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Physiology Final Exam Study Guide

by: Sierra Mongeon

Physiology Final Exam Study Guide BIOS 213

Marketplace > University of Nebraska Lincoln > Biology > BIOS 213 > Physiology Final Exam Study Guide
Sierra Mongeon
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Here is the comprehensive final exam study guide! I hope it helps you study. Good luck on the test!
Human Physiology
Dr. Tony Zera
Study Guide
Physiology, Renal system, Cardiovascular, Muscular System, regulation
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This 17 page Study Guide was uploaded by Sierra Mongeon on Friday April 29, 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 89 views. For similar materials see Human Physiology in Biology at University of Nebraska Lincoln.

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Date Created: 04/29/16
BIOS 213 FINAL EXAM STUDY GUIDE Homeostasis: dynamic constancy of internal environment; always slightly changing but body keeps things relatively constant. • most phys. mechanisms are to maintain homeostasis! • Negative/positive feedback • Antagonistic processes = fine control Membranes and Transport • Phospholipid bilayer = cell membrane. o Proteins embedded in (integral) § Transmembrane = span entire membrane; transport things inside/outside cell § Fluid mosaic model o Permeable to (these diffuse through); small polar or non-polar molecules (H20 and urea), lipids. § Charged molecules (ions) can’t just diffuse through • Diffusion and Osmosis o Concentration gradient : highà low o Osmosis = diffusion of water across membrane § Solute concentration = osmolarity § H20 moves from less concentrated to more concentrated (lowàhigh osmolarity) § Hyperosmotic or hypo-osmotic § Osmotic pressure § For osmosis: membrane only permeable to water, solute concentration determines water flow • Transport Mechanisms o Pores (aquaporins) o Channels § Ligand or Voltage gated (which organ systems use which type?) § Cystic Fibrosis = faulty Cl- channel o Carrier proteins: CMT (carrier mediated transport) § Facilitated diffusion (with conc gradient, no ATP) § Active transport (against conc gradient, uses ATP) • Example: Na+/K+ pumps; 3 Na + goes out, 2 K+ goes in o Sets up conc and charge difference across membrane. o What is the function of Na/K pumps in the body?(Kidney, neurons, muscles etc.) • Primary and secondary active transport o Primary = ATPase, set up ion gradient o Secondary = energy comes from the ion gradient set up by primary § Co- or counter- transport • Example = glucose co-transport with Na+ in kidney • Bulk Transport: Exo- and endo- cytosis o Endo- can be receptor mediated Renal Physiology Osmoregulaton (Water regulation) • Total water content and distribution of water • Conc of osmolytes • Water= polar. o Universal solvent, heat retention, transport etc. very important o 80% in ISF, 20% in blood o lost d/t breathing, metabolism o need constant amount to maintain blood volume (BV) and B/P • Kidneys main osmoregulation organs o Reg. water and ions o Reg. blood pH o Biosynthesis (gluconeogenesis) • Nephron o Bowman’s capsule + glomerulus § Filtration; porous capillaries • Filtrate pushed out of blood, into capsule • Isotonic with blood § GFR can be changed by restricting flow to glom. o PCT § Reabsorption • All glucose, amino acids • 65% water, NaCl • regulated reabsorption: bicarb and H+ (pH control) o DLOH § Water reabsorption by osmosis (hyperosmotic medulla) • Permeable to water only, not ions • Filtrate hyperosmotic to blood @ bottom o ALOH § Na+/ K+ pumps § Na+ pumps out, K+ reabsorbed • Na+ trapped in medulla; countercurrent multiplier • Urea also in medulla § At top of ALOH, filtrate hypo-osmotic o DCT § Regulated reabsorption NA+/ Secretion K+ § Aldosterone: increase K+ secretion, increase Na+ absorption in blood o Collecting duct § Regulated reabsorption of water (aquaporins) § ADH = insertion of more aquaporins Vasa Recta o Capillaries surrounding LOH; contributes to hyperosmolality of medulla pH balance; Bicarbonate buffer system • Law of mass action o Bicarb chem. reaction • What is pH? • Metabolism produces acid, body needs to keep pH relatively constant, uses buffers o H+ variable secretion, bicarb variable reabsorption o Renal system controls these, also CO2 exhaled by lungs • Body’s response to: o Acidosis: increase breathing, increase H+ secretion and bicarb production, make new bicarb § also can use other buffers o Alkalosis: don’t reabsorb bicarb (excrete it), absorb H+ ions o Normal conditions: all bicarb reabsorbed, much H+ secreted • Bicarbonate shuttle: can’t be directly absorbed, so forms CO2 and H2O to cross membrane. Once inside, converts back and H+ secreted back into lumen. Hormones affecting kidney • Aldosterone: responds to low blood volume, regulates Na+/K+ reabsorption o more Na+ absorbed, K+ secreted (Na/K pumps, Na channels) o more Na+ in blood = water moves in by osmosis = raise B o Renin-angiotensin system; renin triggered by baroreceptors o ANP: opposite effects, when BV too high • ADH: more aquaporins in CD = more water reabsorbed, regulates total body water o triggered by osmoreceptors o diabetes insipidus: malfunctioning ADH receptor, high vol. dilute urine Nervous System Neuron • anatomy; know how the parts work • organization of nervous system (CNS and PNS) o CNS = brain + spinal cord, coordination and integration, interneurons o PNS (peripheral nervous system)= somatic (conscious) and autonomic (subconscious) § autonomic = SNS (sympathetic)and PsNS (parasympathetic) § SNS = fight or flight § PsNS = relaxation, “rest and digest” o PNS has afferent (to CNS) and efferent (away from CNS) Bioelectricity • charge difference across membrane= membrane potential • resting membrane potential = Vm, uneven distribution of particles inside and out of cell o Neuron, Vm = -70 mV • membrane impermeable to ions (needs channels/pumps) • Graded potential o small changes in membrane potential o amplitude (strength) depends on strength of stim. § can be summed (summation) § excitatory or inhibitory • excitatory = depolarizes, closer to threshold • inhibitory = hyperpolarizes, farther away from threshold • Ion Equilibrium Constant o determines how ions will move o Na+ = +60 mV o K+ = -90 mV § Why Na+ moves inside cell and K+ moves out (Na+ moves inside to Endocrine system • Hormonal response d/t how receptive tissues are to hormone (example: Type 2 diabetes) and hormone titer o Regulated by negative feedback, except during ovulation of menstrual cycle • Can have sequential effects: uterine “priming” by estrogen so it’s more receptive to progesterone • Physiological and pharmacological effects o Phys. = normal effect of hormone, low conc. o Pharm.= abnormal effects due to high conc. of hormone § example: anabolic steroid abuse, convert testosterone (T) into estrogen (E) • Hormone types and Modes of Action o Peptide hormones (polar hormones) § produced from DNA as inactive pre/prohormones, then are activated. § act via secondary messenger systems (don’t enter cell by themselves!) • binds to receptor à G protein activated à adenylate cyclaseàcAMP from ATP à protein kinase which activates or deactivates proteins (enzymes) • Examples of polar hormones: o Epinephrine – adrenal medulla, “fight or flight”, increase force of heart contraction and plasma glucose o insulin and glucagon o ADH o all pituitary hormones o Lipid Hormones § hormones enter cell (receptors inside) • Receptor 2 parts: ligand binding and DNA binding • Ligand = hormone, binds to receptor, causes it to bind to DNA à produce mRNA and increase protein synthesis • Examples of lipid hormones: o Steroids of adrenal cortex (glucocorticoids: increased production + release of glucose, cortisol) § “fight or flight”, from adrenal cortex § inhibits immune response; reduce inflammation o mineralcorticoids § Aldosterone!! o thyroxine o Gonadal steroids § estrogen = uterine lining growth § progesterone = prep for fertilized egg § testosterone = increase metabolism, male reproduction 1. Pituitary gland a. Anterior = “trophic” hormones i. FSH, LH, ACTH (stimulate adrenal cortex to make cortisol), growth hormones ii. release mechanism: hypothalamus à releasing factor (RF) hormones into portal vein. Graded release of RF d/t neural stimulation of hypothalamus iii. RF hormones bind to anterior pituitary cell receptors à release trophic hormones into general circulation 1. target tissues 2. Amplification: small amount of RF à greater amt. trophic hormoneàlarge amt. of end hormone (estrogen, cortisol etc.) b. Posterior i. neurosecretory cells: bodies in hypothalamus, release vesicles (similar to release of NT) ii. 2 key peptide hormones: Oxytocin and ADH • Endocrine disorders o Anabolic steroid misuse § T à E § growth of female-like breasts, shrinking testes, sterility § high blood cholesterol (because it’s a steroid hormone! steroids come from cholesterol) o Pituitary Problems § pituitary dwarfism = inadequate growth hormone (GH) or tissue insensitivity to GH § gigantism= over-secretion of GH in children § acromegaly= over-secretion GH in adults, thickening of bones/soft tissue (facial features) • similar phenotype in athletes takeing GH o Diabetes Mellitus § Background on insulin/glucagon • beta cells à insulin • alpha cells à glucagon • these hormones work together to regulate blood glucose levels o elevated blood sugar = insulin release; uptake of glucose/fatty acids (FA) into cells, lowers BG (blood glucose) o low BG = glucagon release, glucose/FA released into blood, raises BG § 2 types: • Both types: hyperglycemia, frequent urination, ketoacidosis (severe only-can’t fully metabolize lipids, blood pH drops, hyperventilation) • Type 1: Insulin dependent o autoimmune disease; body destroys B cells à no insulin produced o 10% of diabetics, juvenile onset o insulin injections • Type 2: Non-insulin dependent o 90% diabetics; link w/ obesity (remember adipose tissue is an endocrine organ) o tissue less sensitive to insulin § from adipose tissue hormones o resting (fasting) BG is high (200+; normal is 100) o high B/P (more glucose in blood = more osmolar), leads to vascular damage o measure with oral-glucose tolerance test, A1C hemoglobin (hemoglobin with glucose attached) • Menstrual Cycle § Cyclic changes of gonadotropins FSH and LHà cyclic change in estrogen/progesterone secretion à cyclic change in ovaries and uterus § Follicular phase – FSH decreases, granulosa cells produce estrogen à more as follicle matures (positive feedback between estrogen and LH) § ovulation – right before ovulating, a surge of LH, FSH and estrogen, egg ejected leaving empty corpus luteum § luteal phase- corpus lutem secretes progesterone, which inhibits FSH, LH and estrogen (so only one follicle matures at a time) § Uterine stages • proliferative – high amts estrogen = growth, production of progesterone receptors (uterine priming) • secretory- endometrium thickens, prepares for implant • menstruation – death and sloughing of endometrial cells § Birth control • The pill – simulates luteal phase, LH prevented so no ovulation • RU486 “morning after pill”-blocks progesterone receptors,, which are needed for pregnancy maintenance § Pregnancy tests = hCG (hormone only produced by fetus) • Autocrine/Paracrine Regulation o act within organs that produce them (local) o Examples: § cytokines (immune cells), growth factors § endothelium of blood vessels (vasodilation/constriction) § Prostaglandins –wide variety of function (immune, reproduction, digestive) • Activity inhibited by NSAIDS (aspirin, ibuprofen), COX enzymes needed to function o NSAIDS inhibit COX enzymes o COX 1 = general function, COX 2 = inflammatory, blood clotting function (why aspirin is good for your heart!) • Endocrine disruptors: mimic hormones Immune System • distinguish btwn. self and foreign Ag (antigens) o recognize and defend against • 2 types: o Innate § prior exposure not required (born with it) § general defense § Cellular and non-cellular components • non-cellular = skin, mucous membranes, stomach acid etc. • cellular = phagocytes/macrophages, neutrophils (all are leukocytes-WBC) o some are anchored (immobile) in lymph nodes, some in blood o engulf and destroy, attracted to general features of “foreignness” (Ex. bacterial lipopolysaccharides) o release pyrogens (cause fever) and cytokines (fever, fatigue, reduce iron conc, paracrine regulators) histamine (makes capillaries more leaky) • Interferons- interfere with viral replication o Acquired/Adaptive/Specific § Antigen-specific defending cells (lymphocytes) • B cells – kill at a distance o “antigenic determinant”= Ag binds, induces Ab production o memory cells § stay in body, induced if contact same pathogen again o plasma cells- produce Ab o Clonal selection theory § pre-existing population B lymphocytes (born with)àintroduce Agàcauses production of the clone that is sensitive to that Ag • T cells – directly kill o kill cancer, viruses, transplanted cells (rejection) o cannot bind to free Agàforeign object must be brought to T cell o killer and helper § Primary and Secondary responses • Primary= slow, latent period (body needs more time to recognize and fight infection). Low Ab titer • Secondary = already have memory cells, high Ab titer, pathogen quickly destroyed o basis behind vaccinations (induce primary response with vax so you already have Ab) § Antibodies (Ab) = immunoglobulins • Y shape, 2 Ag binding sites, 4 protein chains o C chain = constant, defines basic shape o V chain = variableàspecificity of Ab to pathogens § several hundred genes mix and match to code for V region § somatic mutation- mutation during B cell division increase Ab diversity • Complement System o Binding of Ab to Ag à activates complement proteins § compliment proteins: produce hole in bacterial cell wall o induce chemotaxis of macrophages o release of histamine • MHC complex – prevents body from attacking itself o immunological tolerance-Body recognizes “self and non self”, tolerates its own antigens o no two people exactly the same; leads to tissue transplant rejects § immunosuppressive drugs, genetically related people o helps macrophages present antigens to T cells • Local inflammation = how innate and acquired work together o pathogen enters, mast cells à histamine (leaky capillaries, increase blood flow) o macrophages à cytokines o specific immunity (B cells) kick in, enhance phagocytosis + Ab activate complement system o macrophage presents weakened pathogen to T cells • Tumors = malfunctioning cells d/t de-differentiation (resemble cells prior to development of immunological tolerance) • Autoimmune diseases = body doesn’t tolerate own Ag, attacks self o cross reactivity with self antigens, Ab against self • Passive immunity = you don’t make Ab, they are put into you/given to you o from mother à child o antiserum/antitoxin for emergencies • Ab in research o immunoassays – blood type, pregnancy test o need monoclonal Ab (very specific, study one Ag) • Allergies o hypersensitivity to Ag o lots of histamine (runny nose, watery eyes), use anti-histamine drugs Muscular System 3 types: skeletal, cardiac, smooth myo-, sarco- = muscle function: contraction, force generation 1. Skeletal a. striated, multinucleate b. myofiber = muscle cell/fiber, myofibrils = bundle of contractile proteins, myofilament = actin or myosin strand c. Motor units – larger = power but less control, small= control, but less power i. one motor neuron innerv. multiple muscle fibers – axon collateral branches ii. meet muscle at NMJ iii. can be recruited to increase force of contraction of whole muscle d. Excitation- contraction coupling i. AP in motor neuron meets muscle at NMGJ à end plate potential at motor end plate (nicotinic receptors)à AP generatedàAP spreads across sarcolemmaàdown T- tubulesà contacts terminal cisternae of sarcoplasmic reticulumàCa++ ions releasedàtravel to sarcomere 1. when contraction complete, Ca++ àback to term. cisternae e. The Sarcomere i. Bands (know the names and how they change during contraction), actin and myosin (A/M) ii. sliding filament theory = A/M themselves don’t actually shorten, but slide past each other 1. myosin forms crossbridges with actin iii. Contraction: 1. Ca++ binds to troponin 2. Troponin changes shape à tropomyosin changes shapeàactin binding site exposed a. Allows myosin to form cross bridge 3. ATP attached to myosin hydrolyzed (ADP + P) à cross bridge formed 4. Release of P à power stroke a. ADP falls off after myosin moves 5. Binding of new ATP causes myosin to detach à relaxation a. No new ATP to bind = rigor mortis 6. Ca++ removed by Ca++ ATPase (pump) à back into terminal cisternae f. Whole muscle contraction i. muscle twitch = basic unit of contraction 1. 1 AP = 1 twitch, all or none ii. differences in force and speed 1. summation of twitches 2. differences in fiber type (diameter, fast vs. slow) a. thick =stronger 3. recruitment iii. Neural control 1. upper + lower motor neurons (upper in brain, lower synapse directly with muscle) 2. muscle spindle apparatus = length 3. golgi tendon organ = tension on tendon 2. Cardiac 3. Smooth Exercise Physiology • Skeletal muscle o fiber types: fast and slow § know differences between the two § how do they affect performance? o Aerobic and anaerobic metabolism § anaerobic à lactic acid § aerobicà CO2 o Energy sources: § aerobic = lipids (triglycerides) § anaerobic = carbs. (sugars, glycogen) o Fuel use § low intensity = aerobic = primarily fats § medium intensity = 50/50 anaerobic/aerobic= 50/50 fats and carbs § high int. = carbs (lots of glycogen) • Measuring intensity o VO2 max = aerobic capacity § max rate of O2 use § intensity = % VO2 max o lactate threshold = % VO2 max where you start making lactic acid (anaerobic), usually at 50-70% VO2 max • Fatigue- what causes it? o run out of creatine = high intensity § creatine phosphate = high energy molecule, used to make ATP o glycogen depletion limits mid-high intensity exercise (marathon running) Cardiovascular System function = transport blood, nutrients, O2 • Heart = 4 chambers -2 atria(A) 2 ventricles (V) o A = blood from veins, pump to ventricles o V=blood from atria, pump into arteries § veins = toward heart, arteries = away from heart • 2 circuits: pulmonary + systemic (know which blood vessels carry oxygenated/deoxygenated blood) • Heart valves prevent backflow of blood o AV valves § close when V pressure> A pressure (systole)à 1 heart sound o Semilunar (SL) § close when artery pressure > V pressure (diastole) à2 heart sound • Systole/Diastole = contraction/relaxation (refer to ventricles) o 80% ventricular filling during diastole; AV valves open o blood pumped into arteries during systole: SL valves open Electrical activity of heart/heartbeat • heart muscle joined by gap junctions o all atrial/ventricular cells attached, 2 separate pumps) • insulating region btwn A and V – allows delay/separation of contraction of A and V • pacemaker cells in SA node o spontaneously depolarize • CAP = cardiac action potential o different than normal AP § longer refractory period, plateau d/t slow Ca++ channels, causes sustained depolarization • pathway: o SA nodeàatria depolarizeà AV nodeàbundle of HisàPurkinje Fibersàventricle depolarizes from apex to top • ECG/EKG (same thing) o P wave- atria depolarize o QRS complex-ventricles depolarize=systole(atria repolarizes but hidden) o T wave-ventricle repolarize 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. Arrythmias = irregular heart beat a. flutter = fast, but still pump b. fibrillation= uncoordinated, not pumping i. A fib= less bad, but risk of blood clot ii. V fib = death in minutes, blood not pumped to body/brain c. Tachycardia/Bradycardia (too fast/slow) d. AV node block (signal can’t get through AV node) e. artificial pacemakers deliver shock to V 2. Ischemic Heart disease = insufficient O2 supply à anaerobic metàcell deathàMI Cardiac Output • CO = HR * 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 à AChàmuscarinic receptoràopens K+ chann (hyperpolarize) o SNS = adrenaline, norepinephrine § increase HR, also increases contraction strength (influence SA node and directly influences muscle) • Starling relationship: Regulation of SV o more blood in ventricle @ end-diastole = more forceful heart contraction § heart contracts more strongly when stretched (different than skeletal muscle) o makes sure blood doesn’t pool/clotàall blood pumped out of ventricles o allows for flexibility in force of contraction + SV § SNS can influence Starling, cause variation Blood Flow • venous return = return of blood to heart = affects SV by determining end diastolic blood volume (BV) o veins = 70% body’s blood, capacitance vessels • venous blood returns to heart 3 ways o SNSà vasoconstriction o skeletal muscle pump + valves o diaphragm contracts à pressure diff. • TPR = total peripheral resistance o arteries = resistance vessels § arterioles = main regulatory vessels!! o Vasodilation/constriction = regulate diameter § dilation decreases resistance, constriction increases o SNS role: divert blood away from non-essential organs during fight or flight o intrinsic reg. § myogenic control – smooth muscle in arterioles, keep constant pressure (such as in cerebral circ) § metabolic – response to acidity = dilation § paracrine = nitroglycerine/nitrous oxide à dilation Blood volume • influences B/P and flow, tightly regulated • ADH and Aldosterone o ADH = total body water; water reabsorption, indirectly effects o Aldosterone = salt reabsorptionàincrease blood osmolalityàwater flows in, increase BV (directly effects) • Body water: 80% in ISF, 20% in blood o H20 pushed out through arterial side, diffuses back in through venous side o Excess fluid in tissues = edema § Result of many conditions (CHF, vein obstruction, starvation etc.) § Treat with diuretics (drugs that increase urine volume, pee out excess water) • Hypovolemic shock = too low BV o direct consequences = decreased BP and CO o body’s responses (to maintain homeostasis)= tachycardia, cold clammy skin Blood Pressure • baroreceptors in aortic arch, carotid sinus à medulla à vasoconstriction/dilation • Taking B/P= sphygmomanometer, Korotkoff sounds Changes during exercise • More blood to skeletal muscles, less to guts/kidneys • CO increases, increased HR and force of contraction Vascular disorders • Arteriosclerosis/atherosclerosis o hardening of arteries, caused by plaque à reduce blood flow, site for blood clots o cholesterol – LDL (bad), HDL (good); it’s not the cholesterol, but the type of carrier it’s bound to • Hypertension – high B/P o damage small Bv’s- silent killer o treat with beta blockers (block beta adrenergic receptors in heart; SNS, responsible for increased heart rate + high contraction force), lifestyle changes • Congestive Heart Failure o CO insufficient, blood gets “backed up” o leads to edema from increased venous pressure § fluid in lungs/ankles Blood • cells o RBC = oxygen carriers (discussed later) o WBC = leukocytes, part of immune system o platelets = cell fragments, blood clotting o plasma= mostly water, keeps blood liquid and is solvent Lymphatic system • takes ISF back to blood o lymph ductsàfiltered through lymph nodes (contain lots of immune cells) before returning to blood via subclavian vein • fat transport (lacteals in intestine) Respiratory System • primary function = gas exchange o also acid/base balance • Anatomy: o alveoli = site of gas exchange, fluid lined sacs close to capillaries § filled with surfactant à decrease surface tension, gases dissolve in this fluid § not enough = collapsed alveoli § premature babies don’t produce enough surf. = infant respiratory distress • Lung volumes + capacities: measured with spirometer, used to characterize normal and abnormal lung function o RR = respiration rate o Tidal volume (TV) = depth of each breath at rest o Minute volume (MV) = rate of air exchange/min. § MV =RR * TV o vital capacity (VC) = max amt. air forcefully exhaled after max. inhalation; used to diagnose lung disorders • Restrictive disorders = VC reduced (damage to alveoli) o emphysema § destruction of alveoli d/t smoking usually o Pulmonary fibrosis § fibrous conn. tissue in lung d/t inhalation small particles • Obstructive = VC normal, decreased exhalation rate (flowrate) o asthma § obstruct air flow through bronchioles; treat with bronchodilators Gas Exchange • Oxygen o Hemoglobin (Hb) § binds 99% of O2 in blood, heme group with Fe++ binds 2 O2 § with O2 = oxyHb; w/o O2 = deoxyHb • CO2 o 10% dissolved in plasma o 20% bound to Hb o 70% as bicarbonate! § carbonic anhydrase § bicarb. buffer system • Occurs by passive diffusion down conc. gradient (highàlow) o partial pressure (PP) = conc. • O2 Pathway o alveoli à blood plasma à RBC à Hb binds it, removing from plasma (keeps PP low, maintains conc. gradient)àback to plasma when it gets to tissuesàISFàcellsàmitochondria o CO2 is reverse the O2 pathway • O2 binding to Hb o not covalently bound – spends some time off Hb and some time on § law of mass action o dissociation curve = O2 carrying capacity, O2 uptake/release § % saturation = P02; strength of binding, highest in arteries (Hb saturated) § Normal curve = 75% saturation (only 25% released) § Right shift = more O2 released (can be local or global), lower % sat • local - occurs where low pH, increased temp • global – DPG (regulatory molecule, increases O2 release in conditions where O2 is lower than normal- anemia, high altitude) § Left shift = more O2 bound/stronger binding, less released, higher % sat • occurs in fetus and myoglobin (both have stronger affinity for O2 than regular Hb) Neural Control o rhythmicity center in medulla o I and E neurons o I = inspiratory, causes contraction of diaphragm (active) o E = expiratory, causes relaxation (inhibits I neuron; passive) Chemical Control o peripheral chemoreceptors – carotid and aortic bodies (remember these are diff. than sinuses that are baroreceptors) o monitor CO2 conc. in blood, send info to medulla o central receptor – in medulla o very sensitive : CO2 can cross BBB, enter CSF which is very close to medulla à dissociates into carbonic acid (with help of CA-carbonic anhydrase) Clinical = Ondine’s curse o can only breathe when you’re consciously thinking about it o mech. respirator when sleeping Acid/Base (pH) regulation o resp. and renal systems work together o correct imbalances created by the other system (example = high altitude) o bicarbonate buffer : CO2 à carbonic acidàbicarbonate and H+ o maintains normal pH o pH maintained by changes in breathing rate o breathe out CO2 (acid) o hyperventilation = combat acidosis o hypoventilation= combat alkalosis o (Remember how kidney combats acid/alkalosis!) § secretion/reabsorption of H+/bicarb Exercise + respiratory function o increased rate of breathing; 2 theories o Neural control § sensory nerves in muscles stim. respiratory centers o Humeral control § pO2, pCO2 and pH important, but changes too small to be measured


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