but still controlled by SA node iv. …Or when pacemakers outside of the SA node take over (ectopic pacemakers) 1. ventricular tachycardia (V tach) 2. ventricular fibrillation (V fib) a. d/t damaged heart cells, ectopic pacemakers, dilated heart b. circus rhythms: recycling nerve impulses, normal refractory period overcome. c. Reset with defibrillator; shock depolarizes heart all at same time, restores rhythm v. Also caused by AV node block 1. Diagnostic EKG: multiple P waves 2. Impulse slowed, can’t make it to ventricles 3. Atria paced by SA, vent paced by ectopic 4. 3 degree = most severe, nothing can get through AV node b. Artificial pacemakers: deliver electrical stim to vent i. Early versions: fixed rate ii. Modern: demand pacemakers, only deliver shock when needed Cardiac Output (CO) • CO= heart rate (HR) * stroke volume (SV) o SV = vol. of blood pumped from each ventricle per contraction o HR = beats per minute (bpm) • Regulated by PNS/SNS o PNS = vagus nerve. Slows HR, takes longer to reach threshold § ACh à muscarinic receptor. Opens K+ chann = hyperpolarize § Influence on SA node o SNS = adrenaline, norepinephrine. Increase HR, fight or flight § Increase slope of pacemaker potential = faster to reach threshold § Increases SV ß increased venous return, TPR. § Increases strength of contraction § Influences both SA node and directly innervates heart muscle • Regulation of SV: Starling relationship o Strength of contraction varies directly with how much blood is in ventricle at the end of diastole § Makes sure ventricles pump out all blood that’s in them so it doesn’t pool/clot § Balances systemic/pulmonary circuits § Allows adjustment for peripheral resistance o Stretching of myocardium = greater force (more stretch d/t more blood in ventricles = stronger contraction) o SNS can also increase contractility/ influence SV (variation in relationship) Blood Flow • Venous return = return of blood to heart via veins o Affects SV by determining end diastolic blood volume (BV) o Veins = 70% of total BV; distend o Veins = capacitance (reservoir), regulate total circulation § arteries = resistance, regulate B/P o Return to heart by 3 mechanisms § SNS à vasoconstriction § Skeletal muscle pump, valves in veins § Diaphragm contraction (breathing) à pressure differential • MAP = mean arterial pressure (force of pumping) • TPR = total peripheral resistance (diameter of vessels) o Organization of vascular system: shutting off blood supply to particular organ o Arterioles = main regulatory vessel!!! § Reduce B/P from arteries before it gets to capillaries; so it doesn’t blow them out! o Vasodilation/Vasoconstriction: regulate diameter. § Dilation decreases resistance, contraction increases o Role of SNS (Extrinsic regulator_ § Divert blood from organs/skin to skeletal muscles o Intrinsic regulators § Myogenic control: using smooth muscle in arterioles to keep constant pressure (important in brain) § Metabolic: response to acidityàvasodilation, increase flow so you can get rid of CO2 § Paracrine: Nitric oxide: produced by endothelium, dilates • Nitroglycerine à treat angina Blood volume • Influences B/P, flow. Tightly regulated (too high/low causes problems) • ADH, aldosterone and their role o ADH = total body water; water reabsorption o Aldosterone = salt reabsorption à increase BV with osmosis § Released when too low B/P is sensed • Body water o 20% of total in blood; 80% in ISF § wateràISF through capillary pores; is pushed out (arterial side= higher pressure) § ISFàwater back to capillaries via osmosis • Blood more osmolar than ISF, on venous end (less pressure o Excess fluid accumulation = edema. Caused by: § problems with blood osmolality (not osmolar enough d/t starvation or infection) § pressure (high arterial pressure), § congestive heart failure (reduced SV) § venous obstruction • Hypovolemic shock = too little blood volume o d/t bleeding, dehydration etc. o direct effects: decreased CO and B/P o indirect effects (body’s attempt to get back to homeostasis) § tachycardia, vasoconstriction in skin/non-vital organs Blood Pressure • Regulated by baroreceptors (pressure sensors) in aortic arch, carotid sinus o Signal to medulla, affect vasoconstriction/dilation o Regulation of common/normal changes in B/P, also tell kidneys to release ADH/Aldosterone (receptors in renal artery) • directly proportional to volume, cardiac rate, TPR (if one increases, B/P also increases) o Clinical indicator o Measured with sphygmomanometer; inflate cuff to compress artery o Korotkoff sounds: First = systolic, Last = diastolic § Sounds created by turbulent flow Changes during exercise • more blood flow to skeletal muscles (About 80% instead of 15%), less to guts/kidneys • CO (cardiac output) increases b/c of SNS o Increased heart rate, force of contraction Cardiac (Vascular system) Disorders 1. Arteriosclerosis/atherosclerosis a. Hardening of arteries b. Plaque- reduces blood flow, site for blood clots i. Slow blood flow = pooling ii. Plaque caused by: smoking, high LDL cholesterol, diabetes iii. Infectionj connection 1. Inflammatory damage 2. C- reactive proteins = marker of systemic inflammation c. Cholesterol: good and bad i. LDL = bad, receptors in blood vessels, it’s deposited there and then oxidizes to form plaque 1. High sat. fat diets, genetics ii. HDL = good; removes bad and takes it to liver, no receptors in blood vessels 2. Hypertension (high B/P) a. 20% US adults: lack of exercise, poor diet, obesity b. “silent killer”: damages small b/v’s (kidney, eyes), can lead to stroke, heart disease c. treatment: lifestyle change, beta blockers (block beta adrenergic receptors in heart; SNS, responsible for increased heart rate + high contraction force), diuretics (get rid of excess fluid) 3. Shock (discussed under blood volume) 4. Congestive heart failure (CHF) a. CO insufficient, blood gets “backed up” i. Congestive = backup à increased venous pressure/volume ii. Left ventricle = pulmonary vein backup, fluid in lungs. Also systemic backup (swollen ankles) b. d/t valve probs, hypertension c. drugs increase contraction, vasodilators, diuretics Blood components • Cells o RBC (red blood cells) = oxygen carriers/hemoglobin o WBC (white blood cells)= leukocytes § Granular/agranular (based on staining) § Part of immune system (phagocytes, tissue macrophages etc.) o Platelets = cell fragments; blood clotting o Plasma = mostly water, some Na+ organic molecules and proteins § Water = keeps blood liquid, solvent (gases + electrolytes dissolve), rapid source of heat exchange (body temp regulation) Lymphatic system • ISFà blood o Lymph capillaries take ISF in, merge into lymph ducts o Filtered through lymph nodes • Immunity o Lymph nodes = phagocytes o Thymus, tonsils, spleen = site of lymphocyte production • Fat transport o Lacteals • Movement by peristalsis, valves • Fluid empties into subclavian vein, back into blood


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