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UNC / Biology / BIOL 252 / unc biol 252

unc biol 252

unc biol 252


School: University of North Carolina - Chapel Hill
Department: Biology
Course: Fundamentals of Human A&p
Term: Fall 2015
Tags: Biology, anatomy, and Human Body
Cost: 25
Name: Biology 252, Anatomy notes by body system
Description: These are the notes in order for exams 2, 3, and 4 for the course
Uploaded: 04/26/2017
123 Pages 182 Views 1 Unlocks

Bone Tissue ∙ Functions of the skeleton bones o Protection skull encases brain, ribcage protects lungs and heart o Support helps us stand upright o Movement o Electrolyte balance calcium and phosphate are used o Blood formation bone marrow consists of blood forming cells ∙ Histology of osseous tissue (bone tissue) oss=bone o Osteogenic cell- multipotential stem cell  o Osteoblast- active…builds. Secrets bone matrix, actively  producing bone tissue  o Osteocyte- mature cell residing within bone tissue  Lives trapped in lacunae (gaps in spongy bone)  Makes connections with other osteocytes ∙ Lacunae= holes in the spongy bone tissue ∙ Canaliculi= channels (space between dendrites) ∙ Bone matrix= the solid white area o The cells are connected to each other through gap junctions so  that things can pass from cell to cell ∙ Osteoclast: develop from macrophage-like cells (White blood cells) o Live on the bone surface (external or internal) and eat away at  the bone matrix the matrix Calcium Organic compounds  (mostly collagen) Phosphate Other Other Other Other Other Other Other Other Other Other Other Other Other Other ∙ Organic compounds o Collagen: a strong string fiber that provides flexibility ∙ Two components that make up the extracellular matrix o Fibrous o Aqueous (ground substance) ∙ Then….there is a mineral component that precipitates into a salt o Total inorganic= 67% ∙ Sun exposure is important for Vitamin D intake 1o Vitamin D is pretty much the same thing as calcitriol increases  blood calcium levels o This calcium absorption is crucial ultimately for bone strength ∙ Bones have a mineral component (for strength and hardness) and a  collagen fiber component (for flexibility) ∙ Osteogenesis imperfecta: excessively brittle bones because of  improperly formed collagen ∙ Long bone structure o Epiphysis: the head made of spongy bone  Made of red bone marrow: blood cells  Trabeculae: BEAMS in the spongy bone o Diaphysis: the long shaft of the bone  Made of yellow bone marrow: mostly fat  Made of compact bone  A marrow cavity runs down the middle  Nutrient foramina: holes on the outside of the bone  The outside covering *oss=bone! ∙ Periosteum: the outermost piece o Thin connective tissue where blood vessels and bone cells are ∙ Then you have….endosteum: the inner layer ∙ Then you have…yellow marrow= THE INNERMOST ∙ Flat bone structure (in skull) o [All of this is part of the bone matrix] o Suture o Outer compact bone o Spongy bone (diploe)  Provides a little bit of flexibility because of how it is  arranged  Has trabeculae  All of the spaces are filled with bone marrow   o Inner compact bone ∙ Histology of compact bone o Osteon: mode of alternating layers of bone marrow cells  This is done for strength! o The circular pattern= osteon (Haversion system)  These osteons are strong when they are together  Rigidity against compression forces ∙ Chondrocyte: mature cell of cartilage ∙ Osteocyte: mature cell of bone 2∙ Spongy bone o These spaces within are much larger o Slivers= spicules o Beams= trabeculae *do NOT confuse with lacunae!! (holes) o Provides strength and minimal weight ∙ Compact bone have osteons (provide resistance against compression) ∙ Mechanical design o Trabeculae follow a path to provide strength ∙ Children have red bone marrow all throughout ∙ As you grow, you develop to have more yellow bone marrow ∙ Bone marrow o Yellow bone marrow: the way to store fatty acids for energy o Red bone marrow: has lots of blood producing cells  RBCs, WBS, and platelets are all produced here ∙ Perichondrium: layer of connective tissue surrounding cartilage o *chond=cartilage! Ossification (osteogenesis): the formation of bone ∙ Intramembraneous ossification o Connective tissue  bone o Happens specifically in the vascular tissue (blood vessels are a  part of it) o Mesenchyme: a connective tissue precursor o Mesenchyme turns into osteoblasts (deposit bone matrix---fill it  with minerals) **making bone cells o The osteoblasts then secrete **osteoid o It **calcifies and calcium phosphate crystals form o Spongy bone forms around the blood vessels o Compact bone continues to form on the top and the bottom  (filling the space above and below the spongy bone in the  middle) o Sandwich! ∙ Endochondral ossification o Generic connective tissue  cartilage  bone o Mesenchyme, then osteoid, then hyaline cartilage forms o Primary ossification center: an area of future bone that is in the  middle of the precursor  This will eventually be the diaphysis o Bony collar forms a thin shell around the precursor o Then, even further out the periosteum forms on the outermost  part  This is where blood vessels enter 3 Osteoclasts and osteoclasts are in there o Cartilage: has no blood vessels…they get nutrients by diffusion o The periosteum allows for the blood vessels, nutrients, and  minerals to get into the precursor  Blood vessels move in and the marrow cavity is made o Secondary ossification center: recap of same series of events,  but it happens on the ends of the bone (picture a compact bone) o Compact bone forms on the outside and forms toward the  inside…but it stops forming so that a marrow cavity remains o Metaphysis: region of transition from cartilage to bone at each  end of the primary marrow cavity  Ex: in a long bone, it is the transitional area between the  diaphysis and the epiphysis o Bone formation in epiphysis, and more bone formation in  diaphysis o Remaining cartilage goes to:  Epiphyseal plate: growth plate that separates the epiphysis from the diaphysis  Articular cartilage: covers the epiphysis o Invading cartilage, hollowing out bone ∙ X-ray highlights the epiphyseal plate o Eventually it goes away after you have fully grown and turns into the epiphyseal line ∙ Bone growth of epiphyseal plate (AFTER endochondral ossification) o This happens over time as you grow o There is growth of the cartilage, so the plate is expanding in  thickness  Enlarging cells= hypertrophic o Plate is expanding from within, but it is dying on the margins  The entire bone is growing in length from the big picture  The bone grows toward the epiphyseal plate, but the  epiphyseal plate does NOT lose its thickness  Bones elongate due to growth of bone toward the  epiphyseal plates  Eventually when you are done growing ∙ Where the cartilage cells are dying, the bone is  moving up to replace it ∙ Bone growth o Interstitial growth: growth happening in the space in between  cells  Bone elongation results from cartilage growth, which is  when the bone grows outward toward the epiphyseal plate  This results in deposition of new matrix in the interior (gets minerals) 4o Appositional growth: deposition of bone matrix on outside  surface of bone  Bone is added on top of existing bone  Growth of cartilage and bone at the surface  You will NEVER find osteoblasts within bone matrix…they  are always on the outside ∙ Remodeling: purpose is to repair microfractures (tiny cracks), reshapes  bones, releases minerals into the blood o BOTH osteoclasts and osteoblasts needed o Reshape bone based on stresses placed on them  When a bone is of little use to a person osteoclasts  remove matrix and get rid of unnecessary mass  When a bone is heavily used osteoblasts deposit new  osseous tissue and thicken the bone o Bones adapt to withstand stresses o We reshape outside, and also inside the trabeculae ∙ Wolff’s Law: states that the architecture of the bone is determined by  the mechanical stresses placed upon it o Architecture changes based on forces placed on the bone ∙ Bones are a source and a sink of calcium and phosphate o We can control bodily electrolytes ∙ Mineralization (calcification)= MINERAL DEPOSITION!: the process  of calcium concentration leaving the blood and going into the  bones….bones are being mineralized o The amount of calcium increases in bones deposition o Whenever we are depositing bone matrix, we are getting calcium from blood and it is going into bone o **The hardening of bone o Dynamic equilibrium: there is constantly calcium coming in and  out ∙ Mineral resorption: putting calcium back into the blood o Also involves dynamic equilibrium o Bone is dissolved because an acid digests the collagen matrix,  and minerals are released ∙ Bone resorption: process where osteoclasts break down bone and  release the minerals resulting in calcium going out to the blood ∙ Calcium levels in blood o Important because this affects the rate at which synaptic vesicles release the neurotransmitter across the synapse, which affects  the action potential ∙ Resorption and deposition are used to maintain Ca2+ homeostasis ∙ **We also use calcium for muscles o Smooth muscle and cardiac muscle use calcium for contraction ∙ We NEED to keep calcium levels in check 5∙ We use calcium in the release of vesicles ∙ Hypocalcemia: low levels of calcium (deficiency) o Fewer Ca2+ ions are available to mask (-) charges  There is excessive excitability o This causes the Na+ ions to enter too freely ∙ Results in a smaller RMP (less polarized…so it is more positive) o Muscle cells and neurons may become hypersensitive to stimuli o The (-) glycogeal membrane structures still there o We lose calcium from the extracellular fluid since there is a low  calcium amount o This means that there is less bonding/matches between the  calcium and the glycogen o Ex: RMP is -60 instead of -70 (it is more positive because calcium is not coming into the cell and so too much sodium is coming in) o Causes us to be closer to the threshold, so it takes a much  weaker stimulus to get to an action potential  Muscles become hypersensitive ∙ Even worse…. Tetany: inability of muscle to relax because calcium  concentration falls to 6 mg/dL ∙ Hypercalcemia: an excess of calcium in the blood (too much) o Excessive amounts of calcium bind to the cell surface which  increases the charge difference across the membrane o Ca2+ binds to the Na+ channels and inhibits them o **Can also happen when there is a high increase in osteoclast  activity (a lot of calcium leaving the bone) ∙ Homeostasis of Calcium o Resorption: Ca2+ going back into the blood *osteocloasts do this o Deposition: formation of Ca2+ in bones *osteoblasts  Mineralization or calcification ∙ Phosphate levels are NOT regulated tightly ∙ Movement of calcium o Dietary absorption: small intestine absorbs and calcium goes into the blood when you eat o Excretion: blood is filtered through the kidney and most of the  calcium stays in the blood. HOWEVER  There is also some calcium lost in the excretion of urine hormonal signals regulate this o Osteoclasts regulate resorption and osteoblasts regulate  deposition ∙ **These 3 systems work together ∙ ex: when blood Ca2+ falls, body releases Ca2+ from the bones, increases Ca2+ absorption from intestines, and decreases excretion by the  kidneys ∙ Hormones 6o Calcitonin: released by the thyroid gland  LOWERS the blood calcium concentration by osteoclast  inhibition (because osteoclasts usually allow for the release of calcium from the bones)  “tones it down” …and is alooooone   Negative feedback…it is released when blood calcium  levels are high o Parathyroid Hormone (PTH): released from the parathyroid gland  RAISES the blood calcium concentration  It is released when the calcium concentration is low and  needs to be raised  This is done by reducing the kidney excretion (we do not  want calcium to get out easily!!)…so we want the kidneys  to stop getting rid of our calcium. o We get Vitamin D from the sun and also from… o Calcitriol: this hormone has been converted from Vitamin D to  calcitriol  RAISES the blood calcium concentration  Stimulates osteoclasts  Stimulates more calcium absorption in the digestive  system ∙ Poll Ev: Person has hypercalcemia? What explains this? o Answer= He had a recent partial thyroidectomy.  o Thyroid releases calcitonin, which lowers Ca2+ levels o If this hormone is inhibited, your body does not know how to  lower calcium levels ∙ Osteoporosis: bones become brittle and fragile o Happens because of over-activity of osteoclasts, or also because  of a decrease in estrogen o Holes form in the spongy bone where they aren’t supposed to be  Micro-fractures happen and over time they build to be a big fracture o Spongy bone breaks down o Vertebral column can cave in o Best treatment is strength exercise, but you can also treat it by  increasing estrogen ∙ Rickets (in children) and Osteomalacia (in adults) = softening of bones 7Muscular System ∙ What muscles do o Excitation: neurons stimulate muscle cells to produce action  potentials (APs) o Excitation-contraction coupling: APs trigger Ca2+ to allow  contraction o Contraction: involves proteins within the cells sliding past each  other and generating force ∙ Muscle fiber: lots of cells that have joined and fused together o Myofibril: one cell/strand within the big muscle fiber  Made of proteins which are called myofilaments ∙ Myofilaments o Thick filament= myosin  Two myosin are intertwined together and then there is a  head/body. The head is where the ATPase activity occurs  Converts chemical energy into mechanical energy o Thin filament= actin (F actin)…the most populated protein  Also made of two fibers intertwined together  2 proteins located ON the actin  Tropomyosin: blocks the myosin binding site  Troponin: calcium binds to troponin and slides  tropomyosin out of the way….so then the myosin is able to  bind!  BOTH of these two are regulatory proteins that either stop  or allow contractions to take place ∙ Each thick filament is surrounded by thin filaments ∙ Z-disc: the ends of the sarcomere, they bind to the thin filaments ∙ M-line: binds myosin (thick filaments) together ∙ Sarcomere: one unit of thick and thin filaments within a myofibril o It is the distance from one z-disc to the next z-disc o It is a unit of contraction ∙ So….it goes muscle fiber myofilaments myofibril sarcomere ∙ A band= the dArk band o Consists of the region of mainly myosin, but also have actin o DEFINED by the presence of myosin…it is dark because it is  soooo dense ∙ I band= the lIght band 1o The absence of myosin!! o Consists of actin and of the z-discs ∙ Alternating dark and light bands ∙ How the sarcomere works o The myosin walks along the filaments and the muscle contracts ∙ TEST TIP o You have to know the terminology to be able to figure out and  get through what the question is asking ∙ Poll Ev: When a muscle contracts, I band shortens because it is… o Answer= part of two sarcomeres o This happens because the z-discs connect the actin filaments,  and so they are causing the sliding o The z-discs cause the moving o Myosin is NOT involved in the shortening ∙ Contractile forces transferred to whole muscles o Endomysium: the tissue that surrounds the muscle cell o Then you have linkage proteins o Then the dystrophin: transmits force from the actin filaments to the extracellular fluid via the linkage proteins  **very important!! ∙ Cell (muscle fiber): surrounded by endomysium ∙ Fascicle: surrounded by perimysium ∙ Organ (ex: tendon): surrounded by epimysium ∙ All of these collagen fibers are continuously running from  bonetendonmuscle o Force is transferred due to the shortening of the fibers 2Nerve-Muscle Relationship ∙ Motor unit: each somatic motor neuron (affecting skeletal muscle)  branches out to A LOT (a large number) of muscle fibers o The unit can be large or small…this tells us about the precision at which the muscle is used o BUT each indiv. muscle cell gets the same number of action  potentials over time from the neuron ∙ Neuromuscular junction: the synaptic knob of the neuron + the  membrane of the muscle fiber o Motor end plate: the region responsible for receiving the signal  **this is the same as the “post-synaptic knob” for a  neuronal signal  This is where we have the ACh receptors  There are junctional folds on the membrane for more  surface area ∙ All along the folds, the membrane is filled with ACh  rececptors  This is WHERE the end plate potentials (type of local  potential) occur ∙ ***Excitation, contraction, and relaxation happens INSIDE the  sarcolemma ∙ Excitation of muscle fiber **this is the signal going from the motor  neuron to the motor end plate on the muscle cell o Action potential (AP) arrives Ca2+ enters synaptic knob synaptic vesicles are released ACh is in the synapse o There are nicotinic receptors on the muscle cells (motor end  plate) o ACh binds to the receptor (ligand-gated channel on the motor  end plate) channel opens to allow Na+ to move through the  membrane (depolarization) then K+ moves into the cell through  the membrane o But…the movement of Na+ is the most important o Opening of the voltage-regulated ion gates  Ion movement across these voltage gates is what creates  an action potential! o End plate potential: this rapid fluctuation in voltage o Since there is no intervening cell body involved (there is no post synaptic neuron…instead, it is the motor end plate), the distance between the motor end plate and the voltage-gated channels is  smaller  This means it is easier to produce an action potential ∙ Flaccid paralysis: the inability to move muscles 1o Issues that interfere with the neuromuscular junction o Botulinum toxin: secreted by bacterium (clostridium botulinum)  BLOCKS the release of ACh  Prevents wrinkles because it prevents the nerve from being able to send ACh across the synapse to the motor end  plate  This affects the facial muscles o Myasthenia gravis: autoimmune disease, degeneration of  muscles characterized by muscle weakness  PREVENTS ACh from binding to the receptor  Antibodies bind to the nicotinic receptors (on the motor  end plate) and precent ACh from getting to the cell and  being able to conduct the signal  The ACh receptors are being attacked by the immune  system  The eyelids are the first thing affected…they are the 1st symptom o Curare: from plants  PREVENTS ACh from binding to the receptor  Competes with ACh for receptor sites and binds to the  receptors where ACh wants to bind  It does not stimulate anything…it just blocks the ACh ∙ Spastic paralysis *the opposite o Muscles become hyperactive and can produce strong painful  contractions o OVERstimulation of the neuromuscular junction o Organophosphates: bind to and inhibits Acetylcholinase (a  degrading enzyme)  Since ACh-ase is inhibited, there is a crazy high amount of  ACh in the synapse  ACh is unable to get out ∙ Poll Ev: a man has myasthenia gravis. What makes his condition  better? o Wrong= Removal of thyroid (because this would cause less  calcium release, which would cause less vesicle release) o Answer= Treatment with an organophosphate  Myasthenia gravis is when there is when there are a lot of  inhibitors preventing ACh from binding to the receptors.   We want organophosphates because then more ACh is  available  Even though you have less receptors (because the  inhibitors are still present on some of the receptors), you at least now have MORE ACh available so there is a better  chance of ACh being able to bond 2∙ Excitation-Contraction Coupling o The action potential (AP) extends into the cell through T-tubules  which are extensions of the cell membrane (cytosol) o T-tubules come in contact with the sarcoplasmic reticulum (SR)  T-tubules: conduct the AP into the interior of the muscle  fiber o Terminal cisternae: bulges of the sarcoplasmic reticulum that  surround the T-tubules (think of the 3D structure)  Contain the calcium channels o Sandwich… Terminal cisternae (of SR)~T-tubule~Terminal  cisternae (of SR) o We need to get Calcium out of the muscle o Action potential stimulates the voltage-sensitive protein in the  SR the voltage channel opens then Calcium can release down  the concentration gradient out of the terminal cisternae Calcium goes into the cytosol o THIS HAPPENS IN THE CYTOSOL  Ca2+ binds to troponin (moves tropomyosin out of the  way) this makes the active site available for the binding of myosin (frees the myosin binding sites) myosin is able to  bind to actin ∙ **Rapid influx of Calcium in muscle cells triggers the contraction! ∙ Sarcoplasmic reticulum (SR) o (1) Releases Ca2+ when stimulated by an action potential o (2) After a contraction, a pump in the membrane of the SR uses  ATP to pull Calcium out of the cytosol (it sequesters it! Takes it  and hides it away) o (3) Stores Calcium ∙ Important spatial arrangement between SR and the T-tubules o Terminal cisternae: specialized portions of the SR that are next to the T-tubules ∙ Contraction (4 phases) o For it to occur:  Calcium has to be available  Action potentials- a lot have to be sent for it to happen  Have to wait until binding sites are available o Myosin head is an enzyme that breaks down ATP  In the initial stages of contraction, ADP and P are present.  Then the myosin head uses the ATP in order to detach from the actin at the end of the cycle. It is used to break the  cross-bridge 3o (1) Cross-bridge formation: myosin interacts with actin (due to  the troponin sliding the tropomyosin out of the way)  Cannot be broken without ATP o (2) Power stroke: the sliding of actin over the thick filament  This is the basis for tension generation (which creates the  strength) o (3) New ATP molecule comes in= *important  Contains chemical energy that is transferred to myosin  Necessary for the breaking of the cross-bridge o (4) Hydrolyzes ATP which regenerates myosin  ATP is broken down with the use of water ∙ Relaxation o the pulling of Calcium back into the SR and then it is stored in  the SR until a contraction needs to occur again 4Conditi on Calci um Tropo nin Tropomyo sin AT P Contrac tion 1 - + + + No This is the normal  state of the cell (when there is no  contraction) 2 + - + + No Tropomyosin is  blocking the binding  sites 3 + + - + Yes 4 + + + - No Can’t go through an  entire cycle because  without ATP, the  myosin cannot  detach. This happens  toward the ned of the  cycle. Then you  cannot get a  contraction. 5 - - - + Yes All the other stuff is  just there to get  tropomyosin out of  the way. If  tropomyosin is not  there, then the  myosin will easily  bind, and then the  myosin will detach  from the cross-bridge  with the help of ATP. ∙ What determines muscle contraction o Temperature: heat makes muscles contract more quickly (they  are enzymatic reactions)  Ex: warming up for a sports game  Contractions are more rapid at higher temperatures, and  there are quicker contractions o pH: muscle contraction is weakened when the muscle is not at its optimal pH  Acidosis: blood and body’s tissues become a little more  acidic (low pH) which weakens the muscles ∙ Less contraction strength o Hydration: oxygen and ion concentration are important for  contraction o Relative length of muscle 5o Intracellular Ca2+ concentration: how much Ca2+ is inside the  cytosol affects the contraction of the muscle ∙ Tension in muscle fibers o Tension: how we measure muscle strength (how much force is  produced) o Stimulus latent phase contraction phase relaxation phase ∙ Twitch: one action potential going over a muscle ∙ Myogram records a twitch ∙ Latent period: this is because of excitation-contraction coupling ∙ SR is always pulling in Calcium, but then the calcium is released into  the cytosol during contraction o Calcium is just sitting in the SR, and when it is released into the  cytosol there is muscle contraction o Cytosol= cytoplasm…. this is where the sarcomeres are!!! ∙ We diminish intracellular calcium (calcium in the cytosol) in relaxation ∙ Wave summation: results when stimuli are close together o Never allowing muscle to relax entirely in between stimuli o Calcium inside the cell is slightly moving up and down each time  that a stimuli comes through o BUT each time it moves out of the SR…so the amount of calcium  going to the cytosol is increasing with each stimulus  Tension slowly builds up ∙ Tetanus (incomplete tetanus): represents the complete saturation  of troponin with Calcium o All of the troponin on every single thin filament is filled up and  bound to Ca2+ o This is the maximum contraction a cell can exhibit o Wave summation describes this process…adding TENSION waves together  The building of wave summation ∙ Fatigue: at a point, the muscle begins to fail o Performs at less than what is expected of it o BUT it is still producing the same amount of tension, it just isn’t  increasing 6o Electrolyte level hasn’t diminished…the cell is still receiving  stimuli ∙ Tension in muscle fibers: tells us how muscles work o AP frequency determines the STRENGTH (tension of muscle)  Different tensions ex: picking up something heavy is more  tension in the muscle versus picking up something light  Ex: carrying something heavy with bicep if it is heavy,  there is a high frequency of action potentials and lots of  Ca2+ is given o Muscles have a maximum tension o Despite the above 2 principles, muscles may fail to perform  appropriately (more to come) ∙ Length-tension relationship o Sarcomeres can be stretched outward by antagonistic muscle  pairs  Gravity can stretch muscle fibers o Sarcomere length correlates strongly to the tension it can  produce o There is an optimal length for tension production  It is all about myosin being able to get a grip on actin o Overly contracted  Sarcomeres can be overly compacted if it is contracted for  a while  Interference: myosin could be grabbing onto the wrong  filament  When actin filaments overlap, the myosin head within the  thick filament could be pulling the actin the wrong way o Overly stretched  There are not as many binding sites for the myosin to grab  onto the actin ∙ The bone determines the range of movement o Our joints limit the stretching and compacting of muscles ∙ These 2 conditions are NOT obtainable for the human body to this  extent ∙ Types of whole muscle contractions o Isometric contraction: when you hold something in your hand,  your muscles are contracting, but they are not shortening  We build tension (actin and myosin are sliding past each  other) but then we allow slippage (allow it to let go)  Sarcomeres are producing a tension, but they are not  shortening  The right amount of Calcium is released so that we are not  producing too much tension (optimal tension) o Isotonic contraction 7 (1) Concentric: providing amount of force that is greater  than the resistance ∙ This causes the muscle to shorten ∙ Ex: create lots of Calcium to overcome the force of  picking up a drink and moving it to your mouth  (2) Eccentric: this is for lengthening the muscle ∙ Amount of tension (force) produced is less than the  amount of resistance ∙ Ex: setting a baby down gently (controlling the  decent of an object) ∙ Ex: quads contract to go down stairs ∙ All three of these types of contraction provide the same action of actin  and myosin…BUT the force (tension) produced varies ∙ Muscle contraction centers around the ability to hydrolize ATP ∙ We get ATP from: o Glycolysis (burn up glucose to make ATP) o Aerobic respiration o Phosphagen system ∙ Glycolysis: the breakdown of glucose o **glucose is the substrate o Production of 2 ATP molecules o Then… Pyruvate (Pyruvic  Acid) is formed Anaerobic  Respiration: when  there is no oxygen,  lactic acid is  produced Aerobic  Respiration: when  we use oxygen, 36  ATP are produced ∙ Phosphagen system: transfer of high energy bonds o **ADP and P are the substrates o Myokinases: they take ADP, add a phosphate to it, and then  make ATP from the two reactants  Myo= muscle  Kinase= adds phosphates to things o Creatine kinase: takes a phosphate FROM creatine phosphate   Uses ADP and the phosphate this results in the production of ATP  Creatine phosphate: stored in muscle cells o The ability of this process to occur depends on if we have the  substrate 8∙ Oxygen gets consumed quickly o It is freely floating in the cytosol o Myoglobin: holds oxygen in the muscle cells ∙ Initially, the muscles have consumed the O2 that is in them (in the  myoglobin) ∙ Then we use glycolysis only as the body is adapting ∙ Once we catch up, we can sustain energy for a while because we have  more oxygen due to the use of aerobic respiration ∙ Strength conditioning: during this, your muscles are contracting a lot  and the muscle cells are squeezing tight together (think about your  bicep) o All the blood vessels around your muscles are not able to deliver  blood when muscle cells are close together o Your muscles lack oxygen because it is not able to be transported throughout the blood cells ∙ Oxygen debt: you breathe heavily after a workout because you have  to repay what you have depleted from the cell ∙ Modes of ATP Synthesis from exercise ∙ In initial aerobic respiration, we are depleting ATP because of muscle  contraction ∙ In aerobic respiration at the end, the cardiovascular system has  catches up ∙ Glucose: is in the blood and is also in muscle cells o Needed for glycolysis o It is stored in glycogen glucose is in muscles, not the blood at  this point  Glycogen: lowers blood glucose concentration  Glucagon: pentaGON! Big!! Raises blood glucose  concentration 9∙ Oxygen debt: something that you have to give back because you  borrowed it o We are operating without oxygen for a period of time, so we  deplete other things along the way o Molecules that we deplete  Creatine phosphate: we grab the phosphate to make ATP  Glucose: we use lots of it…it is suspended in the cytosol,  but also is in glycogen  ATP, Oxygen o We need to get muscle back  Store creatine phosphate  Rebuild ATP  Synthesize glycogen for later ∙ Period of heavy breathing because: o We are replacing oxygen reserves o Replenishing phosphagen system o Oxidizing lactic acid in the liver and converting it to glucose  **think like this is part of the respiration cycle ∙ the reverse of anaerobic respiration in order to  restore o Serving the elevated metabolic rate (body temp increases,  appetite increases)  Causes you to have increased consumption of energy  If you are active, your body is expecting to always be  active so you have a high metabolic rate  You are always using energy, and you always need to get  more energy 10Endocrine System ∙ Hormone: a signaling molecule that travels through the blood ∙ What stimulates a cell to release a hormone o Glucose levels (ex: high blood sugar) o Other hormones (a hormone’s job can simply be just to release  another hormone) o Nerve signals (by the brain) o Ions are small molecules…calcium, glucose ∙ Why we release them o Cells respond to glucose levels because they NEED to respond  Homeostasis (negative feedback): response removes/takes  away a stimulus o Response to an external stimulus o A stress response o Control (ex: a hormone that tells us to make body hair) o Growth and development: age and surroundings are utilized to  determine when these hormones are released  Utilizes top down control ∙ Knowing something about the response can tell you what the stimulus  is…they are tied together ∙ Hypothalamus: a nervous and endocrine structure o Forms floor and walls of 3rd ventricle of brain  The walls of the “cone” region o Below it is the pituitary gland o Fight or flight response o Controls water balance, thermoregulation, sex drive, childbirth  A lot of these functions are carried out by hormones  Hypothalamus releases these hormones through the  pituitary gland o Many of its functions are executed by the pituitary gland ∙ Hypothalamus (there are clusters of neurons within it) interacts with  pituitary in 2 ways: o (1) Interacts with posterior pituitary  Cell bodies in hypothalamus neurons run down and  directly stimulate the hormones the axons form a bundle  (tract) and they terminate to comprise the posterior  pituitary *axons go MUCH further  Hormones released from axon terminals: ∙ Oxytocin ∙ Antidiuretic hormone  Go into blood capillaries to go out to the body (*venous  blood) 1 Posterior pituitary is a neuroendocrine organ: made of  nervous tissue & is an endocrine organ o (2) Interacts with anterior pituitary  Neurons in hypothalamus release hormones within  hypothalamus they go into the blood they go into  capillary beds they diffuse out of the capillary beds and  into the anterior pituitary  Hormone A travels down as an intermediate and tells  anterior pituitary to release Hormone B  Axons primary capillaries (in hypothalamus) secondary  capillaries (in anterior pituitary) hormone released ∙ Posterior pituitary: made of nervous tissue ∙ Anterior pituitary has… o Glandular epithelium: a bunch of cells stuck together  Glandular= it secretes stuff o Made of NO neurons (and NO neuron cell bodies) except for axon  terminals  There also are glial cells ∙ Antidiuretic hormone (ADH) released by POSTERIOR pituitary o Hypothalamo-hypophyseal tract sent down synaptic vesicles o Osmoreceptors: responsible for this detection  Sensitive to high sodium levels o Blood osmolarity: how much solute you have dissolved in blood  If there is a lot of solute in the blood, you will need to try  and retain water to dilute it  Sodium is a good indication of other substances in the  body  If blood osmolarity increases, ADH is released o Diuretic: something that makes you pee  Anti-diuretic…keeps the fluids in you!  It suppresses the release of salt from the blood 2stimulus= • high blood  osmolarity (A  LOT of solute in  the blood) messenger=  ADH •Works against  the production  of urine • Helps us retain  water • If salt  concentration is  too high, ADH  will stimulate  kidneys to  retain water response= • increase in  water retention • increased thirst:  happens  because ADH  tells the  hypothalamus-- > this causes a  behavioral  response ∙ Kidneys have the ability to retain water or lose water o Retaining water= makes the blood more dilute ∙ Poll Ev: What condition would directly stimulate ADH release?  o Answer= consuming caffeine (a diuretic)  This causes us to lose more water…you are peeing more  and so you are losing water, BUT you are retaining salt in  your body  This high concentration of salt means you need to increase ADH which will dilute your blood o Hyponatremia: when there is not enough salt  Natrium: where we get the Na (sodium)…which is what  controls osmolarity o Hypersecretory pituitary tumor  Since we are talking about ADH, we know that we are  talking about the posterior pituitary. In the posterior  pituitary, there is one LONG axon, so the hormone goes  directly into the blood  You cannot have a posterior pituitary tumor because a  tumor cannot be on the axon  If you had a hypersec. tumor, it would have to be in the  hypothalamus ∙ The hypothalamus is where the cell bodies are o Thirst: cannot be the answer because thirst is a response…NOT a condition  It is not an indication of the stimulus and therefore it does  not cause release  Remember…there is an increase in thirst when the  hypothalamus is alerted about the release of ADH from the  posterior pituitary 3∙ Oxytocin (OT) released by POSTERIOR pituitary o Responds to the needs of the nervous system…nervous system  TELLS it when to release  Greatest example of something that responds to the neural reflex o Responsible for smooth muscle contraction (uterus, reproductive  ducts, etc)  Ex: stimulates the release of milk from the mammary  glands o Promotes emotional bonding!! cute baby with dogs  o Neural stimulus OT smooth muscle contraction ∙ Anterior pituitary hormones: under the control of hypothalamic  hormones (ex: ADH, oxytocin) o These hypothalamic hormones: primary job is to signal to the  anterior pituitary ∙ Anterior pituitary hormones are released when stimulated by  hypothalamic hormones ∙ Hypothalamic hormones in the anterior pituitary o Can be inhibiting or releasing…which means it inhibits or allows  for a certain anterior pituitary hormone o Whenever it ends in inhibiting or releasing, you know that it is a  hypothalamic hormone and will be signaling the anterior  pituitary ∙ Anterior pituitary hormones (6) o FSH (follicle stimulating hormone): stimulates secretion of  ovarian sex hormones, development of ovarian follicles, and  sperm production o LH (luteinizing hormone): stimulates ovulation, stimulates corpus luteum to secrete progesterone, stimulates testes to secrete  testosterone  These two are hormones used in reproduction o ACTH (adrenocorticotropic hormone): stimulates the adrenal  cortex to secrete glucocorticoids  “adreno” (adrenal) “cortico” (cortex)  Tropic= stimulates one hormone to release another  hormone o PRL (prolactin): “pro” “lactation”  After birth, stimulates the mammary glands to synthesize  (MAKE) milk, enhances secretion of testosterone by testes  BUT oxytocin causes smooth muscle cells around the  mammary glands to squeeze which allows for the RELEASE of milk 4o TSH (thyroid stimulating hormone): stimulates secretion of  thyroid hormone o GH (growth hormone): stimulates mitosis and cellular  differentiation  It is important for growth through childhood of the somatic  tissue (bone, cartilage, muscle), but also for  repair/maintenance as a person is an adult  causes ∙ ALL have common regulatory theme o Hypothalamus pituitary organ ∙ Control of thyroid gland exemplifies the interactions of the  hypothalamus-pituitary-organ axis ∙ How the thyroid hormone is released o TRH (Thyrotropin releasing hormone)  Its name tells you what it does…it causes the release of  thyrotropin o Thyrotropin is called TSH *tropic= one hormone causes release  of another o TSH (thyroid stimulating hormone) goes to the thyroid stimulates the release of T3 and T4 which combine to make up  the thyroid hormone  We have negative feedback inhibition to maintain  homeostasis of hormone levels  Negative feedback tells us to try and remove that stimulus  to prevent hormone levels from going out of control  Then, once we need the hormone again, the stimulus  comes back to trigger the steps that cause the release of  thyroid hormone ∙ How the growth hormone is released o GH and IGF-I (somatomedin) are only released when the  conditions are right for growth and repair o FIRST *both of these are hypothalamic hormones  GHRH (high protein meals, hypoglycemia, sleep,  exerciseall good things!  GH leaves pituitary and causes  growth/maintenance/repair of tissue tissue ∙ Released when conditions are good= protein, sleep,  exercise *if you are already old, it is growth in terms  of cell division  Or……GHIH (poor nutrition, not enough fats, high carb  meals) ∙ Released when conditions for growth are not present, so you will not grow  ∙ GHIH is stimulated when this happens o In tissue: IGF-I (somatomedin) is the intermediary 5 Growth of cartilage, bone, and muscle  Repair of tissue o IGF-I mediates the somatic effects of GH ∙ GH= the short term hormone (only lasts an hour or so)…it then  stimulates IGF-I ∙ IGF-I= the long term hormone *somatomedin “somato”  “medin”mediates SOMATIC effects of GH ! o Hormones have similar effects ∙ ADDL FUNCTION OF GH o GH and IGF-I cause our bodies to use:  Fats for energy  Spare proteins for repair/growth  Spare carbohydrates for later o Proteins, fats, and carbohydrates are used for fuel o GH regulates all 3 of these *think…the purpose is to promote  growth&repair Molecules  affected What GH/IGF-I does Rationale Proteins  production, degradation Make proteins available  for growth Fats Fatty acids released from  adipocytes *if you consume fats, you burn fats *goes out to body and is  consumed for fuel *preferred to be used for  energy…. “protein sparing”  effect and  *“glucose sparing” effect:  resisting the use of glucose for fuel Carbohydrates Reduces tissues use carbs  (glucose in particular) for  energy The sparing effects  means that we want to  AVOID using protein and glucose for primary fuel Fats are abundant…so  storage is unnecessary o SO……fats are the preferred method to get fuel and use it for  energy, and carbs are only use when necessary. Also, use  proteins to grow, repair, and divide cells. o NOTE= brain, liver, kidneys, and RBCs always use glucose for  energy ∙ Hypothalamus and pituitary gland control a lot of these other organs ∙ Pineal gland: converts serotonin  (happy hormone) to melatonin 6o Establishes the circadian rhythms o Serotonin: promotes high mental activity, mental arousal, and  alertness  Much more abundant in daytime hours o Melatonin: “mellow”  Low light, mental “depression”, sleep ∙ Seasonal affective disorder (SAD) : occurs in winter or northern  climates o Melatonin is present much more often than serotonin o Symptoms: depression, sleepiness, irritability ∙ Thyroid gland: located up around the trachea, composed of T3 and T4 producing follicle cells o Follicle: the little dots that go all around in a circle  The spherical arrangement of cells  Single layer of epithelial cells make up the border o Colloid: the inside of the circles which contains proteinacious  fluid ∙ Process o Hypothalamus detects temperature TRH released when  temperature is low travels to anterior pituitary (the only  target) TSH then goes to blood and then to the thyroid T3 and  T4 (together called TH) o *Target cell for TH is the whole body!! ∙ Purposes of thyroid hormone: o  metabolic rate: increase reactions that produce and consume  energy (glycolysis, increase number of enzymes, activate  enzymes)  EACH cell is consuming more energy because of TH  Heat is a byproduct…and the temperature is increased.  The heat energy is needed to stimulate other chemical rxns ∙ So…there are temperature effects! ∙ Also…oxygen effects! (we are consuming more  oxygen) o Respiratory rate and heart rate go up o  appetite o  GH secretion ∙ **Great blood supply in endocrine glands…and great blood supply in  thyroid! ∙ T3 and T4 production is a multi-step process o Blood capillary and thyroid follicle relationship 1. Iodide absorption: iodine absorbed by follicle cells (we get iodine  from food) 2. Thyroglobulin synthesis (tyrosine-rich amino acids) 7a. Thyroglobulin rests in that little follicle 3. Iodine added to tyrosines of thyroglobulin a. Sometimes we get 4 iodines, and sometimes we get 3 b. The cells only really use 3…they just remove the 4th if they  get it 4. Thyroglobulin uptake and hydrolysis (taken apart/broken down) 5. Release of T4 and small amount of T3 into blood ∙ **iodine is important! ∙ Poll Ev: Patient exhibits hyperactivity and elevated body temp. Blood  test is done. Elevated TH and TSH. Low levels of TRH. Which part of the body has the problem? o Answer= anterior pituitary  You know the hypothalamus produces low amount of TRH  because of negative feedback and homeostasis. It is still  doing its job. Hypothal makes low amount of TRH to  balance out the elevated levels of TH and TSH.   Hypothalamus RESPONDS to TH levels…if there is a lot of  TH, hypothal will lower TRH (thyroid releasing hormone)  TH should inhibit the pituitary, which is not happening ∙ Like…if there is a lot of TH, then the anterior pituitary will not release TSH!  TRH stimulates TSH, and if TRH is low, you would expect  low amounts of TSH  **Hyperpituitary secreting gland is suspected/assumed ∙ Thyroid gland continued o One big concept to remember….  When osteoblasts build more bone matrix and calcium  levels increase in the bone, that means that there are  lower calcium levels in the blood o Has C cells (parafollicular cells) that produce calcitonin (lowers  blood Ca2+ concentration) o Calcium  calcitonin  osteoblast activity, PTH o High levels of calcium is not usually the problem  But if it is, we build bone matrix (osteoblasts) and increase  calcium that goes into bones  PTH: increase blood calcium concentration. Levels of this  hormone decrease when calcitonin is secreted since they  are antagonistic o Thyroid gland has TWO parts  90% devoted to production and release of thyroid hormone o Follicle cells (dots lining the follicle): produce thyroid hormone o Parafollicular cells (C cells): respond to calcium  Calcitonin released 8o Calcium in blood  happens because osteoblasts are using the  calcium to form bone matrix ∙ Parathyroid glands: produce PTH (raises blood calcium  concentration) o Calcium conc  PTH  osteoclast activity, Ca2+ reabsorption  from kidneys, Calcitriol o the increase in calcitriol: increases calcium in the blood, also  increases calcium uptake in the intestines o ALSO mimics and repeats the increase in osteoclast activity and  the increase in calcium reabsorption by the kidneys ∙ Pancreas: 2 organs in one o (1) digestive function  Exocrine cells: made of ducts (99% of pancreas cells are  connected to ducts)  Produce digestive enzymes and mixes them with what  comes out of the stomach o (2) endocrine function  pancreatic islets: a gland that secretes insulin and  glucagon DIRECTLY into the blood ∙ Endocrine cells: NO ducts  Alpha cells: secrete glucagon (increases blood glucose  concentration)  Beta cells: secrete insulin (decreases blood glucose  concentration)  ANTAGONISTIC hormones o Insulin: little peptide hormone  Stimulates cells outside the body to pull in glucose  Takes glucose out of the extracellular fluid and into the  cells  After we eat a meal, glucose needs to be absorbed and  pulled in by the cells ∙ Insulin is utilized to do this  Muscle cells take in the most glucose, especially when you  are active ∙ They need more ATP than most cells ∙ We store a lot of glucose in the muscles as glycogen  Liver pulls in glucose too (but this depends on how big the  meal is) ∙ Turns it into glycogen and stores it ∙ glucose conc (hyperglycemia)  insulin  hypoglycemic events… effects are in the direction of hypoglycemia (but eventually become  normoglycemic) 9∙ Another function of insulin: o Suppresses usage of stored fuel (fat, protein, carbs)  They are NOT used when there is abundant glucose ∙ POLL EV: Sally has just eaten a meal. What will happen as a result? o ANSWER= glycogen synthesis will increase  Makes sense….take in all the glucose from the food and we want to store it away as glycogen o Glycogenolysis: breakdown of glycogen  “glycogen”= stored glucose “lysis”= break down  Glycogen becomes glucose IN THE LIVER  This process is increased when you have low amount of  glucose. You need to release more glucose from the stored  glycogen. o Gluconeogenesis: production of new glucose from fatty acids  A form of glucose synthesis that mainly happens during  starvation or high stress o We know….that if you eat a meal, glucose levels go up o Adipose cells releasing lipids  Not the result, because glucose is the first thing we use,  and then fats are used as a second resort  So…this would be used when we need to increase glucose  in another way o Glucagon’s hyperglycemic effects (the effects glucagon has to  raise glucose)  Stimulate glycogenolysis  Gluconeogenesis would be the second/last resort  Stimulate fat catabolism and release of fatty acids ∙ POLL EV: What would not result in high levels of glycogenolysis? o Answer= you are on a high carb diet o You have lots of glucose readily available for use in the blood, so  you do NOT need to break down the glycogen (the stored  glucose) o Plenty of carbs avail ∙ Lipogenesis: when you have an excess of glucose, it is stored as fat Andrenal gland: sits on top of the kidneys and has 2 parts ∙ Adrenal medulla: has chromaffin (post-ganglionic neurons) o Chromaffin releases Epinephrine and Norepinephrine  catecholamines o Neural stimulus catech. E and NE sympathetic effects (dilating  of pupils, suppress digestive activity) o Releasing fats and adipocytes they go into the blood for the  purpose of providing fuel to the body 10o E and NE: make fuels available for the body o Effects of E and NE:  Fat mobilization (fatty acids are stored in adipocytes) ∙ Release fatty acids from adipocytes that go into the  blood purpose= provide fuel for the body  Glucose production in the liver ∙ Glycogenolysis and gluconeogenesis ∙ Seems excessive to release BOTH of these…but it is  fight or flight and we need fuel  “glucose sparing effect”: inhibits insulin secretion ∙ keeps glucose in the blood during intense exercise  (we are consuming lots of energy) o BUT without the insulin, your muscles cannot  uptake glucose o **make sure to think about how the hormone  works in BOTH directions…blood to muscles,  and muscles to blood ∙ During exercise, we primarily use fats for energy. ∙ BUT the brain can only use glucose…so fat is used  for energy in order to protect the brain which needs  the glucose ∙ Muscles use fats so that we do not deplete glucose o **normally, insulin is needed to increase the glucose that goes  into the muscles and glands (because insulin decreases blood  glucose concentration…so therefore it increases the glucose that  goes ino muscles) ∙ Adrenal cortex: has 3 classes of hormones (but total of 20 hormones) o Mineralocorticoids ex: Aldosterone: concerned w/ mineral  levels and  electrolyte balance o Glucocorticoids ex: Cortisol: concerned with glucose levels o Sex hormones ex: DHEA, Estradiol: concerned with sex  activity and  development  They are a supplement to what ovaries and testes  produce they produce the same hormones  Women= this gives them their major source of DHEA  Men= this gives them their major source of estradiol o While aldosterone is concerned with mineral levels, we can  monitor mineral levels as a whole mainly by being concerned  with Na+ levels 11o Na+ OR K+  aldosterone  reabsorption by kidneys so there is  less sodium that is lost. We want to retain sodium levels in the  body.  ∙ Poll Ev: If blood Na+ levels are very low, what should the body do to  achieve homeostasis? o Answer= secrete aldosterone AND inhibit ADH  Think about it…a diuretic is something that causes you to  pee a lot (caffeine). There becomes a high concentration of sodium in blood, since water is leaving blood. So…ANTI diuretic hormone increases water concentration…and it  wants to decrease Na+ levels!  Low sodium levels stimulates aldosterone release…the  body reabsorbs sodium from the kidneys  If we inhibit ADH, we prevent the hormone from working.  ADH tends to decrease urine secretion and increase the  amount of water in the blood. ∙ Stress: physical and mental o Physical stress: any kind of injury, being malled by a bear  Brain is aware of the damage to the body, so hormones are released o Mental stress: happens to us all the time o Cortisol= “the stress hormone”…main function is to deal with  stress o When under stress, cortisol stimulates the breakdown of fat and  proteins for fuel o Negative effect: diminishes/reduces the immune system function o Physical/mental stress  CRH released by hypothalamus, ACTH  released by anterior pituitary (adrenocorticotropic hormone)  cortisol (secreted by adrenal cortex)  fat and protein  breakdown, gluconeogenesis (glucose production from fat) o Cortisol effects:  Mobilizes fat: takes fat stores and releases them to the  blood  Breaks down proteins  Breaking them down for energyresult is  Gluconeogenesis: you are going to have to make glucose  from the fat. The brain and other organs REQUIRE glucose  for function…so we cannot function without glucose  production Hormone Effect on glucose utilization Rationale GH *Focused on dietary conditions *Other fuel is abundant 12Epinephrine  &NE *Decreases glucose usage in  the body. When GH present, we  use fat for energy and to grow  and do functions of the GH.  *Decrease glucose usage to  most cells. Instead, use fats.  Make glucose available for the  nervous system.  *Hypoglycemia *“Glucose-sparing  effect”: shift in fuel  usage. Leave glucose  for the cells that HAVE  to have it…and use the  abundant fat for fuel *Fight/flight has a large  energy demand *You are running from a  bear…you cannot use  up all of the glucose to  run away, because the  brain needs it Cortisol *Decrease glucose usage *Usually present when you have been malled by a bear and you  need fuel..because it’s the  stress hormone!! *Glucose is scarce;  spare it for nervous  system ∙ Usually low glucose is not the case. Usually us people in the normal  world have too much glucose soooo so much…because we have high  carb diets. So that extra glucose gets stored as fat ∙ General Adaptation Syndrome (GAS) aka stress response 1. Alarm Reaction: epinephrine rises, sweaty palms, breathing  heavily  Goes on for a short period of time  Defined by elevated levels of Epin and NE they prepare  the body for fight or flight 2. Resistance stage: brain stimulates release of ACTH and cortisol  Alternative fuels mobilized…we have to break down fats  and proteins 3. Exhaustion stage: protein alone is available.   Muscle wasting=muscle diminishing in size broken down  into amino acids amino acids used for fuel  Death is imminent= hormones aren’t able to be released  and you cannot maintain homeostasis ∙ Hormone chemistry: classes of hormones o Steroid hormones: derived from cholesterol (cholesterol is  produced in the liver)  Secreted by gonads (testosterone, estradiol, etc) and  adrenal cortex (ex: cortisol) o Monoamines: made from amino acids (biogenic amines)  Derived by tyrosin and tryptophan 13 Secreted by adrenal medulla, thyroid, and pineal gland o Peptides and glycoproteins: amino acid chains  Secreted by pituitary, hypothalamus, and others ∙ Poll Ev: If you were in the exhaustion phase, what hormones might you  have trouble synthesizing? o Well…in the exhaustion phase protein is being utilized for  energy…there is a drastic decrease in protein synthesis. Because the proteins are being USED! o ANSWER= ADH  We have trouble synthesizing this because it is it is  secreted by the pituitary, which means it is a peptide  hormone  Cholesterol is produced by the liver…so we have the  building blocks for cholesterol! So we are able to make the  steroids.  ∙ Cortisol, aldosterone, testosterone, estrogen= ALL  steroids Hormone receptors and effects ∙ Hydrophobic hormones: steroid hormones and TH o Require a transport protein to get through the blood o This transport protein masks the hydrophobic effects of these  hormones o BUT since its hydrophobic, it is able to pass through the plasma  membrane easily o Receptors are intracellular bond is formed o The hormone enters the target cell and goes straight to the DNA  in the nucleus o This hormone affects transcription **has an effect on the GENE  level! This is a big deal!! o Have major changes on cells (ex: puberty and everything that  happens) ∙ Hydrophilic hormones: peptides and catecholamines (Epin, and NE) o Travel freely through the blood, but then they are unable to  penetrate the plasma membrane o Hormone binds to transmembrane receptors on the cell surface  o The hormone is the 1st messenger o This is linked to the 2nd messenger (the intracellular messenger)  There are a variety of 2nd messengers  Calcium is one of them  This happens because there are different types of  responses  **we do not want 2 hormones to go to the same 2nd messenger 14∙ How the hydrophilic hormone does its job 1. Hormone-receptor binding activates G protein 2. G protein activates adenylate cyclase 3. Adenylate cyclase produces cAMP 4. **cAMP activates protein kinases a. kinases have SELECT number of proteins that it affects b. job is to go around and phosphorylate other proteins…they  either activate or deactivate enzymes c. kinases phosphorylate enzymes!!! 5. The enzymes that are activated catalyze reactions ∙ Hormones involved: ACTH, FSH, PTH, TSH, glucagon, calcitonin,  catecholamines o Ex: PTH increases blood calcium concentration. Think about it  as…it does this by breakin down bone matrix stimulates  osteoclasts and releases calcium into the blood **osteoclasts  does this by dumping acid HCl onto bone matrix……it just tweaks the existing apparatus within the cell ∙ “Amplifying effect”: lots of cyclic AMP goes around to activate the  protein kinases then lots of kinases go out and phosphorylate the  enzymes o This is what causes a hormone to have an effect ∙ The number of receptors for a hormone is not static o Hormones can have an effect on their own strength o Ex: exercised muscle cells upregulate insulin receptors  Insulin stimulates glucose uptake into the muscles…the  number of receptors for insulin will increase if the muscle is used often this increases the response to be greater  This type of muscle needs more glucose than the average  muscle cell ∙ Diabetes: when cells downgrade insulin receptors o This means that muscles are unable to get enough glucose o Insulin= responsible for glucose uptake 15The Heart ∙ Sequence of blood flow *starting with oxygenated blood leaving the  heart and going out to the body o Left ventricle: chamber that provides pressure for most of  circulation o Oxygenated blood leaves the heart through the aorta o Systemic capillaries: place where O2 goes from blood to most of  the tissues in the body o Deoxygenated blood comes back into heart through the superior  vena cava o Moves into the right atrium o Right ventricle o Deoxygenated blood leaves the hearth through the pulmonary  trunk o Pulmonary capillaries: take blood to lungs and pick up O2 o Oxygenated blood goes back to the heart through the pulmonary  vein o Left atrium ∙ Path of blood: the double circuit ∙ When blood goes through the whole circuit one time, it goes through  both circuits 1∙ The blood goes through 2 circuits before getting back to the start ∙ Job of the heart= pumps blood provides the pressure o It is pressurizing the blood ∙ Input of pressure to system is done at 2 locations because there are 2  circuits ∙ Arteries: have the highest pressure o As you get further and further from the heart, pressure gets lower  and lower ∙ Pressure gradients (differences in pressure between two things or two  sides of things) are what move blood o Because blood moves from area of high pressure to area of lower  pressure ∙ Heart location: more or less in the middle of the body (a teeny bit off to the left I guess maybe…) ∙ Thorax is the area from the neck to the abdomen o Subdivision of the thorax= mediastinum ∙ Mediastinum: the middle cavity (region) where the heart resides o The central compartment of the thoracic cavity o Anterior to vertebra and it is in between the lungs o It contains the heart, esophagus, and trachea, etc ∙ Pericardium: the outer covering that encloses the mediastinum *has  2 parts o Fibrous: tough, resilient, outer sac covering  Doesn’t allow heart to stretch/limits the heart’s expansion  Dense irregular connective tissue= resists stretching in all  directions o Serous pericardium: inner covering that secretes serous fluid  Reduces friction as the heart is always moving around and  pumping  We want the heart tissues to last and make sure they don’t  wear away  2 layers: parietal pericardium and visceral pericardium  (epicardium) ∙ Heart layers o Fibrous pericardium o Parietal pericardium *serous layer o Visceral pericardium *serous layer o Myocardium *where the cardiomyocytes are o Endocardium ∙ The fist! balloon= parietal pericardium o Outer covering of balloon that surrounds fisit= visceral  pericardium o The skin that covers the fist= myocardium ∙ Action potentials stimulate contractions 2o Conduction system: very specialized cells within the heart  It functions like neurons conducting APs  Electrically conductive  **Conduction cells: haven’t fully taken on characteristics of muscles (such as contraction) o Cardiomyocytes: electrically conductive cells that contract!  Located in the myocardium  **Cardiomyocytes: cells for contraction ∙ The heart sets its own heart rate by producing action potentials o Conduction system sends APs to specific parts of the heart o Cardiomyocytes take the signal from the nodal cells and contract ∙ Cardiomyocyte cells are much shorter than skeletal cells…they only  have 1 nuclei in each cell o They are striated…so they have sarcomeres that shorten and can  contract ∙ Intercalated discs: connect the individual cells o The junction where one cell meets the next O|O|O|O|O| o Contains gap junctions and desmosomes o (1) Highly folded surface area allows more and more surface to be  available  This allows for more gap junctions and more desmosomes o (2) Gap junctions: functional junction allows electrical impulses to pass from one cell to the next  They allow the AP to be propagated from cell to cell  Allows for the passage of ions o (3) Desmosomes: intercellular junction (mechanical type of  junction) they anchor/join cells together and connect myocytes  If one cell contracts, the cells all contract together  Transfer the force from one cell to the next without  destroying the cell ∙ Cardiomyocytes are connect BOTH electrically and physically o Glycogen- lots store in them o Mitochondria- have a lot of them because the heart is always in  aerobic metabolism ∙ Electrical activity in the heart *conduction cells o System found in certain places in the heart o Job of conduction cells (nodal cells): pattern distribution of APs  along the conduction system pathway  They spread the signal to the myocardium o SA (sinoatrial) node starts the conduction of the signal located  in the right atrium  Establishes the frequency of APs o Pathway 3 SA node AV node Bundle of HIS Bundle branches Purkinje fibers ∙ Sinus rhythm: normal heartbeat set by the SA node o Intrinsic electrical rhythm of the heart with NO outside influence ∙ BUT…there is still extrinsic influence on the heart sympathetic and  parasympathetic innervation o But really we do not need it for the heart to actually beat o Job of symp and parasymp: speed up or slow down the heart rate due to what is going on in the external environment  They need to do this in some circumstances  Fight/flight, rest/digest influence blood pressure/heart rate ~Antagonistic effects ∙ Cardiac nerves: innervates sympathetic part o Speeds up the heart rate ∙ Vagus nerves: innervates parasympathetic part o Slows down the heart rate ∙ **Usually a person’s heart rate at normal content conditions is slower than the sinus rhythm o Parasympathetic tone: the normal constant slowing of the heart  at rest  The parasymp system at rest is slowing the heart down at  an intrinsic rate (internally) o So…if you took the heart out of the body, it wouldn’t have  parasymp effects so the heart rate would speed up a little bit ∙ Pacemaker cells (nodal cells): they do things alone (meaning they  do not have a stimulus…they work involuntarily) o They are the pacemaker (set the pace of the signal) for the heart o Have an unstable RMP o Have a lot of Na+ leak channels  On a graph, the RMP is no longer a flat line that it is in  neuron cells 4 Instead, they have an inclined pacemaker membrane  potential o Normal cell= flat line with RMP -70 mV o Pacemaker cell= line inclining upward, starting at -70 and then  getting to -55  THEN the AP happens  Threshold= -55 mV o The membrane potential really isn’t resting…it is always  depolarizing (causing a slow upward, more positive increase in  membrane potential) ∙ Pacemaker cells are special because… o *Unstable RMP o *Large number of Na+ leak channels allow the cells to climb up  toward threshold ∙ AP after AP after AP from pacemaker cells o This is what causes the sinus rhythm to be able to happen! ∙ (1) Pacemaker potential: SA node cells gradually depolarize from the  slow Na+ leak channels during the incline ∙ (2) Depolarization: voltage-regulated Na+ and Ca2+ channels open right at the threshold and keep going until they hit the peak o But…mainly the influx of Na+ ∙ (3) Repolarization: K+ flows out of the cells ∙ Changing frequency of APs o We change the frequency of the APs in order to pick up the pace o We can make the threshold happen faster, which then makes  more APs able to happen in a shorter amount of time 5o How we do this= we let more Ca2+ into the cell during the  pacemaker potential phase in addition to the Na+ inflow that is  happening  Ca2+ influx!!!  We get to the threshold sooner faster depolarization ultimately speeds up the heart rate ∙ Poll Ev: Explain how the heart rate is increased. _____ increases Ca2+ leak channels in pacemaker cells o Answer: NE from cardiac cells  We know that the heart is sped up by NE (NOT ACh)  We know it is cardiac because cardiac cells are innervated  by the sympathetic nervous system (fight/flight)  The sympathetic nervous system SPEEDS UP heart rate o NE stimulates adrenergic receptors those receptors lead to a 2nd messenger system 2 nd 2nd messenger=  1st 1st messenger messenger =  =  the NE  the NE  messenger=  the activation of  the activation of  more Ca2+ more Ca2+ channels so that  channels so that  pacemaker  pacemaker  potential has a  potential has a  steeper slope and  steeper slope and  increases faster increases faster Effect=  Effect=  heart rate is  heart rate is  increased! increased! o The slope of the pacemaker potential is adjustable…it can have  different steepness depending on how many Ca2+ leak channels  we have during the pacemaker potential ∙ SA node comprised of nodal cells o They have spontaneous APs…do NOT need a stimulus to make  the AP happen ∙ Molecule that tells the heart to go faster= NE (from the symp system) o It causes more Ca2+ channels to be inserted into nodal cells leads to a faster pacemaker potential ∙ Molecule that tells the heart to slow down= ACh (from parasymp  system) o It causes the activation of K+ channels so that K+ leaks out of the  cells (efflux) o Less steep slope in pacemaker potential ∙ IMPORTANT DISTINCTION- 2 types of cells in the heart these are the  cells causing the blood to be pushed through, and then the pressure  causes the blood to go out to where it needs to go o Nodal cells (pacemaker cells)  Only in the nodes of the heart (SA and AV nodes)  They create their own impulse because they do NOT have  a stimulus  Produces signal (the AP) and sends it off 6o Cardiomyocytes  All throughout the conduction pathway ∙ In the walls ∙ They are the lining of the atria and the ventricles  Has a stimulus  Receives the signal, sends the signal (propagates/sends  along)  Also is responsible for contracting: the cells still have  sarcomeres and they are muscle cells ∙ The cells shorten which leads to an overall contraction  of the heart ∙ Cardiomyocytes have an extended “plateau phase” o Cardiomyocyte AP is much greater in response, compared to the  skeletal muscle AP ∙ Plateau phase: has the effect of lengthening the period of time that  we have an AP o The AP is not different in magnitude…it is just stretched over a  longer period of time ∙ Cardiomyocytes have an additional channel o Slow Ca2+ channel: opens at the height of depolarization  (opens right after the peak of the AP…and then it happens during the plateau phase) o Ca2+ moves into the cell o Plateau phase= simultaneous movement of Ca2+ into the cell and K+ out of the cell ∙ Cardiomyocyte pathway o Depolarization (Na+)  Plateau phase (Ca2+ and K+)  Repolarization phase (K+) 7∙ Absolute refractory period (in green): it is very long because  membrane potential goes up and stays up for so long (takes a while for repolarization to start) o Gives time for the ventricles and atria to fill with blood after the  blood has circulated o Prevents against wave summation the contraction will not build  upon other contractions ∙ Tension/contraction happens DURING the absolute refractory period o Happens as soon as the depolarization phase ends ∙ In order for cardiac cells to contract, they need calcium o Source of contraction for cardiac cells= comes from extracellular  fluid an the sarcoplasmic reticulum o These are the 2 sources where the Ca2+ channels can come from  for the slow Ca2+ channels that are utilized in cardiac muscle  cells (cardiomyocytes) o So…there are 2 ways for the cardiomyocytes to achieve  contraction ∙ Contraction takes place in response to calcium ∙ Primary pacemaker= SA node ∙ How does electrical activity of a pacemaker cell (nodal cell) differ from  a typical neuron? o Their RMP isn’t resting…there is a positive slope to it (a small  depolarization) o There are Na+ leak channels that result in steady decrease in the  membrane potential o Ca2+ channels (and also Na+ channels) involved in the  depolarization phase o Independent of nervous system…does NOT require a stimulus  Pacemaker cells spontaneously produce APs ∙ How does electrical activity of a cardiomyocyte differ from a typical  neuron? o There is a longer absolute refractory period  Slow Ca2+ channels at the same time that the K+ is leaving  the cell, so the cell has to hold off on starting repolarization ∙ Electrocardiogram (ECG) o The minimum number of electrodes (things that you put all over  the person’s body) is 3 o The electrodes on the skin tell you what is happening within the  heart  The body is made of liquids inside  The electrical activity of the heart influences ions all  throughout the body, so it is influencing these bodily fluids o P wave: represents in time the depolarization of the atria   Na+ ions move during depolarization 8 The signal from the SA node moves from the top of the  heart and down through the atrium…the cardiomyocytes  carry this signal along the pathway  There are so many cells…an electrical field is created and  disturbed  This electrical field can be detected o QRS complex: atrial repolarization and ventricle depolarization  Ventricle depolarization happens as the signal travels from  the AV node, goes down the branches all the way to the  bottom of the heart, and then spreads upward along the  border of the heart (refer to electrical conduction picture) ∙ The AP goes all the way down to the bottom first  because this allows for a delaying stimulation of the  ventricles ∙ This causes the atria to contraction, followed by the  ventricles so that everything is not messed up and  happening at once o This makes things efficient!  Fibrous connective tissue separates atrial cells from  ventricle cells  The AV node is the one point of attachment o Blood flow happens because of pressure think of a long skinny  balloon…it is getting bigger in a certain direction as you blow  It is going out in that direction because of the air that you  are blowing in the balloon, NOT because of the direction  that you positioned the balloon….the pressure of the air  causes the balloon to go in a certain direction o T wave: ventricular repolarization  The K+ ions flow out of the cell o Keep in mind…cardiomyocytes do not really matter a lot for  conduction. It is NOT their main job ∙ Cardiac arrhythmias o Heart block: failure of conduction to the AV node  The QRS complex is missing when you look at the ECG o Nodal rhythm: failure of the SA node, so the AV node takes over  The primary pacemaker is the SA node, but if it is not  functioning then the AV node takes over because it is the  secondary pacemaker  The P wave is missing, so there is no atrial activity o Ventricular fibrillation: messed up heart rhythm  You can fix this by shocking the heart to get it back on  rhythm ∙ Pressure: job of the heart is to provide the pressure to move the blood  (force/area) 9∙ Flow: volume per time (mL/sec) the rate of the volume movement ∙ Flow is proportional to pressure o Ex: syringe…if we provide pressure to the fluid, it puts pressure  on the container which will increase the flow of the liquid out of  the syringe o If  pressure, it  the rate of volume that moves...it has increased the flow! ∙ In the body, pressure leads to the movement of the blood o In the heart, the pressure comes from contraction o Direction is NOT important….it is the squeezing of the blood that  is important (the magnitude of the pressure) ∙ Systole= contraction *the atria contract together at the same time ∙ Diastole= relaxation • Increased pressure moves blood from atria to  Atria systole,  Atria systole,  ventricles  ventricles  relaxed relaxed ventricles • Blood shifts from area of high pressure to area of  lower pressure • Pressure determines both direction and rate of  movement Atria relax,  Atria relax,  ventricles  ventricles  systole  systole  (contract) (contract) • Blood pushes AV  valves closed Ventricles  Ventricles  continue  continue  contracting,  contracting,  semilunar valves  semilunar valves  pushed open pushed open • Blood pushes the  semilunar valves  closed ∙ Semilunar valves: one way passage from the ventricles out through the aorta o They prevent blood from flowing in the opposite direction o There are TWO of them  One is between the left ventricle and the aorta  One is between the right ventricle and the pulmonary trunk ∙ After this process…THEN the pressure from the heart drives the blood  flow to the body and to the lungs ∙ Poll Ev: When would you predict the opening and closing of the  semilunar valves? o Answer:  Open during…ventricle contraction  Close during…ventricle relaxation o Once the blood is released from the ventricles, pressure pushes  backward and the semilunar valves close as the ventricles relax 10∙ S1 sound= when the AV valves close, there is such turbulence that we  get a sound ∙ S2 sound= when the semilunar valves close, there is also a huge amt of turbulence o The right and left sounds happen simultaneously (because there  are two circuits and 2 sets of valves happening at same time) Phases of the cardiac cycle o (1) Ventricular Filling  1a. Rapid filling & 1b. Diastasis (slower filling) =passive  filling phase ∙ Ventricles are ENTIRELY relaxed during this, atria are also  relaxed ∙ Ventricles cannot fill unless they are relaxed ∙ Blood flowing passively through the veins into the right  atrium, and then into the right ventricle ∙ MOST of the filling (75-85%) of ventricles happens up here  1c. Atrial systole ∙ Happens as the atria contract…adds additional volume to  the ventricle ∙ Happens because of depolarization followed by the  plateau phase ∙ End diastolic volume (EDV): the volume of the ventricle achieved at the end of ventricular diastole…when the  ventricles are relaxed but they are ABOUT to contract. So  they are VERY full of blood ∙ Another way of thinking about it: o Happens at end of atrial systole…happens at the end of the contraction of the atria ∙ The peak ventricle volume is achieved at the end of this  phase ∙ Volume of ventricle is constantly changing  o (2) Isovolumetric Contraction  Contraction of the ventricles with no change in volume  because we are increasing the pressure in the ventricle  The creation of pressure is what allows for the contraction  The blood will move when the pressure is so great that the  semilunar valve is pushed open  VERY short phase, but important because we go from a very  low pressure to a very high pressure  No blood will move out of the ventricle until the pressure in  the ventricle has exceeded the pressure in the aorta or  pulmonary trunk o (3) Ventricular Ejection 11 When the blood moves out of the ventricle and into the aorta  or pulmonary trunk  End systolic volume (ESV): the volume left in the ventricle  following ejection o (4) Isovolumetric Relaxation  There is a great pressure change…we are rapidly dropping  pressure in the ventricle in this phase ∙ Volume is staying the same  Ventricles resting in diastole  It can begin the filling phase, but there has to be a pressure  change  No blood will move into the ventricle until blood pressure in  the atria is surpassed by ventricular pressure… this would  then cause the AV valve to open  We can only transition back into the filling phase after the  pressure in the ventricle has dropped to be lower than the  pressure of the atria ∙ Phases of cardiac cycle based on ventricular volume ∙ V&L are flat horizontal lines…because “iso” so no volume change! ∙ Stroke volume: the amount of blood (the volume) that leaves the  ventricle o It is the volume that enters the aorta or pulmonary trunk. It is the  volume that we contribute to circulatory system with each  heartbeat o SV= EDV – ESV 12o EDV: volume of ventricle at the end of its rest (when it is fullest) o ESV: volume of ventricle remaining in the ventricle after the  systole (contraction) ∙ Cardiac output: tells us how much blood the heart pumps out  (mL/min) o CO (mL/min) = HR (beats/min) x SV (mL/contraction)   Heart rate tells us how fast or slow  Stroke volume tells us how much ∙ Cardiac reserve: the amount of blood that you have o At rest: CO is approx. 5 L/min o At max: CO is approx. 25 L/min o An athlete can increase oxygen carrying ability due to increased  cardiac output ∙ If the heart rate goes up, it helps deliver more oxygen to the blood  faster o This will increase our cardiac output…look at eqn! ∙ Heart rate or Stroke volume to increase cardiac output ∙ Chronotropic agents: things that affect heart rate (rate of cardiac  cycles) o **Affect pacemaker cells o Chrono= time o Have an effect on the nodal cells o SA node establishes this o Sympathetic nervous system  Releases hormones (NE and TH) which heart rate  TH: If you increase metabolic rate, you also increase the  demand for O2….so it elevates metabolic rate at same time  that it increases heart rate o Parasympathetic nervous system  Releases ACh in order to  heart rate ∙ Tachycardia: too fast of a heart rate ∙ Bradycardia: too slow of a heart rate o Abnormal heart rates ∙ Regulation of heart rate does NOT happen within the heart ∙ Cardiac centers: the areas in the brain that regulate heart rate o In the brain stem (medulla) o Respond to proprioceptors (receptors that give us info on  movement and stress on joints)  Located in muscles and joints 13 Then…this tells the heart to speed up or slow down (if it needs more oxygen, brain will tell the heart to speed up)  PATH= a lot of movement (the stimulus)  proprioreceptors  send signal to cardiac center in medulla  signals the heart to  increase heart rate  more O2 is delivered to the body/muscle  cells o ~Your environment has an effect on your heart rate and what you  perceive based on your sensory receptors affects heart rate o Respond to chemoreceptors: tells us about blood chemistry  (MAINLY pH , and also CO2)  Located within blood vessels  CO2 levels go up…means that pH goes down (becomes more  acidic)  When you dissolve CO2 in blood, blood becomes more acidic  CO2 and water leads to production of an acid so the blood  becomes more acidic  Hypercapnia: high blood CO2 ∙ Acidosis: blood very acidic  High CO2 levels build chemoreceptors cardiac centers response= cardioacceleration ∙ ***Sympathetic nervous system deals with this  Cardiac centers signal to the heart  Cardioacceleration: the nervous system telling the heart to  go faster ∙ Increases heart rate which increases cardiac output…more blood goes through the lungs ∙ This allows for CO2 to go away more quickly ∙ This is negative feedback!! o Respond to baroreceptors: tells us about blood pressure  Located within blood vessels  Hypertension Cardioinhibition ∙ High BP (Hypertension)…too much tension as there is so  much blood hitting against the blood vessel walls (this  also involves high cardiac output) baroreceptors  stimulated  provide the cardiac center with information  on BP ∙ We want to lower cardiac output by lowering heart rate ∙ Cardioinhibition: cardiac centers decide to slow down  heart rate  ∙ This is part of the parasympathetic nervous system ∙ ACh goes to SA node and slows down the pacemaker  potential 14 Hypotension Cardioacceleration o Chemoreceptors and baroreceptors= BOTH entirely homeostatic… happening all the time for appropriate output ∙ Inotropic agents: affect how strongly the cardiac muscle contracts o **Affects the cardiomyocytes o Cause changes in stroke volume (amt of blood that leaves the  ventricle) o NE (major agent)  Causes an INCREASE in stroke volume  Can come from sympathetic nervous system or adrenal  medulla  Increases contractility o ACh (small effect on atria)  Causes a DECREASE in stroke volume  Parasymp. nervous system can diminish contractility of  cardiomyocytes ∙ Intrinsic regulators: within the heart parts IN the heart that control  the heart o Nervous system is NOT involved!! o Preload: pressure of the filled ventricles that stretches the  myocardium (the preload is the state of the ventricles before ventricular contraction)  FIRST- the pressure arrives at the ventricles ∙ This causes the stretch of the ventricles ∙ The strength of the pressure can vary, which causes the  stroke volume to vary ∙ The preload varies based on venous return  BP causes ventricle walls to stretch (the pressure of filled  ventricles stretches the myocardium) o Frank Starling Law: the greater the EDV (the greater we fill the  ventricles), the greater the stroke volume  EDV- happens at the end of the ventricular rest…so it’s the  point when the ventricles are filled the most o The more the heart muscle is stretched, the more strongly it will  contract  Length-tension relationship: the more you stretch the  muscles, the cardiac cells are lengthened and become  stronger ∙ NO additional stimulus from nervous system…nervous  system NOT involved!!!  Response= more blood comes in, and then more blood goes  out of heart 15∙ Effects on cardiac output: afterload opposes ventricular ejection and  reduces the stroke volume o Afterload: the BP in the aorta and pulmonary trunk that resists  the ejection of blood from the ventricles  **Elevated aortic pressure  The afterload varies based on aortic blood pressure (the  pressure on the other side of the semilunar valve)  The ventricles are pushing against the BP in the aorta and  pulmonary trunk….when pressure is greater inside ventricle  compared to aorta and pulm trunk, blood moves out of  ventricle (moves from area of high pressure to area of lower  pressure)  Ventricle contracts and pushes against semilunar valve o Hypertension: condition that ALWAYS increases afterload  (increased blood pressure)  Pressure in aorta increases the afterload  Decreases contractility **all of this described below ∙ When pressure in left ventricle goes way up, we transfer blood to the  aorta ∙ If we increase aortic pressure:  o Lengthens the isovolumetric contraction phase o Diminishes the period of ventricular ejection  This is because incr aortic pressure increases afterload  (which means there is more pressure in the aorta)  *Decreases the amount of blood that is ejected from the left  ventricle ∙ Valvular insufficiency: failure of valves to completely prevent  backflow o Causes: 16 Stenosis: narrowed opening of semilunar valve surrounded by  scar tissue ∙ There is a small narrow gap in the semilunar valve that is  supposed to be closed  Valvular prelapse: valve flaps do not stay closed correctly and  stick together the wrong way, so there are unwanted openings in the valve  Congenital malformation: during embryonic development, 2  cusps form in the formation of valves, or when 3 cusps form,  but they form incorrectly o Vegurgitation (another name for it) because some blood seeps  and moves in the wrong direction  Bad because blood only supposed to flow ONE way through  the valves ∙ Poll Ev: Phil was diagnosed with atrioventricular valvular prelapse.  Which of the following would you not predict? o Answer: His ventricles would be enlarged  …this would only happen when your heart has to pump more  strongly (due to blockage or HR) o His cardiac output would be within normal range  Yes, because this is what we are compensating for  HR greater than normal  BP in his aorta would be within normal range ∙ If you have valvular prolapse, your heart needs to compensate o This is because the net amount of blood leaving the ventricles  lowers (because some of the blood goes back in)= Stroke volume o In order to fix this, you HR so that you can Cardiac output and  get it back to a good amount…because cardiac output= SV x HR  Since stroke volume is low, you need to increase heart rate to  make up for the decrease in SV ∙ What indicates low cardiac output o CO2 in the body o Baroreceptors stimulated (affect changes in BP, and therefore CO) ∙ Enlargement of heart happens when heart has to work harder o Ex: exercise 17Blood Vessels ~all about moving BLOOD! (even though…these  capillaries are also used to (1)move air  in ventilation and (2)move molecules of gas in respiration) ∙ 3 layers o Tunica interna: made of squam epithelium AND loose connective  tissue o Tunica media: the THICKEST layer, made of smooth muscle,  collagen, and elastic tissue…the “muscle layer” o Tunica externa: made of loose connective tissue ∙ Arteries: carry blood away from the heart o HIGH pressure o The farther you get away from the heart, the lower the pressure  o Tunica media (middle layer of artery): made up of smooth muscle,  collagen, and elastic fibers  As you get further from the heart, they are less elastic and  more muscular  Large vessels are stretchier (so that they can handle the high blood vol)  Smaller vessels have more muscle so that we can change the diameter easily o 3 classes **from closest to heartfarthest from heart  Conducting (elastic or large) arteries: BIG guys, aorta,  pulmonary trunk, etc  Distributing (muscular or medium) arteries: “distribute” blood to specific organs  Resistance (small) arteries: have a lot of resistance  because the most vasoconstriction and vasodilation  (diameter changes) happens in these arterioles and  capillaries…the resistance is in the tissues where these  artioles are located ∙ Capillaries: connect arteries to veins (where exchange takes place) o MODERATE pressure o Oxygen, CO2, sugars, wastes, nutrients, gases, hormones o Exchange between the blood and the tissues surrounding it o 3 types *permeability varies among them!  Continuous capillaries: in most tissues (ex: pericytes which have elongated tendrils that wrap around the capillary)  Fenestrated capillaries: have filtration pores that allow for  rapid passage of molecules through the walls of the  capillaries (rapid absorption and filtration)  Sinusoids (discontinuous capillaries): irregular blood filled spaces in liver and spleen∙ Cells have LARGE fenestrations (pores)so for example,  RBCs are able to pass through the walls and get into the interstitial fluid ∙ Veins: carry blood toward the heart o LOW pressure o 3 types  Large veins  Medium veins  Muscular and post-capillary venules o ***take note: veins can be blue OR red….because you can have  oxygenated blood in veins  ex: pulmonary trunk (the vein that goes from the lungs back  into the heart), pulmonary arteries o As veins (vessel) get larger, the vessel wall becomes less muscular (more elastic) and the pressure decreases ∙ Arteries are more elastic than veins because they have a pulsatile  pressureit goes up and down, big fluctuation ∙ Sense organs: located in the walls of the arteries o In aortic arch= where blood leaves the heart and goes to the  systemic part o In carotid artery (goes to your head)=  Carotid sinuses: sense organs that contain baroreceptors  ∙ Baroreceptors: little patches of cells that respond to  changes in BP (respond to a sensory change) and then  they send signals to the brain ∙ BP  baroreceptors signal brain HR and also this will  lower the blood pressure. Also leads to vasodilation… which decreases pressure ∙ **Systemic responses…so it happens in the vessels all  over your body  Carotid and aortic bodies: sense organs that contain  chemoreceptors ∙ Chemoreceptors: respond to changes in blood chemistry (pH, CO2) ∙ CO2 (hypercapnia) and pH (acidosis)  chemoreceptors send signal…we want an increased  heart rate ∙ Capillary beds: at any time only 25% of capillary beds are perfused  (have blood flowing through them) o This is because it would take too much blood volume to fill all the  capillaries at onceo Precapillary sphincters: shut off capillaries so sometimes the blood goes straight through from the artery to the vein through a  thoroughfare channel  They cycle between open and closed…blood constantly being redirected o Veins= where most of the blood resides they are capacitance  vessels ∙ Circulatory routes o Venous and arterial anastomoses  Anastome: creates variety of circulatory paths  Can be venous to venous or artery to artery  Arterial anastomoses: creates a variety of circulatory paths ∙ Common around the brain ∙ During gestation= baby pushes around on things and so we need these anastomoses so that blood can be  redirected sot aht it is still continually circulated o Arteriovenous anastomosis (shunt)  Redirect blood away from fingers and toes when it is cold  out…bypass fingers and toes to conserve heat o Portal system  Example of portal system: hypothalamus and anterior  pituitary there is a 1st and a 2nd messenger  2 capillary systems involved  Way of directing substance of blood directly to somewhere  else so that the hypothalamic hormones do not have to go  through the whole body o Typical  Blood leaves heart through the artery capillaries veins blood goes back to heart ∙ Ohm’s Law o V (voltage) = I (current…the flow of ions) x R (resistance) ∙ ΔP (pressure difference) = F (flow of blood) x R (resistance) o Hypertension: high blood pressure o Hypotension: low blood pressure ∙ Blood flow  o Flow is proportional to change in pressure  ΔP, F o Flow is INVERSELY proportional to resistance  R, F ∙ Syringe: blue fluid has pressure and the air has pressure o If we provide high pressure with our hand onto the syringe (high  pressure inside of syringe), the flow will increase  o If we have lower resistance (ex: increase diameter of the syringe),  we get a greater flow∙ Flow happens because of a pressure gradient….a difference in pressure ∙ Flow is OPPOSED by resistance ∙ Poll Ev: What does not contribute to blood pressure? o Cardiac output (HR x SV) o Volume of blood o Resistance o Answer= Level of oxygenation ∙ Blood pressure is not a single value…there is variation throughout the body o Blood pressure in the aorta is VERY high o Pressure diminishes with distance from the heart o Blood pressure measurement= cuff on arm…it is measuring the  blood pressure in a major blood vessel that goes to your heart o Systolic pressure / diastolic pressure is your blood pressure  Systolic: top of pressure ∙ This is when the left ventricle contracts…it is fully  expanded and at its pressure peak. It is at its highest  pressure  Diastolic: bottom of pressure ∙ When blood is at the different parts of the body, the  pressure in the heart drops in the ventricle and is very  low. There is no blood in there o These two are farther apart for the vessels that are very close to  the heart, because there is a big difference between the highest  and the lowest o Pulse pressure: the difference between systolic and diastolic  pressureo Mean arterial pressure: the mean of the systolic and diastolic o Pulsatile nature ends at the capillaries…this is important because  if they had this pressure, they would rupture  Capillaries ONLY have the tunica externa…they do not have  the muscle layer or the connective tissue layer o Normal BP for adults: 120/80 mm Hg  The minimum blood pressure in a normal person that it can  drop to is 80 ∙ When you think of large arteries they are stretchy! Like a rubberband.  They are NOT rigid o Elasticity helps moderate the big pressure differences that these  arteries experience over the distance of the artery o They stretch and recoil Variables that affect/determine BP o (1) Cardiac output (=HR x SV) **SV= amt of blood that leaves the  ventricle  CO means that BP because you have a higher volume  moving into the same space over time ∙ You are cramming more blood into the vessels in a short period of time ∙ So…if you have a valvular prolapse, you have less CO so BP o (2) Blood volume (=water in – water out)  When there is not a lot of water in the blood, there is a lower  blood volume ∙ Low blood volume (from dehydration, or from an injury  where you lost a lot of blood) leads to BP  Source of water intake for the body: drinking and eating  Ways we lose water: sweat, urinate, bleed, cry ∙ (3) Peripheral resistance *peripheral= happening out in the tissues (think  peripheral nervous  system…but this isn’t the nervous system, this is vessels instead) o Many types of resistance…they all are used to alter the peripheral  resistance so that blood can flow more easily or less easily o Friction: interaction with blood against the blood vessel wall o Vessel length  A long series of blood vessels has more friction than a short  series  Ex: long swirly straw is hard to drink out of…or trying to drink water out of a garden hose! Really hard  If we  or  length, resistance is affected. Therefore, blood  pressure is affected  As length, resistance o Angiogenesis: the formation of new blood vessels, which either  increases or decreases the length of them  We do this because of metabolic need, the growth of new  tissue, etc  It is only done when needed o Vessel diameter **Most important factor of periph. resist!!!  Smaller diameter has resistance because we are increasing  friction ∙ A lot of blood is in contact with the surface of the vessel  walls  The main way that we change blood pressure in the body=  vasodilation and vasoconstriction of blood vessels…which  change the vessel diameter!  Systemic effects  As diameter , resistance  o Viscosity  The more viscous the fluid, the less easily it is going to get  through  Viscous fluids: stick together…they flow slowly because the  forces are greater and it is harder to separate the molecules  Blood is more viscous than water ∙ It is about 5x as viscous  What determines viscosity ∙ Hydration (blood is thinner when there is a ton of water  because the water dilutes the blood more and thins it  out) ∙ RBC count ∙ Albumin concentration (protein in the plasma of the  blood)  As viscosity , resistance  Raise or lower BP? BP Gain 50 lb (muscle or fat) because increasing length of blood  vessels, so you are gaining tissue and you need more vessels Fight/flight  increases cardiac output,  vasoconstriction occurs (which  means there is increased resistance  and increased BP) Dehydration Could be either; change in  viscosity. Most normal= Blood vol so BP Anemia low # RBCs  because decreases viscosity, decrease in resistance would lower  BP because there is an easier flow Polycythemia high # RBCs  because increases viscosity,  increase in resistance would raise BP Limb amputation  less vessel length, so less  peripheral resistance. Not a lot of  pressure needed to move the blood Participation in water drinking  contest  BP, because blood volume Blood donation w/ fluid replacement No change Blood donation w/o fluid replacement BP, because blood volume (since  the amount of water in the blood  decreases) ∙ Regulating blood pressure and flow o Vasomotor centers: located in the medulla o (1) Autoregulation (local control): individual blood vessels  (arterioles) constricting and dilating  Local= no signal, it doesn’t matter what is happening with rest  of the body…this allows tissues to be profused based on need  Happens in response to certain things ∙ In response to metabolic byproducts o They stimulate vasodilation o Ex: sometimes capillary beds are shut off. Tissues  build up CO2 and lactic acid these can be signals that cause vasodilation so that blood will be sent to the  body ∙ In response to local vasoactive chemicals o They control response to injury/infection ∙ In response to oxygen needs o Angiogenesis happens: the growth of new vessels to  meet the oxygen demands of tissues  Only involves individual capillary beds o (2) Neural control  Signal from brain  In response to pressure or chemical changes ∙ Sympathetic NS controls vasomotion (vasodilation and  vasoconstriction)  Chemoreceptors respond to pH and CO2 ∙ The HEART system’s response to these changes= the  signals were going to the cardiac centers ∙ **Same receptors, but different action∙ The VESSEL system’s response to these changes= the  signals from the chemoreceptors go to the vasomotor  centers in the brain ∙ CO2 (hypercapnia)/pH (acidosis) stimulate  vasoconstriction everywhere, except NOT in the lungs  Baroreceptors provide info on blood pressure ∙ The HEART system’s response= signals sent to cardiac  centers  ∙ The VESSEL system’s response= signals sent to vasomotor  centers ∙ BP leads to vasoconstriction to raise BP ∙ BP (high BP) leads to vasodilation to lower BP  Medullary ischemic reflex: medulla is one of the few places in  the body where we have something specifically measuring its  own O2 levels ∙ This is where these vasomotor centers are ∙ There are specific receptors for oxygen…it can redirect  blood to the brain if oxygen levels are low ∙ O2 in medulla stimulates HR and vasoconstriction o (3) Hormonal Control **everything that starts with A  Several hormones affect BP by impacting vasomotion or  salt/water balance  To maintain homeostasis  ∙ In response to osmotic changes (solute concentration) o Aldosterone: wants to increase blood osmolarity o ADH: causes water retention and vasoconstriction in  order to increase blood osmolarity (want to keep  everything in…because it is ANTI diuretics..and  diuretics make you pee) ∙ In response to pressure changes o Hormones that affect pressure changes to maintain  homeostasis, respond to hypo- and hyper- tension o Angiotension II o Natriuretic peptides (ANP, BNP)  To redirect blood ∙ E and NE o They respond by causing vasoconstriction in order to  redirect the blood (EXCEPT no vasoconstriction in  blood vessels serving skeletal and cardiac muscle) ∙ When blood vessels constrict, not ALL blood vessels  constrict ∙ Very often the heart and the brain vessels will remain  dilated even if vessels around the viscera constrict∙ Capillary exchange o With distance from the heart, there is a decline in pressure o Lots of exchange= water, nutrients, waste, ions, antibodies,  hormones o This exchange does not rely on diffusion alone o We can actively push fluid out of the capillaries ∙ Arteriolecapillaryvenule ∙ Filtration: fluid leaves the capillary on the arterial side o It goes into the interstitial space ∙ Reabsorption: where fluid is reabsorbed from the interstitial fluid into the blood ∙ Due to 2 big forces o Hydrostatic pressure: the fluid pushing on the walls of the vessels  It is in 2 places: inside the blood AND in the interstitial fluid o Osmotic pressure: water moves from an area of less solute  concentration to an area of more solute concentration…it moves  down the concentration gradient  OR…think about it that it moves from an area of high water  concentration to an area of low water concentration  Water moves freely across the semi-permeable membrane Filtration in arteries ∙ 2 forces…one pushes in and the other pushes out ∙ Net Hydrostatic pressure (in arteriole) *pushes OUT o High hydrostatic pressure in the blood o Low hydrostatic pressure in interstitial fluid o SO…the net (the diff between the pressures) gives you a value called  the net hydrostatic pressure. This fluid will move OUT of capillary and  into the interstitial fluid because it moves from area of high pressure  to area of low pressure  ∙ Net Colloid Osmotic Pressure (oncotic pressure) *pushes IN o Colloid proteinacious nature of blood o Ex: if there is fresh water on the left and interstitial fluid on the right,  the water will move TOWARD the interstitial fluid…because there are  more salts on that side  Na+, F, Ca2+ o Ex: fresh water on left and blood on the right  Water moves toward the right because there is not a high  amount of water in the blood ∙ Major difference between interstitial fluid solutes and blood solutes=  blood has protein and interstitial fluid does NOT ∙ Blood and interstitial fluid next to each othero Water will move from interstitial fluid to the blood because blood has MORE solutes (than the ISF) and less water…those solutes=  proteins!!! Solutes do NOT have to be just salts and ions ∙ Net filtration pressure: net hydrostatic pressure (fluid that leaves  capillaries b/c of pressure) + net colloid osmotic pressure (fluid that goes into the blood in the capillaries b/c of solute conc) Reabsorption on the venous side ∙ Net hydrostatic pressure: drives fluid out of capillary o A lot lower than the net hydrostatic pressure in the arterioles because there is a lot less fluid (low volume)…the initial huge hydrostatic  pressure caused the fluid to move out o Now, there is a lower volume and therefore a lower pressure ∙ Net colloid osmotic pressure: drives fluid into capillaries (water wants to  move toward the high amt of solute so that it can dilute it) o Same effect in the vein side of the capillaries  ∙ Filtration and reabsorption (the absorption of veins and interstitial fluid  back into the venous side of capillaries) o Capillaries reabsorb about 85% of filtered fluid o The other 15% goes to lymphatic vessels they suck up interstitial  fluid and return it to circulation…they are intertwined all within the  capillaries  Lymphatic system drops the fluid back into your veins near your heart  There are lymph nodes along the way to screen the fluid with  the immune system…this is good!  The 15% that is lost is regained entirely…this is just another  way of recycling the fluid ∙ Edema: swelling in the tissues due to accumulation of fluid…there is not enough capillary reabsorption o High pressure in the cells is bad o You have lost the fluid volume you are hypovolemic ∙ Capillary filtration (amount of fluid that leaves the capillary)= capillary  reabsorption + lymphatic absorption (the extra) o Whatever we lose, we have to gain. If this balance does not happen,  then you have edema ∙ Veins are LOW pressure o How to move low pressure venous blood to the heart  Pressure gradient  “Skeletal muscle pump” & one-way valves ∙ Skeletal muscles contract, which elevates pressure in the  leg∙ Veins have their internal hydrostatic pressure, but we can  aid in elevating this pressure by squeezing our muscles  “Respiratory pump” ∙ Helps move blood toward heart during inspiration ∙ When you inhale, the pressure around your lungs is  negative. This pulls blood within the vessels toward the  heart (because the blood has increased pressure) ∙ Pressure around the heart is negative when you breathe ∙ Also when you inhale, the diaphragm moves down so the  pressure from the abdominal cavity pushes blood toward  the heart  Vasomotor- vasoconstriction and vasodilation  Gravity  Cardiac suction ∙ Shock: we do not have high enough BP and enough blood flow to meet  the demands of the body **we have a LOW BP!! Uh oh!! (1) Circulatory shock o Cardiogenic shock: circulatory shock that starts with the heart o Ex: myocardial infarction (heart attack) blockage in a blood vessel  (either vein or artery) in the heart which leads to plaque build up  This means that no blood is going to an area, and so a part of  the heart becomes dead o Coronary vasculature (the arteries surrounding the heart) can have  clots, and then that part dies o Dead heart muscle directly lowers stroke volume (affects  contractility), which means it lowers cardiac output (contractility of  the heart) low BP this can lead to circulatory shock o Stroke: an example of a type of shock that affects blood vessels in  the brain ∙ Compensated shock: responses in order to recover from the shock o The baroreceptors send signals to the cardiac centers which BP and  then this causes BP so that we can get rid of this blockage in the  vessel o ALSO…signals sent to vasomotor centers which leads to  vasoconstriction (increases resistance, increases BP) ∙ Uncompensated shock: if these two things do not successfully get the  person out of the shock (2)Low Venous Return Shock: NOT a problem with the heart o Circulatory shock that happens when the venous return of blood is  insufficient (not enough blood going back to heart) o Amount of blood leaving the heart and amount of blood going back to the heart should be equal Venous return= cardiac output (stroke vol: amt that goes out of  the heart) o Low venous return a decreased stroke volume o Hypovolemia: low blood volume  Hemorrhage, dehydration, knife wound  Hypovolemia decreased stroke volume, decreased BP LVR  shock  Hypovolemia (low vol)  Hypotension (low BP!!) o Brainstem tumor: it pushes on different things and compromises their function. This messes with the cardiac and vasomotor centers, which  are in the brainstem.   Could prevent normal response, so you have low BP LVR shock o Sepsis: bacterial infection where bacterial toxins get into the blood  An immune response to these toxins= vasodilation this is good to get rid of the bacteria, but bad because it can  low BP  (blood unable to circulate correctly) which LVR shockRespiratory System ∙ RECAP o Blood volume movement of blood o Ventilation movement of air to the alveoli o Respiration movement of molecules of gas (1)between alveoli  and capillaries and (2)between capillaries and interstitial fluid ∙ Diaphragm: only muscle necessary for “quiet” ventilation o Has to seal off the throax from abdomen o Responsible for inhalation (contraction of the diaphragm) o Exhalation/expiration:   Bones, cartilage, ligaments, prefer to be collapsed and  small  Relaxation of the diaphragm and elasticity of the ribcage ∙ “Forced” respiration: a lot of muscles involved to move the ribs (ex:  abdominal muscles) o Abdominal muscles push everything up and the volume of the  thorax is diminished= in exhalation ∙ Inspiration: o Diaphragm contracts (moves down)…makes sense because it is  making more room in the thoracic cavity for the air to fill up as you  inhalesize of thorax incr. ∙ Expiration: o Diaphragm relaxes (moves back up to the flat normal position) and  the size of the thorax decreases ∙ Ventral respiratory group (VRG) (control center in medulla): controls  respiratory rhythm o Makes decisions about whether to  or  signals to the respiratory  centers o Primary job= setting the rhythm! o Sends info to the integrating center: place in the spinal cord that  stimulates muscles o Reverberating circuits alternate between stimulating contraction  (inspiration) and allowing relaxation (expiration)**inhibitory signals o On off on off signals constantly leaving the ventral respiratory  system o Circuit of neurons that form a loop= time keeping mechanism o Expiratory neurons: stimulate integrating centers o Send signal that participates in the circuit 1W h a t in f o r m s th e D R G & P R G ? o Ultimately stimulates the inspiratory neurons o Inspiratory neurons: they then start another action potential D R G ( in m e d u lla ) P R G ( in p o n s ) ∙ **these two have control over the rhythm established by the VRG ∙ DRG: dorsal respiratory group ∙ PRG: pontine (pons) respiratory group ∙ Factorsthese inform the DRG and the PRG 1. Motor cortex: voluntary part of muscle control. a. Informs nuclei to stop and allow a signal 2. Hypothalamus: seat of control of ANS, causes release of  hormones a. When you have a fight or flight response, the DRG and PRG  detect this so that your ventilation rate will be affected  when you are in this state 3. Irritant receptors: detect smoke, dust a. When lungs are irritated, you want to breathe more  shallowly 4. Stretch receptors: if you keep inhaling and your lungs are very  stretched, you have a strong urge to exhale 5. Peripheral chemoreceptors: in the aortic arch and carotid artery a. Peripheral= OUTSIDE of CNS b. The SAME chemoreceptors! c. Tell us to do something different based on blood  chemistry…so the response will be to CO2 or O2 6. Central chemoreceptors: in parts of the CNS, medulla pH!! 2∙ Poll Ev: A patient has hypercapnia (CO2). Which region of the  brainstem is NOT stimulated? o All of these EXCEPT the answer are stimulated by sensory neurons o Vasomotor center: works to BP so that we get rid of the CO2 faster o Cardiac center: BP o Dorsal respiratory group: receives the signals o Answer= Ventral respiratory group: this is going to take action  BASED ON the 6 factors…it is not initially stimulated. It acts in  response to the DRG and PRG to  or  rhythm o This shows you how the different centers and factors affect the  respiratory system and the movement of blood, which carries the  gas molecules o CO2  stimulates chemoreceptors  blood vessels, heart, resp.  system ∙ 3 types of chemoreceptors…across different areas of the body. But they all do the same thing ∙ F (flow) = ΔP/R o Flow is directly proportional to pressure change o Flow is inversely proportional to resistance ∙ Boyle’s Law about ventilation o Volume, Pressure o Decrease in vol (gas molecules squish together) because increase in pressure o PIVI = PFVF ∙ Thorax: increases volume, and pressure decreases which gives us the  pressure within our alveoli o The pressure is low relative to what is outside…so the air moves  from high concentration in the air/thorax  to lower concentration  in the alveoli o Magnitude of the difference in pressure between the alveoli and  the atmosphere will give you a greater or lesser flow o During inspiration= = Patmosphere > Palveoli o During expiration= Palveoli > Patmosphere  so the air moves OUT of  the body and from high pressure to low pressure…the alveoli are  filled with carbon dioxide that needs to be released ∙ Differences in pressure by changing dimensions of the thorax ∙ Sources of resistance o Diameter of bronchi/bronchioles (air passages that come off  of the trachea and go to the lungs)  Made of muscles and cartilage there is less and less  cartilage as you move down bronchioles…and so there is  MORE muscle at the ends of the bronchioles  3 Bronchodilation (makes passageway bigger) ∙ Caused by NE released by the sympathetic nervous  system ∙ Think…fight/flight and you need more air faster  Bronchoconstriction (makes passageway smaller) ∙ Things can affect air passages: cold air, irritants,  histamine ∙ ACh released by the parasympathetic nervous system in order to constrict the bronchi o Pulmonary compliance: stretchability of lungs (their ability to  expand given a certain pressure)  With big expansion of thorax, air is being pulled in  Compliant lungs: expand and stretch quickly to fill up the  entire space of the thoracic cavity **stretchy!! ∙ Expand easily with expansion of thorax  Less compliant lungs: do not expand as easily ∙ Happens because of stiffness in connective tissue ∙ Ex: you get old and your lungs lose connective tissues and lose elasticity ∙ Young people can expand more… o Respiratory rate of young people is slower than  that of old people because young people take in a lot of air with each breath ∙ Surface tension: contributes to non-compliance of lungs o This is present when you have an interface between the space  and the air o There is a thin aqueous film of watery mucus that lines the alveoli on their surface  Molecules within the lining are attracted to each other and  exhibit surface tension o Because each alveolus has this fluid, there is a force that wants to pull the alveolus closed (since the molecules are attracted to one  another) this makes the lung less able to expand. BUT….. o Great alveolar cells: solve this problem  They sit in the alveolar lining  Make surfactant, which reduces surface tension and  compliance  Surfactant is little molecules that mix in with the fluid lining ∙ Keeps the alveoli from collapsing inward ∙ Compliant lungs have alveoli which have the thin film of fluid AND the  surfactant o Premature infants do not have surfactant production, so they  cannot breathe correctly 4∙ “Conduction zone”: the area outside of the alveoli where air is moving through…moving air to its destination o Nasal passages, trachea, bronchi, and bronchioles o 150 mL of air o *note: this is part of ventilation, so it has to do with air moving,  NOT exchange ∙ “Respiratory zone”: where you have gas exchange; between alveoli and capillaries ∙ Anatomical dead space…negative effect of the conduction zone o Consequence= we have a built in inefficiency o We have to perform work/expend energy to move air through the  conduction system to get to the respiratory zone o BUT some air will not make it to the respiratory zone…it will not  be able to participate because it has to occupy the dead space o Dead space because there is no gas exchange…it is just air that  has to move in order for respiration to be able to occur o The space is NOT a constant  How to change volume of dead space= bronchodilation and  bronchoconstriction!!! (diameter)  Bronchodilation under sympathetic control is what can  change our dead space…when you run, tidal volume, and  dead space also ∙ Alveolar Ventilation Rate: tells us how much air is going into or out  of alveoli over time o It is under sympathetic control when you are active or have a high AVR ∙ Tidal volume: the amount of air that you breathe in and out (think of it like the waves or the tide of the ocean continuously going in and out… it’s the same volume every time!) o Can vary with level of autonomic stimulation o At rest: 500 mL/min ∙ AVR= (TV- Anat. Dead space) x breaths/min ∙ More air is moved to alveoli when there is a lot of physical activity…and you have a lot of breaths per minute ∙ Spirometry: how we measure various volumes (pulmonary ventilation) ∙ (1)Tidal volume: how much air you normally breathe in and out ∙ (2)Inspiratory reserve volume: when you inhale as much as you can ∙ (3)Expiratory reserve volume: you exhale as much as you can ∙ Vital capacity: the sum of the inspiratory volume, expiratory volume,  and tidal volume o Maxiumum amount of air you can move if you actually want to ∙ (4)Residual volume: exists so that your alveoli do not collapse 5o You need air on each side of your alveoli so that you prevent  surface tension o If you get rid of the air entirely, then the alveoli cannot expand o **also, it is important because it is there in between the lungs and the thoracic cage. When the thoracic cage is relaxed, it will not  allow that air to leave 2 1 3 4 ∙ Various pathologies affecting spirometry o Restrictive Pulmonary Disorders: reduce pulmonary  compliance  Surfactant disorder (insufficient surfactant)= restricts your  ability to inflate your lungs…lungs are inflated when alveoli are inflated!  Tuberculosis: bacterial infection that results in an immune  response ∙ Causes fibrosis: build up of connective tissue  (collagen) that results in scar tissue ∙ =compliance (lungs cannot expand as much!!) …  inspiratory reserve volume is most directly affected o Obstructive Pulmonary Disorders: affect resistance by  affecting diameter of the airway they narrow it  Forced expiratory volume: normal person can exhale A  LOT demonstrates that their airways are not blocked ∙ This is a RATE  Ex: asthma narrowing of airways due to inflammation,  which affects resistance. It takes this person a lot longer to  reach vital capacity ∙ Poll Ev: What would result in a condition resembling “obstructive  pulm. disorder”? 6o Answer= bronchitis o Pulmonary fibrosis o Insufficient number of great alveolar cells o Broken ribs o **the first one is the answer because all of the other options  have to do with compliance (expanding of lungs), not resistance  (diameter of bronchi) ∙ Gas exchange and transport: happens in the alveoli o 4 major gases make up air: 78% N2, 20% O2, 0.5% water vapor,  0.04% CO2 o At sea level= 760 mm Hg of pressure (1 atm) ∙ Partial pressure: how much pressure is exerted by each component of  the air o Dalton’s Law: sum of the partial pressures= total pressure ∙ Ex: for air, 20% of 760 is the pressure that oxygen exerts (partial  pressure of oxygen) ∙ Alveolar air is NOT the same as the air that is coming in from the  atmosphere…this is because alveolar air involves gas exchange so the  concentrations are changing o There is more CO2 in alveolar air o There is less O2 in alveolar air, compared to atmospheric air ∙ Po2 of alveolar air= 104 mm Hg  this is lower than the atmospheric air (760) because of the oxygen leaving the alveoli and going into the  blood to be transported ∙ Henry’s Law: how a gas moves from a gaseous environment into an  aqueous environment o They move in and out of a solution according to:  Partial pressure: varies with air pressure…a gas’s pressure  is what drives it to dissolve a liquid  Solubility: depends on the molecule (picture the graph… CO2 is very soluble)…and solubility depends on strength of  IMFs ∙ Equilibrium pressure in a container with a molecular solution partial pressure and concentration of molecules are proportional o So… partial pressure means concentration of molecules  (because there are more molecules in the container and more  molecules colliding in a small space, so the individual pressures  must increase since the total pressure is increasing) ----------- ∙ The partial pressure and solubility are what drive a gas to dissolve in  the blood o Daltons Law sum of partial pressures is total pressure o Partial pressure is a matter of a gas’s concentration in the air 7∙ Alveolar air: moves by the process of respiration o Ventilation is the process that got the air from the atmosphere into  the alveoli…now the air is going to be moved through the entire  body by respiration ∙ O2 moves from the alveolar air to the blood ∙ CO2 moves from blood to the alveolar air (in order to leave the body  through the lungs) ∙ The big picture ∙ For gas exchange, we need to compare the partial pressure of oxygen  in the air to the amount of oxygen in the blood coming into the lungs o 104 mm Hg only 95 mm Hg of oxygenated blood that goes by  pulmonary veins to the heart  There is mixing of the blood, so we lose a little bit of the  oxygen. But this 95 is the amount of oxygen that we want  to unload to the tissues o This is external respiration because it is happening with outside air ∙ Gas exchange happens in two places o At alveoli: external respiration happens (exchange between  capillaries and external air) o At systemic capillaries: internal respiration happens (exchange  through systemic capillary walls) ∙ Gas exchange at alveolar capillaries o Po2 changes substantially over the length of the alveolar capillaries 8o Remember…this is happening inside the lungs!!! So the  deoxygenated blood is coming into the lungs and the capillaries  are intertwined onto the alveoli…they have a PO2 of 40 mm Hg o Then the alveoli give the oxygen to the capillaries…so then the  arterial capillaries have a PO2 of 104 mm Hg o Blood picks up oxygen in the lungs at the alveoli through  capillaries ∙ Normal cardiac output= 5 L/min ∙ If the cardiac output is 4x the resting rate, will blood be fully  oxygenated when it reaches the end of the capillary? o YES! We can always use vasodilation (less resistance…which  decreases blood pressure and cardiac output) to slow down the  blood moving in the lungs in order to oxygenate the blood o Very efficient system…this is because we have a ton of surface  area on the capillaries and the alveoli ∙ Factors that affect gas exchange o Pressure gradient of gas: matters to the efficiency of the process  The large difference in pressure is what causes more  movement of oxygen (pressure change means that there is a strong movement of the oxygen…it wants to move SO  bad!)  Situations where the alveolar air has a lower PO2 High  altitude, COPD, lung removed, respiratory arrest  Affects efficiency o Solubility  How substances interact in aqueous environments  Carbon dioxide is highly soluble o Respiratory membrane thickness  Respiratory membrane: collective area of gas exchange  within the lungs 9 The membrane of the alveoli is very thin…this allows for  diffusion to happen very quickly over the small distance  Changes in membrane affect speed of gas exchange o Membrane area  Surface area for respiration is BIG lots of area where gas  and blood interact  Normal alveoli: make up clusters called alveolar sacs  Emphysema: walls between the alveoli have been broken  down there is a diminished surface area and there are  only partial alveoli ∙ Not as much gas can be exchanged o Ventilation-perfusion coupling  Ventilation: the movement of air  Perfuuuuusee… “to spread”…it fills up with blood and gets  taken over by the blood! ∙ When you spray perfume, you have been “perfused”  because the scent spreads all over to fill your body ∙ Filling of capillaries with blood  If ventilation, then PO2 and therefore the PCO2 in the  alveoli  There will be LESS blood flow in the capillary to the  alveolus if it is a poorly ventilated alveolus…makes sense  because the blood is not going to go to an area to get  oxygen if there is no air in that area ∙ We will send blood to the areas where there is a high  amount of oxygen in the alveoli…we can change  blood vessels in response to “fresh air” levels in  alveoli  In reverse, the alveolus can respond to a blood vessel…we  send more air to a good alveolus, instead of sending air to  an alveolus that is resistant to air flow  Changing blood vessel diameter and changing access to  alveoli through smooth muscle contraction  to maximize  gas exchange 10Gas transport ∙ This part= external respiration o O2 moves from air into alveolar capillary A l v e o l u s   A l v e o l a r   c a p i l l a r y   1 . 5 %   D i s s o l v e d O 2   g a s O 2 +   H H b O 2   9 8 . 5 % H b O 2 +   H +  ∙ Oxygen moves from the air alveolus through respiratory membrane blood plasma of capillary (low capability to hold O2) into the RBC  ∙ Majority of the oxygen combines with deoxyhemoglobin (HHb)  98.5% o Deoxyhemoglobin= “without” oxygen…which is why there is an  H+ for the oxygen to bind to o **Equilibrium reaction ∙ Plasma o Only holds 1.5% of the oxygen o Oxygen has a low solubility so it cannot dissolve in that plasma so it cannot be kept there ∙ Hemoglobin: made of 4 peptide chains, has “heme” groups in the  center o **This is where the O2 is bound to the RBC!! o Located in the cytoplasm of the RBCs o The “heme” group has Fe2+…this is where the oxygen is bound  4 molecules of O2 can bind to the hemoglobin 11How O2 is Carried in the Blood ∙ Oxyhemoglobin dissocation curve: shows the relationship between Po2 and O2 saturation of hemoglobin  A n o x y h e m o g lo b in d is s o c ia tio n c u r v e s h o w s th e r e la tio n s h ip  o At different partial pressures of oxygen that make up the air and  b e tw e e n P O 2 a n d O 2 s a tu r a tio n o f H e m o g lo b in then go into the blood, we get different amounts of oxygen  binding to hemoglobin H H b + O 2 ⇌ H b O 2 + H + 2 5 % 7 5 % 1 % 9 9 % ~ 2 5 % O 2 u n lo a d e d to s y s te m ic tis s u e s =   u t i l i z a t i o n f r a c t i o n ~ 7 5 % r e m a i n s b o u n d a s H b O 2 =   v e n o u s   r e s e r v e ∙ Left side of equation= when hemoglobin and oxygen are separate ∙ Right side of equation= when oxygen is bound to hemogrlobin ∙ When hemoglobin is 100% saturated with O2…all 4 of the heme groups are bound with oxygen ∙ Blood plasma in lungs= pressure of 104 mm Hg **because that’s the  partial pressure of the oxygen in the alveolar air ∙ The BLUE= refers to oxygen in the systemic tissues o 75% of systemic tissues are saturated with O2 o 25% is not saturated with O2 ∙ The GREEN= refers to oxygen in the alveoli o 99% saturated with O2 o 1% is not saturated with O2 ∙ Utilization fraction: the amount of oxygen that is released from the  blood and unloaded to the systemic tissues =25% ∙ Venous reserve: the amount of oxygen that is held onto hemoglobin  and is STILL found bound to the hemoglobin even after the unloading  of the capillaries o We may use this during respiratory arrest when you stop  breathing, we are still alive because we have this backup amount  of oxygen to use that is waiting in the hemoglobin =75% 12∙ How CO2 is carried in the blood o (1)Dissolved in the plasma (it is highly soluble…remember graph) o (2)Bound to hemoglobin  Binds to the amino acid protein “globin” part=  carbaminohemoglobin o (3)Converted to bicarbonate ion  CO2 + H2O --[carbonic anhydrase]-- H2CO3  HCO3- + H+  Remember… CO2 means that reaction shifts to the right,  there are more H+ ions, and so the pH (becomes more  acidic) Systemic gas exchange- between capillary and tissue o Oxygen unloading and CO2 loading L o a d in g o f C O 2 in s y s te m ic c a p illa r ie s ∙ CO2 is loading and LEAVING systemic tissue and going into capillaries o The most common and main way that CO2 is carried is through  bicarbonate S y s t e m i c   t i s s u e C a p i l l a r y   b l o o d C O 2 7 %D i s s o l v e d C O 2 g a s C O 2 + p l a s m a p r o t e i n C a r b a m i n o c o m p o u n d s C O 2  2 3 %  C O 2 + H b H b C O 2  C l – C h l o r i d e s h i f t  C l –  H C O 3–  a n t i p o r t C O 2  H C O 3– + H +  7 0 % C O 2 + H 2 O  H 2 C O 3  ∙ If we accumulate the product (bicarbonate), we slow down the  reaction so a transport protein takes the bicarbonate. This happens  because of… o Chloride Shift: chloride moves into the RBCs. At the same time,  Bicarbonate is moving out of the RBCs o This chloride shift happens and the bicarbonate moves out so that  the reaction of CO2 moving from the tissue and into the capillaries  can continue to happen  CO2 gets into the blood and is carried to the lungs where it is expelled ∙ O2 is unloading and going INTO systemic tissue 13U n lo a d in g o f O 2 in s y s te m ic c a p illa r ie s o The tissue has used up oxygen for processes, and now it needs  more oxygen H C O 3 – + H +  9 8 . 5 % O 2  O 2  1 . 5 %  O 2 + H H b H b O 2 + H +  D i s s o l v e d O 2 g a s ∙ In addition to oxygen unloading because of (1)leaving hemoglobin and  (2)the dissolved oxygen gas there is a third reason o It is NOT just diffusion that causes oxygen to move!! ∙ Bohr Effect: H+ (high CO2 conditions) facilitates the hemoglobin  unloading O2 o Process happens starting with the curved arrow in the picture o We want to get rid of the bicarbonate o H+ assists in the unloading of the oxygen from the hemoglobin o the H+ comes from the formation of bicarbonate o **enhances getting rid of O2 so it goes into the tissue ∙ The more acidic the environment, then more oxygen will be unloaded o So if there is O2 in the tissues, there will be more oxygen  unloading from the blood o If your tissues are really active, they will get more oxygen o There is also more unloading of CO2 at these tissues CO2 leaves  tissue and goes into blood ∙ Oxygen does NOT move directly to the interstitial fluid…it goes from  RBCplasma interstitial fluid ∙ Summary o High tissue CO2 CO2 loading of blood (goes to plasma, or to  hemoglobin, or binds with water to make bicarbonate) o Low tissue O2 O2 unloading from the blood  ^these 2 things happen by simple diffusion o High blood CO2 (H+) **think pH!!!  enhances O2 unloading from  the blood  The H+ binds to oxyhemoglobin…so then oxygen leaves  blood and goes into tissue 14Alveolar gas exchange- between alveolus and capillary O 2 lo a d in g & C O 2 u n lo a d in g in a lv e o la r c a p illa r ie s o Oxygen loading and CO2 unloading o Happens in the reverse!! 7 %  C O 2  2 3 %  D i s s o l v e d C O 2 g a s C O 2 + p l a s m a p r o t e i n C a r b a m i n o c o m p o u n d s C h l o r i d e s h i f t  C l –  C O 2  C O 2  7 0 %  C O 2 + H b C A H C O 2 + H 2 O H 2 C O 3  H b C O 2  C l –  H C O 3– + H +  H C O 3–  H C O 3– – C l–  a n t i p o r t  O 2 O 2 + H H b H b O 2 + H +  O 2  1 . 5 %  D i s s o l v e d O 2 g a s H a l d a n e e f f e c t : H ig h O 2 c o n d itio n s f a c ilita te s  C O 2 u n lo a d in g ∙ CO2 moves in the same 3 ways, but it moves OUT of the blood and into  the alveoli so that it can leave the body o Carbaminohemoglobin gives up its CO2 so that it can move into  alveoli ∙ O2 moves from the alveoli into the blood so that it can go to the body o Formation of oxyhemoglobin ∙ Haldane Effect: high O2 conditions facilitates the hemoglobin  unloading CO2 o This is an enhancing effect…drives bicarbonate reaction to the  left o The H+ from the dissocation of oxyhemoglobin it is used to  move CO2 into the alveoli through the reverse bicarbonate  reaction o **enhances getting rid of CO2 so it goes into alveoli ∙ NOTE: the chloride shift happens in BOTH types of gas exchange…but  in different directions o For alveolar gas exchange, CO2 is unloading, so bicarbonate is  coming into the cell and chloride is leaving the cell o In systemic capillary gas exchange, the chloride is coming in so  these systemic arteries have a large amount of chloride ∙ Summary o Low alveolar CO2 blood unloading of CO2 o High alveolar O2 blood loading of O2 o High blood O2 (due to the process of air leaving alveoli and going  into blood) enhances CO2 unloading by the blood 15

Where important? Why important? Bohr Effect Systemic capillaries O2 unloading to the tissues is enhanced by CO2/H+ Haldane Effect Alveolar Capillaries CO2 unloading to the alveoli is enhanced by O2

What will happen as a result?

∙ Poll Ev: What condition would directly stimulate ADH release?

What makes his condition better?

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16The Urinary System ∙ Medulla: deeper tissue, cortex= superficial tissue ∙ Excretion: movement of chemicals out of your bodily fluids o Respiratory system: CO2, small amounts of other gases, and water o Integumentary system: water, inorganic salts, lactic acid, urea in  sweat o Digestive system: water, salts, CO2, bile pigments, cholesterol, other metabolic wastes o Urinary system: many metabolic wastes, toxins, drugs, hormones,  salts, H+, and water =99% of excretion ∙ Kidney functions o Excretory: filter blood and remove wastes o Cardiovascular: regulate BV, BP, osmolarity of fluids (ideal solute  concentration= 290 milliosmoles/L…measure of everything  dissolved), acid-base balance o Endocrine: stimulate RBC production ∙ 10-20% of blood passes through the kidneys ∙ Nitrogenous wastes: something that has nitrogen in it o We break down a protein (catabolism) ammonia is formed and is  toxic o The carboxyl group is important o The amino group is taken off and is wasteit becomes ammonium  (NH4+)  Having lots of ammonia makes us form ammonium…this is not  good because then we have more stuff to get rid of  o Ammonia: from the breaking down of a protein o Urea: formed from ammonia in the liver, not as toxic as ammonia o Uric Acid: formed from nucleic acid metabolism (the breaking down  of DNA) o Creatine: formed from the breakdown of creatine phosphate  In ATP production we used the phosphate, and then now we  have this creatinine portion to get rid of ∙ The nephron: consists of a tubule and its associated vasculature (blood vessels) o This is where we do all the functions of the endocrine system ∙ Vessels of the nephron o Renal artery: big vessel that brings blood to the kidney o Renal vein: brings blood out of the kidney o Afferent arteriole: the blood supply to the nephron  Afferent (sensory)…bringing blood TO nephron  Efferent (EXIT) arteriole…takes blood away o Glomerulus: the site of filtration of the blood 1
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