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is the study of how the body functions. |
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Homeostasis is the constancy of the internal environment. - cells and only survive within a narrow range of conditions |
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Examples of states that must be maintained for the cell to survive |
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pH, temperature, carbon dioxide, oxygen, blood pressure, wastes, intra and extra cellular fluid volumes. |
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Disease is a failure to maintain homeostasis |
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systems that maintain homeostasis |
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nervous and endocrine systems |
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examples of why you might need to derive from homeostasis |
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sudden fright, growth and pregnancy |
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1)Change in internal or external environment must be detected or anticipated 2) NS and/or endocrine response alters system(s), responsible for that condition. 3) For an anticipatory response: Ex. You get an increase in resp. rate just before you start exercise. What normally blood gases are reasonable for change, but because you haven’t started yet this is before they are changed. Because you have proprioceptors they signal movement. These receptors can be learned and even behavioural. (ex. Putting on a coat before going out in the cold.) 4) Feedback mechanisms (both NS and endoc mechanisms) - these are mechanisms that respond to change in the system |
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a range of values of the variable, which do not bring about a response. So this is where you are in HS, it is “normal” |
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monitor information (input) and sends is back to the NS or and endocrine system |
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the most common HS control mechanism. The result of the output moves the variable back toward the set point that is in the opposite (negative) direction, to the change that triggered the initial response. Hence negative, going in the opposite direction. |
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True or false: the set point can not be reset |
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- less common and it is NOT homeostatic - output intensifies the input |
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Components of the Cell membrane |
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1)phosolipid bilayer 2) membrane proteins 3) membrane carbohydrates 4) bulk flow |
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- continuous layer - a barrier to water soluble molecules |
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Types of membrane proteins: |
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a) transport proteins b) receptor proteins c) enzymes d) joining proteins e) identifying proteins |
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transport proteins I) channels - form a pore in the membrane - permit the movement of water and ions - lots of them are specific channels that allows certain ions - they can be gated (open or close like a door) - they can be non-gated (always open) II) Carrier proteins - bind solute and carry it across the membrane Ex. Glucose transport - facilitated diffusion or active transport |
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- can bind specific intracellular molecules (hormones or neurotransmitter- nt) Ex. Insulin binds to a receptor that is specific to it, it only binds to insulin, and binds it to receptor on sk.muscle or adipose tissue which triggers movement of glucose transporters into cell membrane to increase glucose movement of glucose from blood to cells. |
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- control chemical reactions on inner or out surface Ex. Acetichlornesteras which is found on sk. Muscle and on some post synaptic neurons. Na+/K+ - ATPase which is found in every cell in the body |
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- anchor cell membrane to cytoskeleton or to adjacent cell -they can be junctional proteins, which are between cells, they form : I) desmosomes II) tight junctions III) gap junctions - extra cellular fibres (usually glycuproteins) |
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Ex. Major mistocompatibility complex (MHC) proteins, which are on the surface of cells (expect the RBC). These identity cells as being part of the body. The RBC do have identifying proteins but not this kind. |
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Membrane Carbohydrates Fig. 3.4 pg.68 |
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- most commonly glycoproteins but they can be glycolipids - allow cell to recognize type ie. Other neurons, muscles cells….. |
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Passive processes - no energy is required à movement from high concentration to lower concentration (like riding a bike down a hill) |
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Types of passive processes |
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1) simple diffusion 2)Facilitated Diffusion 3) osmosis |
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Simple diffusion (solute movement) fig. 3.6 pg. 71 |
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- solute can cross the membrane bilayer (fig 3.7) - they have to be small and generally lipid soluble (O2, CO2) - OR ions moving across membrane via protein channel by diffusion (from high To lower concentration |
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- big charged or water soluble molecules - molecule moves across the membrane down it’s concentration gradient, using a specific carrier protein. - requires no energy Ex. Glucose transport into liver, sk.muscle |
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Osmosis (solvent movement) |
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Osmosis (solvent movement) - it can get across, but we don’t know how - the movement of water across the semi permeable membrane. A semi permeable membrane is permeable to water and nothing else, this is due to the water concentration difference via pore (protein) or across the bilayer. |
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Osmotic pressure (OP) fig. pg. 73 |
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- the pressure that most be applied to prevent movement of water from pure water solution (S1) across a semi permeable membrane into another solution (S2). |
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- the response of a cell immersed in a solution - depends on the conc’n of solutes (and the permeability of cell membrane to solutes) |
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- cell swells (takes in water), the outside has a high conc’n of water then the inside and the membrane is permeable to water so the water can get in, it has a lower OP compared to the cytoplasm. |
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- the cell neither shrinks nor swells, it is happyJ - for humans 0.9% NaCl is normal saline |
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- the cell shrinks when placed in this solutions and is unhappyL - the outside has a lower conc’n then the cytoplasm, therefore it is more concentration and has a higher OP then the cytoplasm. |
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- swelling and shrinking of certain cells uses to regulate fluid conc’n in the body (tonicity of fluids) - 10% sucrose solution can be used to reduce brain swelling in brain injuring. |
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- movement of fluid due to a pressure gradient |
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pressure of a fluid pressing against a surface ex. Cell membrane, blood vessel wall (BP) |
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Direction of fluid movement into/out of capillaries determined by balance of |
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a) hydrostatic pressure ( fluid on both sides) b) osmotic pressure due to presence of large non-diffusible proteins |
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1) active transport 2) vestibular transport |
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- substances move again conc;n gradient (low to high) - protein- carrier mediates - may be primary (1) or secondary (2) |
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primary active transport fig 3.10 pg. 76 |
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1=pumps - ATP brakedown is part of the transport process Ex. Na+/K+ - ATPase a) Na+ gradient established by Na+/K+ ATPase (ATP use step) |
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secondary active transport fig 3.11 pg.77 |
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2= co transport Ex. Glucose entry at small intestine b) glucose, Na+ both must bind to carrier and they are co transported into the cell à Na+ moving down it’s conc’n gradient drives in glucose against it’s glucose conc’n gradient. This is the transport step, therefore the glucose transport is active. |
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- substance is surrounded by a membrane within a cell (a vesicle) a)endocytosis b)Exocytose |
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- movement into the cell I) phagocytises - large items taken into the cell ex. Bacteria (cell eating) II) pinocytosis - (bulk phase endocytosis) fluids and dissolved substances moving Into the cell (cell drinking) |
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- movement outside the cell Vesicles containing hormones, enzymes, nt ect., fuse with the cell membrane and open to release contents into ECF, this required Ca2+ |
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Electrical properties result from: |
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1) ionic conc’n gradients across the membrane 2) permeability characteristics of membrane to ions 3) ionic conc’n differences across membrane (gradients) |
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ORG- (=A-) = negatively charged proteins Cl- repelled by ORG- so is higher outside than inside Na+ and K+ conc’ns are due to and maintained by activity of Na+/K+ ATPase (pump) on cell membrane |
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Permeability of membrane to ions Fig. 11.8 |
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- always open - more K+ non-gated channels then Na+ non-gated channels - cell membrane is more permeable to K+ then to Na+ at rest - these channels (especially K+) are important in establishing the resting membrane potential |
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gated ion channels (not involved at rest) Fig 11.6 |
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- can open in response to various stimuli I) membrane voltage changes= voltage gated channels II) Chemical changes ex. Binding of nt or hormone = chemical gates III) Other stimuli that can open channels are tempurature (thermal gates), mechanical deformation (mechanical gates) Ions move through channels by diffusion, no energy is required, it is always passive |
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Resting Membrane Potential (RMP) fig.11.7 pg.399 |
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- charge difference just across the membrane when cell is not stimulated =potential (voltage) difference across the membrane (-70mv) ie. Inside = 70 mv more negative than outside |
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Na+/K+ ATPase (pump) - not a channel |
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- brakes down one ATP and uses that energy to pump three Na+ out and two K+ in à both ions are pumped against their conc’n gradients and therefore required energy (ATP) and so it active transport. - maintains concentration gradient of Na+ and K+ ( contributes a little but does not determine RMP) |
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More non-gated K+ channels than non-gated Na+ channels (membrane is more permeable to K+ than Na+ at rest) |
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- K+ is the major determinate of RMP - K+ diffuses out of the cell down conc’n gradient, therefore the cell loses postive charge, but |
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large organic ions inside the cell ex. Proteins (ORG-)=negative, they can not cross the membrane |
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- K+ moves out due to the conc’n gradient and the inside of the cell becomes more negative |
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Diffusion of K+ out ___1__ , and the diffusion of Na+ in ___2___ due to the increasing negative charge. At first, the postive out (K+) is ___3__ than the positive being drawn in (Na+) via the negative charge. Over time the inside of the cell becomes ___4__ enough that the amount of positive moving out balance the amount of positive moving in. - the net movement of charge is 0. (positive is the same in both directions) and at that point you have the RMP) |
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1) slows 2) speeds up 3) greater 4) negative |
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- two poles, one positive, one negative - unequal distribution of charge ( a potential or voltage difference = -70 mv in neurons) - present in all cells |
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Electrically Excitable Cells |
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- can depart from resting membrane potential, which is called action potential (ap), in response to stimuli (changes in external environment) - muscle and nerve cells only |
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When a neuron is stimulated |
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a) mp changes = a graded potential if the membrane reaches a threshold potential b) triggers an action potential |
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Graded potential fig 11.10 p 401 |
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Graded potential fig 11.10 p 401 - a small change in mp (away from resting) - usually occur on a dendrite or a cell body - this small change causes the ions to move, they travel passively a short distance ( current flow) - short lived - magnitude and the distance travelled by the potential ( or current) varies directly with the strength of the stimulus fig 11.11 p.402 |
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changes in the graded potential can be either : |
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a) depolarization b) hyperpolarisation |
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inside face of the membrane becomes more positive than resting Ex. From -70mv to -60 mv (closer to zero) fig 11.9 p.400 |
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- inside face of membrane becomes more negative then RMP Ex. From -70mv to -80mv |
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a return to resting after either hyper or de polarization |
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Why are graded potentials important? |
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- if it is a depolarization and if it is large enough ( or sums to be large enough) I.e. cause by a critical stim à will lead to an action potential You have to get: 1) a critical stim à 2) graded potential à 3) action potential |
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Action potential (impulse) - |
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a large change in MP that propagated along an axon with no change in this intensity - initiates at trigger zone table 11.1 p.342 |
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what are the two possible outcomes of a stimulus? |
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1) hyperpol. Or too small (dies out) OR 2) depolarization to a threshold potential (around -55mv) which means it was a critical stimulus and we get an action potential |
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absolute refractor period |
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- no action potential can be generated regardless of the stimulus size - either 1) all Na+ channels are open (region 2) or 2) they are all inactivated ( cannot reopen until MP passes RMP ) region 3 |
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relative refractory period (region ) |
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- period can be generated, but only by greater than normal stim. - Na+ channels are reactivated when the MP passes RMP on repolarization, therefore they are closed but can be opened - K+ channels are open and the membrane is hyperpolarised - further to go to get to threshold and therefore you need a larger stim. And a larger graded potential |
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All- or not principle of APs |
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- each time an action potential is produced it looks the same, that is it has the same max. depolarisation ect. - strong stim à get AP (looks the same as previous) - weak stim. (below critical) à no AP |
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Compasision of AP and GP (CAG) location |
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ap - axon gp - dnedrites of cell body |
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ap - all or none gp - variable |
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graded - Current dies away | ap- Na+ gates close, K+ gates open |
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graded Chemical, mechanical etc. (anything but voltage) | ap - voltage |
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graded - Short and then dies away | ap - Produced anew on the axon and propagates over long distances |
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Action potential propagation |
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- depolarization during APà positive charge moves toward more negative charge on the adjacent membrane - depolarization à is large enough to reach threshold à get AP on the adjacent resting membrane - get a sequence of AP s along the membrane, each one the same |
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Action potentials move ___1__philologically because the preceding membrane is still in it’s ___2__ |
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1) in one direction 2) refractory period |
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Rate of propagation depends on: |
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1) fibre diameter - the larger the diameter the fast the propagation (less resistant to current) 2) whether the fibre is myelinated a) myelinated fibre AP occurs at nodes of ranvier = saltory (leaping conduction) à fast b) un myelinated fibres Aps all along fibre = continuous conduction = slower |
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- large diameter and they are myelinated à 130 M/sec (most sensory neurons and motor neurons to sk. Muscles fibres) |
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- small diameter and un myelinated à 0.5 M/sec ( autonomic nervous system and some pain fibres) |
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describe synaptic transmition in terms of AP and Ca2+ |
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Presynaptic cell à postsynaptic cell fig 11.18 p. 356 - AP arrives at axon terminal - Ca 2+ enters synaptic end bulb of the terminal via Ca2+ - voltage gates (Ca2+ = low inside) - Ca2+ triggers exocytose of the neurotransmitter à nt crosses cleft, binds to receptor on postsynaptic membrane à chemically gated channels open à graded potential = postsynaptic potential (PSP) |
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= graded pot. Depol. - due to opening of Na+ ( or Ca+) channels, or closing of K+ channels - nt is often = ex. Acetylcholine (ach) |
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= graded potential à hyperpol. - due to the opening of K+ channels or Cl- channels - more difficle to get an AP - nt often ex. Glycine |
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1 neuron has many synapse à sum of all __1__ and ___2__ arriving determines if an action potential will occur at the axon hillock |
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à ach - opens Na+ chemical gates on muscle end plate - grader potential = end plate potential (EPP) Depol. Is sufficient to get an AP on the adjacent sarcolemma - lots of ach is released and therefore you always get an AP from and EPP |
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Interpretation of sensory stim. |
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1. Stimuli detected by receptors 2. Receptors can be a) dendrites on unipolar neurons b) individual cells which synapse to neurons Ex. Hair cells in the ear |
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What happens when a receptor is stimulated? |
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1) the stim. Causes opening of channels (usually they are Na+ channels) on receptor membrane 2) à graded potential on receptor membrane (stim. Becomes electrical) = receptor potential |
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If the stimulus is on the dendrite of a unipolar cell (aka generator potential) then: |
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= graded potential (depol.) which directly generates an AP on that neuron |
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if the stimulus is on an individual cell (aka receptor potential) then : |
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( no AP on the receiving cell) à nt onto the associated neuron à generator potential à AP on the neuron |
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1. phasic receptors 2. tonic receptors |
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- show adaptation (usually decrease in sensitivity) - get decrease in AP frequency to the CNS even though the stim. Is maintained at constant strength Ex. Touch à clothes on skin - receptors respond to a stim. Change (clothes fall off) |
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- do not show adaptation (or takes a long time) - give continuous info Ex. Posture, condition (are things working properly) and painà protective - monitor presence and intensity of stim. |
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How does the brain perceive different types of stim? |
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- mainly by type of receptor stimulated - mostly by the pathway that it takes and where it goes in the brain - the axon activated by the receptor will make the same synaptic connections to the CNS concerned with that sense (hardwired from the receptor to the brain) - always knows “who” is calling (type of receptor) and from where (location) |
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How does the brain perceive stim. Of different strengths? Ex. A feather or a brick on your foot |
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- mainly by the frequency of Aps ( the number per unit time) going to the CNS - stronger stim. Also activates larger number of receptors ex. Pressure and touch |
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Physiology of Vision fig 15.10 |
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1) light image which is focussed on the retina (reduced and inverted) 2) stimulates chemical reaction on the rods and/or cons which produces a receptor potential (graded potential) Receptor potential à nt à bipolar neurons à release nt à ganglion cells à ntà AP à optic nerve (II) à optic tract à visual cortex or occipital lobe) |
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So guys some of the notes are missing cause I missed the first part of class and the way the person that lent my the notes didn't transfer well |
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= adrenergic (ne = norepin por cholinergic |
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function of the post and pre ganglionic neurons |
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Func. prepares body for activity - fight or flight |
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NE- broken down by ____________ in presynapsic neuron |
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- rest and digest “house keeping” |
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Most organs innervated by ans have both SNS and PSNS, and the effects are usually _____________ |
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Effect | SNS | PSNS | Pupils of eyes (iris musc.) | dilate | constrict | |
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Effect | SNS | PSNS | | | | heart | Increase heart rate and force of contraction | Decreases heart rate | |
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SNS- Increase heart rate and force of contraction | PSNS - Decreases heart rate |
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SNS - Decrease motility PSNS- Increases motility |
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Effect | SNS | PSNS |
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| Blood vessels (sm. Muscle) |
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SNS - Vasoconstriction * no innervations (mostly except penis and clitoris) |
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Effect | SNS | PSNS | | | | | | | | | | | | | Glands (sweat) |
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SNS - Increase secretion (cold sweat) PSNS - No innervations |
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Effect digestive | SNS | PSNS | |
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digestive | Decrease except saliva | Increases secretion | |
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genitals | Ejaculation (male) | Erection and lubrication (both) | |
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a) spinal - least complex required sensory input from ex. Muscles spindles b) postural - for balance, posture - require sensory input from ex. Proprioceptors (muscle spindles ), eyes, inner ear à co-ordinated by cerebellum |
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- most complex - no external stim. Required (will) |
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- walking, running, etc. - reflex and voluntary - initiated and ended but cerebrum - sustained without input from cerebrum - input does to the motor neurons from |
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1)Premotor 2)Supplementary Motor 3)Association Areas - these three are level one - they signal to the primary motor cortex, which is level two à - the brain stem nuclei (level 3) à spinal cord (level 4) but the primary motor cortex can also send messages directly to the spinal cord, this is called the cortico-spinal tract - the basal nuclei also get messages from the first level and second level. The spinal cord goes down to the muscles |
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- decides what movement is needed. - Plans sequences of muscle contractions. - Signals the primary motor cortex, it also sends a copy of the plan to the cerebellum |
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a) directly to the motor neuron (corticospinal tract). Fine, skilled movements b) to brain stem nuclei à descending motor tracts go lower motive neurons = indirect tracts (extra pyramidal)- co-ordination of large muscle groups involved in maintenance of posture and locomotion |
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- stores planned movement and compares the actual movement to the plan and then corrects it if necessary. - receives sensory input about balance - it has tracts going into the brain stem |
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- involved in the planning and initiation of that movement |
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Coritospinal (direct) pathway |
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- descending from the cortex to the sk. Muscles - for fine, precise movement |
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1) upper motor neurons ( they are actually inter neurons) |
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- cell bodies in the motor areas of frontal cortex - axons travel down tracts to the sp. Cord |
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à sp. Nerves - cell bodies are located in the ventral horn of the spinal cord |
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1) Destruction of Upper motor neurons will result in
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- reflex arcs are present - get a) spastic paralysis - increased muscle tone (no muscle atrophy) B) exaggerated reflexes |
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2) destruction of the lower motor neurons results in:
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- no reflex arc present - get a) flaccid paralysis - decreased muscle atrophy B) no reflex action |
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- low level of contraction |
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- complex - involves areas in the left cortex in most ppl (99% of RT handed ppl and 66% of left handed) |
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a) prefrontal cortex is reponsable for ____ part of speech |
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- necessary to understand written and spoken words (language) |
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b) wernicke’s area, at the parietal/temporal lobe junction is reasonalbe for ____ part of speech |
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- sounding out unfamiliar words, and comprehension of language |
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c) broca’s area is reasonable for ___ partof speech
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- frontal lobe - formulates words as they are to be spoken - puts words together in a meaningful sentence |
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Damage to wernicke's will result in: |
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person can’t understand spoken or written words, but they can speak, but the words are meaningless, inappropriate or they are mixed but |
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Damage to broca’s area wil result in: |
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person can understand the language, but they can not produce sensible speech (can’t find the words and co-ordination of respiratory and oral movements may be poor) |
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- glands and tissues that secrete hormones which travel in the blood to target cells (= cells with specific receptors) - bind to receptors and change cell activity - regualte growth reproduction, metabolism - receptors - proteins and can be |
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Describe the path sound waves take from the hair cells to the auditory cortex of thf temporal lobe |
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| hair cells in cochlear duct stim. (receptor potential) | | | [image] | | | | | | | | | | | | | | | | | | | | | | | | nt release | | | | | | | [image] | | | | | | | | | | | | | | | | | | | | | | | | generator potential | | | | | | [image] | | | | | | | | | | | | | | | | | | | | | | | | action potential on neuron of cochlear branch on nerve VIII | | | | | | | | | | | | | | | | | | | | | | | | auditory cortex of temporal lobe | | | | |
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Describe how we maintain good posture |
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| | | | | | | | | | | | | Hair cells of semicircular ducts and saccule and utricle | | | | | (= vestibule) | | | | | | | | | [image] | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | receptor potential | | | | | | | | | [image] | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | nt release | | | | | | | | | | | | | | | | | | | [image] | | | [image] | | | [image] | | | [image] | | | | |
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rapid automatic response to stimuli which which the stimulus always causes the same response, usually protective and involving 2 or more neurons |
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Somatic relfex (E= skel. musc) Visceral Reflex (E= sm./ cardiac musc. or glands) |
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Somatic spinal relfexes Autonomic Spinal Relfexes |
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Strech Reflex Flexor (withdraw) Reflex Cross Extensor Reflex |
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| ie: knee jerk reflex (Extensor muscle contracts) (Fig.15.16) | | ╚ Stimulus is tapping patellar ligament | | | | (Stretches muscle which in this case is quadriceps | | | femoris) | | | | | | | ╚ Receptor = muscle spindle (in muscle) | | | | ╚ Effector is skeletal muscle (quadriceps femoris) and it | | contracts | | | | | | | ╚ Ipsilateral (same side) | | | | | | ╚ monosynaptic (1 sensory neuron and 1 motor neuron) | |
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| ie: in leg (flexor contracts) | | | | | ╚ stimulus is standing on a nail | | | | ╚ Receptor = touch, pressure, pain | | | | ╚ Effector is Hamstring (= flexor) and it contracts | | ╚ Ipsilateral (same side) | | | | | ╚ Polysynaptic (more than 1 synapse) | | |
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Definition
ie: in leg (extensor contracts) | | | | ╚ Stimulus is stepping on a nail | | | | ╚ Receptor = touch, pressure, pain | | | | ╚ Effector is quadricep femoris (extensor) and it contracts | ╚ Contralateral (opposite side) | | | | ╚ Polysynaptic means more than 1 synapse | | | ╚ keeps you from falling down when flexor (withdrawl) reflex | occurs | (Fig. 13.19) | | | | |
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Term
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Definition
╚ when muscle (group) contracts → agonist | | | ╚ at same time, antagonist prevented from contracting | | (inhibitory neurons) | | | | | | ie: stretch reflex in quadricep femoris is the agonist | | and it contracts the hamstrings which are the | | antagonists and are inhibited from contracting, | | that equals reciprocal innervation | | |
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Term
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Definition
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Term
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Definition
╚ urinary bladder | | | | | ╚ polysynaptic | | | | | ╚ stimulus = stretch of bladder | | | ╚ Receptor = stretch receptors in bladder wall | ╚ CNS is in the sacral segment of spinal cord (PSNS) | ╚ Effector is Detrusor muscle (wall of | | smooth muscle | bladder) and it contracts | | ╚ Effector is Internal Urethral Sphincter it | relaxes | | | | | ╚ External urethral sphincter under voluntary control | | (ie: not part of reflex) | | | |
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Term
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Definition
╚ auditory and visual reflexes | | | | | → movement of the eyes (visual reflex), head and | | neck (both; auditory and visual) in response to | | visual and auditory stimuli | | | |
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Term
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Definition
╚ functions with medulla to regulate breathing (appneustic, | and pneumotaxic areas used to regulate breathing) | | |
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Term
Functions of the Medulla Oblongata |
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Definition
╚ decussation of motor and sensory neuron tracts | | | ie: Left brain controls right skeletal. muscle and | | received sensory input from right side aswell | ╚ vital reflex centers | | | | | ╚ respiratory area (drives breathing rate) | | | ╚ vasomotor area | | | | | | → controls blood vessel diameter | cardiovascular | ╚ cardiac center | | | center | | | → modifies heart rate | | | ╚ non-vital centers | | | | | → swallowing, vomiting, coughing, and sneezing | |
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Term
Overall function of the Brain Stem (which consists of the midbrain, the pons and the medulla oblongata) |
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Definition
╚ controls life-sustaining processes | | | | ie: breathing, circulation | | | ╚ if brain stem is functional but the higher centers are | damaged the person will be alive but unaware, no | conscious control | | | | |
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Term
Functions of the Hypothalamus |
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Definition
1) Regulates the Autonomic NS (smooth muscles, cardiac | muscles, and glands) | | | | | | | | | | | | 2) Regulate part of the Endocrine System | | | | | | | | | | 3) Regulates Temperature | | | | | | ╚ contains "thermostat cells" | | | | | | | | | | 4) Regulates eating, and drinking | | | | | | | | | | | 5) Part of the limbic system | | | | | ╚ composed of cerebrum, thalamus and hypothalamus | | ╚ is the emotional brain and basic emotions | | | | ie: rage, fear | | | | | | | | | | | 6) Co-ordinates Reticular Activating System (RAS) | | | ╚ reticular formation | | | | | | → in brain stem | | | | | | → alerting | | | | | ╚ RAS is incoming sensory input for awakening | | (includes the cortex, hypothalamus, thalamus, | | reticular formation) | | | | | ╚ receives input from visual system that sets the | | daily rhythms | | | | | | | | | | | | 7) Receives Sensory Input from cutaneous receptors of | nipples, and external genitalia, therefore it is involved | in sexual arousal behaviours | | | | |
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Term
Damage to the hypothalamus will result in: |
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Definition
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Term
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Definition
╚ Preganglionic Neuron is called Cholinergic | | ╚ Postganglionic Neuron is called Adrenergic (NE) | and/or cholinergic (ACh) | | | | ╚ function is to prepare the body for activity | | | → fight or flight response | | | ╚ NE broken down by monoamine oxidase (MAO) | | → in presynaptic neuron | | | |
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Term
Parasympathetic NS (PSNS) |
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Definition
╚ pre and postganglionic neurons = cholinergic | ╚ functions are rest and digestion or "housekeeping" | ╚ ACh broken down by acetylchoinesterase (AChE) | on postsynaptic membrane | | | ╚ most organs innervated by ANS (autonomic nervous | system) have both SNS and PSNS, and effects are | often opposite | | | | | | ie: heart rate | | | | | | → SNS will excite | | | | → PSNS will inhibit | | ╚ mostly of gastrointestinal (GI) tract - PSNS excites, | and SNS inhibits | | | | ╚ ANS regulates internal processes continuously and | automatically | | | | | |
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Term
Sorry the cards are out of order!! I was missing the first part of lecture 4 and just got it. |
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Definition
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Term
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Definition
- peptides, proteins catecholamines (= 1st messenger) - binds to cell membran receptors (do not enter cell) - hormone - receptor complex activates membrane protein eg. G-proteinroteins t G-proteins then acitvate 2nd membrane proteins eg. cyclic amp (camp Ca2+ ect.) |
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Term
Example of 2nd messanger camp |
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Definition
1) hormone binds to cell - surface receptor and activates the G-protein 2) G-protein the activates adenylate cyclase adenylate 3) ATP---------------- camp + PPi - concerntration of camp increase in cell 4) camp (2nd messenger) activates protein kinase in cytosol 5) protein kinase acts on other cyclase proteins (usually phosophorylates) to change their acticity, therefore it changes the acitivty of the cell |
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Term
Why use 2nd messenger systems? |
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Definition
a) hormone can`t enter cell (water volume) b) rapid actiing (enzymes) already present c) one hormone molecule acitvated, multiplies effect of single molecule d) limited - messeng broken down or removed ex. camp broken down by phosphodiesterase in cell |
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Term
B) lipid soluble hormones |
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Definition
- steroids and thyroid hormone - enter the cell; bind to intracellular (nuclear) receptors and activates genes triggers protein synthesis -- takes time, but has long lasting effects |
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Term
Protein synthesis via lipid soluble hormones |
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Definition
1) Hormone binds to receptor in cytosol or nucleus | | | | | | | | | 2) Hormone receptor complex binds to a specific region of | DNA and starts gene transcription | | | | | | | | | | 3) makes mRNA binds to the ribosomes and you make proteins | via protein synthesis | | | | | |
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Term
Regulation of Hormone secretion into the blood |
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Definition
- by stimuli acting on endocrine gland |
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Term
Stimuli acting on the endocrine gland or tissue may be |
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Definition
1) a non- hormone substance in the blood ( a humoral stimulus)
2) the NS 3) a hormones: low metabolism to high metabolism |
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Term
Regulation of hormone secreation into the blood via :a non- hormone substance in the blood ( a humoral stimulus) |
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Definition
ex. if you have high blood glucose ---- beta cells of islets of langerhans (pancreas) Langerhans -- insuline -- lowers blood glucose -ve feedback low blood Ca2+ --- parathyroid gland ----- parathyroid hormone (PTH) -- raises blood CA2+ (raises bone resorption by osteoclasts, lowers osteobast acitivty) |
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Term
Regulation of hormones into the blood via: the NS |
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Definition
resting ---`surprises`` --- SNS (ach) ---- adrenal medulla epi --- THR force of contraction |
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Term
Hormone release into the blood via: Low metabolism to high metabolism |
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Definition
| | Low metabolism | | | | | | | [image] | | | | | | | | | | | | | | | | | | | | | | [image] | | release thyrotropin | | | | | | releasing hormone | | | | | (-) | (TRH) from hypothalamus | | | | | | [image] | | | | | | | | | + | | | | | | | | | | | | | | | Thyroid - Stimulating | | | | | | hormone (TSH) | | | | | | (-) | anterior pituitary | | | | | | | [image] | | | | | | | | | | | | | | | | | | | | | | | | Thyroxine (T ) | | | | | | | | (Thyroid Gland) | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | T → T in target | | | | | | | tissue or liver | | | | | | |
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Term
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Definition
- any exteme external or internal st.m ex. surgery, infections, strong emotions, exams - triggers set of body changes called the general adaption syndrom - all co-ordinate directly or indirecty by the hypothalmus. |
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Term
alarm reactioor fight or flight response - immediate (NS) |
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Definition
CNS - (sensory input - dectect change) ------- hypothalmus (RAS raises alertness) --- SNS -- adrenal medulla --EPI -- organs OR from SNS -- oragns |
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Term
effects of the alarm reactioor fight or flight response |
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Definition
a) raises bood glucose (energy) (SNS inhibits insulin release) glycogen ------ glucose (liver) b) increase HR, force of contraction will increase respiration rate and decrease blood flow to skin, abdominal viscera. therefore more avaiable to skel muscle, heart and brain ----- O2; glucose to working organs and brain c) lowers digestion and urine formation |
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Term
resistance reaction (long term --- endocrine |
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Definition
- initiated by hypothalamic releasing hormones (RN) - recovery from one tissue repair, ect.) or response to longer term stress |
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Term
2) Resistance Reaction (long term this is endocrine) |
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Definition
| | | hypothalamus | | | | | growth hormone | | | | | corticotrophin | | releasing | | | | releasing hormone | hormone | | | | (CRH) | | | (GHRH) | | | | | [image] | | | [image] | | | anterior | | | | | | | | | pituitary | | | | | | | | | [image] | | | ↑ adrenocorticotropic | growth hormone | | | | | hormone (ACTH) | | (GH) | | | | | | [image] | | | | | | adrenal | | | | | | | | | cortex | | | | | | | | | | | | ↑ cortisol | | | | | | | | (= glucocorticoid) | | |
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Term
Although cortisol is released within 30 seconds of stress (i.e alarm reaction) ..... |
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Definition
| | the response is not seen until | | hours have passed because cortisol is a steroid and acts at | | nuclear receptors (turns genes on and off) | |
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Term
The inhibition of insulin results in: |
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Definition
increase blood glucose | | | | | | ╚ liver stimulated to produce new glucose from | | fats and (later) proteins if continuous stimulation | | ╚ little insulin so glucose not taken up well | | | by especially skel. muscle (at rest), and | | | adipose tissue | | | | | |
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Term
The increase in blood glucose results in: |
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Definition
a) glucose spared for use by NS (brain can only use | glucose to make ATP) | | | | b) metabolism of non-nervous tissue | | | directed to fats for energy (combination of growth | hormone (GH), and cortisol that do this) | | | → if stress continues then cortisol inhibits GH | | release and proteins then also used | |
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Term
The use of fats for energy for everything over than the vrain results in: |
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Definition
╚ Increase in blood fatty acids (FA), and amino acids (AA) | | | → provides energy for everything but the brain | | ╚ inhibition of many immune responses, bone formation, formation of | connective tissue (delays wound healing) | | | | ╚ also get release of aldosterone, antidiuretic hormone (ADH) → | reduces salt, water loss at kidney to maintain blood volume and | therefore Bp | | | | | | | | | | | | | | | |
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Term
Long term effects of the inhibition of insulin: |
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Definition
| | | | | | | | | | | | | | | Decreased weight, increased Bp, increased HR, immune | | suppression (due to cortisol), loss of bone density | | | (↑ Bp and HR increase heart attack and stroke) | | |
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Term
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Definition
╚ results from depletion of body resources | | | | | ie: lipid reserves gone, glucocorticoids, loss of potassium | | (aldosterone effect-monitors K+ & Na+ levels), damage to | | organs (specifically heart, liver, kidneys) | | | | | | | (Fig. 16.16-purple is short term) | |
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Term
Endocrinology and Physiology of male reproduction |
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Definition
[image] | after puberty: | | | | | gonadotropin-releasing | | | | hormone (GnRH) | | FSH = follicle | (-) | | | | stimulating | | + | | + | hormone | | | | | | | | LH | | FSH | LH = luteinizing | | | | | hormone | (-) | + | | + | | | | | | | | | testosterone | | spermatogenesis | | (leydig cells) | + | (seminiferous | | | | | tubules) | | | |
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Term
Functions of Testosterone |
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Definition
1) Development of organs of male reproduction tract | | | | | | | | | 2) Development of secondary sex characteristics ) (puberty) | | ie: hair, deep voice, etc. | | | | | | | | | | | 3) Stimulate bone growth, then stops growth, at epiphyseal plate | (converted to estrogen to stop growth (closure)) | | | | | | | | | 4) Protein Anabolism | | | | | | | | | | | | 5) Spermatogenesis (direct effect) | | | | |
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Term
Endocrinology and Physiology of Female Reproduction |
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Definition
Hypothalamus | | Releasing | GnRH (after puberty) | | | [image] | | | | | | | | | | | | | | | [image] | | [image] | | | | | [image] | | | [image] | | | | | [image] | | | | | | [image] | | | | | | | | travels down | | + | | + | | | | | | | | | | | | anterior pituitary | | | LH | | FSH | | | [image] | | | | | | | | | | | | promotes + | | | promotes | | | | | | | | | | Ovaries | | | | ovulation | + | follicles develop | | | | | | | | (primary and | | | | | | | | secondary) | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | estrogen (E) | | |
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Term
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Definition
Stim. Primary follicle to become secondary follicle | | | | | | | | | | | ╚ inhibited when high PROGESTERONE (P) therefore FSH high when | progesterone low | (Fig. 27.22a) | | | | | | | | | | | | | | | | | | | | ╚ LH - stimulate estrogen production from theca and granulosa cells | (follicle cells) | | | | | | | | ╚ surge in LH in middle of cycle that triggers ovulation, and | | formation of corpus luteum | | | | | ╚ in follicular phase estrogen from secondary follicle rises for a | | few days | | | | | | | ╚ it stimulates LH release via increase GHRH → stimulates | | follicle to increase estrogen secretion → increase LH, etc. (+ve | | feedback) | | | | | | | | → LH surge | | | | | | ╚ in luteal phase both estrogen and progesterone inhibit LH | |
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Term
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Definition
╚ required for ovulation | | | | ╚ stimulates growth of and maintenance of endometrium | ╚ development of secondary sex characteristics | | ie: breast development, fat deposition, etc. | ╚ bone growth, closure (stop growth) of epiphyses. | |
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Term
Progesterone - from corpus luteum |
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Definition
╚ prepares the uterus for pregnancy |
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Term
Phases of Ovarian cycle (28 days) |
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Definition
1) follicular (pre-ovaltory) phase (days 1-14 ) 2) Ovulation (day 14) 3) luteal (post-ovulatory) phase (days 15-28) |
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Term
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Definition
a) menstrual phase (days 1-5) b) proliferative phase (days 6-14) |
c) Ovulation (day 14) d) Secretory phase (days 15-28) |
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Term
1) Ovary: follicular (pre-ovulatory) phase (days 1-14) | | | |
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Definition
| | | | | | | | | | | | ╚ Early Phase: estrogen and progesterone low therefore LH, | | FSH, secreted → some primary follicles become secondary | | follicles due to FSH | | | (Fig. 27.22) | | ╚ secondary follicles secrete estrogen therefore blood | | | estrogen rises | | | | | | | ╚ Later: One (usually) secondary follicle becomes graafian | | follicle | | | | | | |
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Term
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Definition
| | | | | | | | | | | | | | | ╚ due to LH surge | | | | | | ╚ LH triggers | | | | | | | | a) completion of meiosis I to secondary oocyte | | | b) rupture of graafian follicle with release of | | | | secondary oocyte | | | | |
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Term
| | | Luteal(post-ovulatroy) Phase
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Definition
| | | | | | ╚ high progesterone from corpus luteum inhibit GnRH | (therefore LH and FSH) therefore no follicles from | developing | | | | | |
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Term
a) menstrual phase (days 1-5) | (Fig. 27.22d) |
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Definition
| | | | ╚ stratum functionalis is shed (outer layer of | | | endometrium) and denuded areas bleed | | | (denuded means made nude) | | | | | → therefore menstrual flow is blood, cells | | | of endometrium, secretions (50-150 ml) | |
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Term
b) proliferative phase (days 6-14) | (Fig. 27.22d) |
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Definition
| | | | ╚ estrogen → repair, and proliferation of stratum | | functionalis | (by way of mitosis in stratum basalis) | |
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Term
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Definition
it's just in here you so remember ovulation is a stage of the uterine cycle too :) |
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Term
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Definition
| | | | | | ╚ progesterone from corpus luteum | | | | | | | | | | a) prepares endometrium for implantation | | | ╚ becomes more vascular, thick | | | stores glycogen | | | | | | | | | b) Inhibits uterine contractions, keeps | | cervix firm, inflexible | | | |
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Term
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Definition
| | | | | | | | | | | | | a) Placenta secretes human chorionic gonadotropin | | (hCG) | | | | | | | ╚ hCG takes over from LH & maintains the | | | corpus luteum (hCG similar structure to LH) | | | | | | (Fig. 27.22a) | | | | | | | | | b) Corpus Luteum will secrete progesterone and | | estrogen | | | | | | | ╚ for ~6 weeks, then placenta begins | | | secretion of progesterone and estrogen | | | | | | | | | c) FSH, and LH inhibited by high progesterone (no | | new follicles develop) | | (Fig. 28.6) | |
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Term
If No Fertilization occurs: | | | |
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Definition
| | | | | | | | | | | | | a) Corpus Luteum degenerates into a corpus albicans | | (scar) (because there is no hCG, low LH) | | | b) therefore progesterone, and estrogen decrease | | | | | | | | | | i) no longer inhibit LH, FSH; LH, FSH | | | increase | | | | | | | | | | | | | ii) No longer maintain endometrium | | | | | → leads to menstruation hCG= human | chorionic | gonadotropin | | | |
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Term
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Definition
| | | | | | | | | ╚ High estrogen and progesterone these inhibit GnRH secretion | | | therefore you get no FSH, LH | | | | | | | ╚ No follicle maturation | | | | | | | | ╚ No Ovulation, (also thickened mucus, so sperm can't get in and reduce | | | motility of reproductive tract) | | | | | | |
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Term
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Definition
| | | | | | ╚ use progestin (synthetic progesterone) | | ╚ similar mechanism | | | |
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Term
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Definition
| | | | | | ╚ has high E and progestin (75% effective), or progestin | | only (89% effective) | | | | | ╚ main action, prevents implantation, ovulation, or | | fertilization | | | | | | ╚ can be taken within 5 days of unprotected sex, but | | is more effective sooner that it is taken, especially | | within the 1st 72 hours | | | | | | → usually 2 doses, 12 hours apart | | | ╚ if pregnancy continues after its use, there are no | | demonstrated -ve effects on baby | | | |
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Term
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Definition
| | | | | | | | ╚ formed from trophoblast and that gives rise to chorion (fetus) | | and endometrium (maternal) | | | | | ╚ blood vessels of mother and fetus in close proximity | | | (No blood mixing) | | | (Fig. 28.7) | |
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Term
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Definition
| | | | | | | | | | | | | | | 1) Exchange of materials between the mother and the fetus | | | for instance: | | | | | | | ie1: gases, nutrients, antibodies (passive immunity) | | | wastes | | | | | | | | | | | | | | | ie2: drugs, alcohol, morphine, nicotine | | | | | | | | | | | | ie3: viruses; measles, polio | | | | | | | | | | | | 2) Secretes hormones | | | | | | | | | | | | | | | a) estrogen and progesterone | | | | | b) hCG (human chorionic gonadotropin) | | | | | ╚ maintains corpus luteum for ~ 6 | | | | | weeks (peaks ~10 weeks then | | | | | decreases) | | | | | | | ╚ detected by pregnancy tests | | | | | ╚ stimulates secretion of | | | | | | testosterone by fetal testes | | |
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Term
Protein synthesis (fig 3.33) |
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Definition
- Proteins: enzymes, structural, signalling molecules, transporters ect. Ex. Actin, myosin, some hormones - involves both DNA transcription and translation |
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Term
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Definition
- DNA to mRNA (fig 3.34) i) DNA uncoils at sit of gene to expose gene base sequence ii) RNA strand formed, using code on DNA template to add complementary RNA nucleotides Ex. ATC GCA (DNA template) UAG CGU (mRNA sequence) |
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Term
a) Translation – mRNA – protein (fig 3.36) |
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Definition
i) mRNA associates with ribosomes – 3 bases on mRNA = base triplet codon ii) tRNA with attached AA and it`s base set is going to be complementary to the codon, it is therefore called an anticodon, binds to the matching RNA iii) a peptide bond is formed between the AAs, therefore by forming a long chain of AAs |
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Term
Synthesised proteins are: |
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Definition
1) Released into the cytosol or go to the nucleus or mitochondria (from free ribosomes) 2) Released into the lumen rough ER (attached ribosomes) - Modified by addition of sugars (not all of them) –» glycoprotein - Then transferred in vesicles to golgi apparatus - In golgi, modified by CHO(carbohydrates) changes/additions, used in part as an address to send them to proper destination and lipids - Modified proteins packaged in vesicles and sent to destination (cell membrane, secretion, lysosomes) |
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Term
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Definition
- Membrane bound organelles containg disgestive enzymes (in acidic environment) |
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Term
Enzymes (names end in ``ase``) |
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Definition
- Speed up rate of reaction but are not used up themselves - Very specific, they will only act on one or two molecules - Synthesis is controlled by the cell (because they are proteins) - Very sensitive to pH and temperature |
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Term
ATP production (adenine +ribose = adenosine and three phosphates) |
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Definition
- ATP is used in reactions by braking the high energy covalent bonds Ex. Protein synthesis, membrane transport muscle contraction) - Little is stored in the body |
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Term
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Definition
- Pathway for production of ATP using glucose |
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Term
How do we use proteins to make ATP? |
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Definition
Proteins – some AA can be converted to pyruvic acid OR the Kerb`s cycle. Depending on what is needed by the body, may form new glucose (liver, kidney) OR makes ATP ( most cells) |
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Term
How do we use fats to make ATP? |
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Definition
Fats – primary storage form of energy in the body (trigylcerides) . It is the fatty acids that get broken down into cetil Coa --» ATP |
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Term
Functions of the Skeletal System |
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Definition
- Support - Protection of vital organs - Attaches muscles - Allows movement - Contains bone marrow, which produces RBC and WBC - Stores calcium (for muscle and nerve functioning) |
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Term
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Definition
- Bone formation begins in about the 8th week and continues until around 20 years of age and contains the phases Intramembranous ossification and Endochondral ossification |
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Term
1) Intramembranous ossification (fig 6.7) |
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Definition
- Flat bones (ex. Skull bones, mandible and clavicle) - Develop from fibrous connective tissue membrane - Osteoblasts produce spongy bone along the fibers - Periosteum forms - Osteoblasts beneath it grown compact bone |
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Term
2) Endochondral ossification (fig 6.8) |
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Definition
- Most bones develop from a hyaline cartilage model - Cartilage is laid down first in the rough shape of the bone to be - Cartilage ossifies to become spongy bone - Periosteum forms and the osteoblasts beneath it lay down compact bone - Articular cartilage and epithyseal plates = cartilage that has not ossified |
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Term
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Definition
1) growth in length 2) growth in diameter |
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Term
1) Growth in length (endochondrial growth because it starts with a cartilage model) |
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Definition
- At epiphyseal plates - Cartilage grows on epithyseal side and matrix near diaphysis becomes bone - Grow in length stops when the epiphyseal plate ossifies into the epiphyseal line, this process is called closure |
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Term
2) Grow in diameter (appositional growth) |
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Definition
- Due to activity of osteoblasts beneath periosteum of long bones - Osteoclasts beneath medullary endosteum resorb bone so that the size of the cavity keeps pace with the growing bone |
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Term
Factors affecting bone grow and remodelling |
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Definition
1) Mechanical stress
2) Nutrition
3) Hormones |
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Term
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Definition
- Moderate exercise - Increase in osteoblast activity in areas of stress (more building then brake down) - Injury that causes no movement of the limb - Decrease osteoblast activity and no change in osteclast activity ( no building but still breaking) - This obviously causes decrease in bone mass |
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Term
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Definition
- Ca2+, PO4- - required for the production of matrix - Vitamin C – required for the production of collagen - Vitamin D – increases absorption of calcium from the small intestine - Lack of vitamin D causes rickets in children (soft bones) |
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Term
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Definition
- Growth hormone, thyroid, estrogen and testosterone --» stim. Bone growth - E and T osteoblast acticity but also cause ossification (e) of epiphyseal plate --» line (closure) - Calcitonin – inhibits osteoclast activity - Increase in calcium movement from blood to bone - PTH – increase bone resorption (destruction of matrix) by increase osteoclast activity and decrease osteoblast activity, their fore it lowers blood calcium |
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Term
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Definition
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Term
Risk Factors of Osteoporosis: |
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Definition
- Increasing age in man and women (decrease in sexual hormones) - Inadequate diet (low in vit D, calcium) - Illness, excess PTH - Lack of exercise - Too much exercise (too little body fat) - Menopause in women , it is a drastic drop in estrogen, a decrease in osteoblast and increase osteoclast activity - Drugs ex. Cortisone |
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Term
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Definition
1) Fracture repair begins with formation of a blood clot. (from blood vessels of periosteum and bone) 2) Clot replaced by callus consists o fibrous network and fibrocartilage islets 3) Callus ossifies --- intamembranous and endochondral ossification 4) Takes 4-6 weeks (longer for long bones) – cast required since movement can refracture new matrix |
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Term
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Definition
1. Ach is broken down by Acetylecholinesterase (AchE) on the sarcolemma (motor end plate) and it is facing the cleft Ach --> acetic acid + choline --> recycled 2. SR actively takes up the Ca2+ (Ca 2+ - ATPase) 3. ATP will bind to the myosin head and that triggers it’s release from actin 4. Tropomyosin moves back to cover the myosin binding sites on actin |
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Term
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Definition
a) Activation of myosin and the power stroke b) Cross bridge release c) Pumping calcium back into the SR to end the signal d) Maintaining the Na+ and K+ ATPase in the muscle cell (helps maintain Na+ and K+ gradient) |
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Term
Rigor mortis (the stiffness of death) |
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Definition
- Myosin heads are activated before death, which means they can bind to actin as soon as the Ca2+ levels rise - no new ATP is being produced (no O2) therefore a) Intracellular Ca2+ increases from ECF and SR b) Myosin heads can’t be released from actin à muscles remain contracted - Starts around 3 hours after death, max at 12 hours - Gradually subsides over days as the cells brake down |
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Term
If extracellular Ca2+ low (like during pregnancy): |
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Definition
you get Na+ entering --> cramps because of contractions |
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Term
If intracellular Ca2+ is too low: |
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Definition
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Term
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Definition
– decrease in Ach receptors because the autoimmune system thinks they are a virus - Flaccid paralysis - Use AchE immigitors (increase binding to remaining receptors) |
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Term
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Definition
- Prevents Ach from binding to the receptors - causes flaccid paralysis - used in surgery |
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Term
Botulism (improper canning, clostridium botulinum) |
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Definition
- prevents ckocytosis of Ach - flaccid paralysis - used to control uncontrolled binking - to correct crossed eyes - botox (cosmetic) |
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Term
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Definition
- binds to the receptors and mimics the action of Ach - muscle contractions which can lead to muscle spasms |
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Term
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Definition
- massive release of Ach - muscle contractions - stopping breathing |
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Term
long term effects of the black widow spider and nicotine: |
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Definition
depress firing due to receptor desensitization |
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Term
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Definition
= the amount of force exerted by a muscle or muscle fibre |
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Term
Factors Affecting muscle tension in a muscle fibre (tension --> determined by number of cross bridges attached) |
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Definition
a) effect of frequency of stimulation on muscle fibre b) Effect of fibre length on tension development (fig 9.22) c) Size of the fibre tension |
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Term
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Definition
- not normally seen in a skel. Muscle - produces a switch (weak contraction and then relaxation) |
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Term
2) 2nd stimulus arrives before muscle completely relaxes |
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Definition
- Reduces 2nd contraction with an increase in tension (no refractory period in contraction) - Mainly due to increase availability of calcium - Increase in tension is called wave summation |
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Term
3) Rapid sequence of stimuli |
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Definition
- Allows partial relaxation between contractions - Tension increases (summation, increase in calium avaiblity) - = incomplete tetans |
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Term
4) Hig frequency of stim. |
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Definition
- No relaxation between contractions (sustained contraction) - Highest tension (3-4 x twitch) - Occurs normally in body = complete tetanus |
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Term
5) Frequency that allows complete relaxation between contractions |
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Definition
- Called trepae = staircase effect - Progressively higher tension (and then uniform tension) - Increase in temp à increase activity of enzymes - Warm up muscles (?) doesn’t actually happen in real life |
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Term
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Definition
– about 2 MSR – period between application of stimulus and contraction - processes associated with excitation and compiling - AP down T-Tubules, Ca2+ release and binding to torponin |
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Term
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Definition
- Mechanical - Cross bridge attachment and sliding filaments - Tension increases |
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Term
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Definition
- Ca2+ pumped back into SR (Ca2+ ATPase) - ATP attaches to myosin heads à release - Decrease in tension |
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Term
Fibre types in a muscle differ |
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Definition
i) Fast fibres – contract, relax rapidly – appear white (little myoglobin) ii) Slow fibre – contract, relax slowly – appear red (more myoglobin) Eg. Postural muscle |
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Term
Effect of fibre length on tension development (fig 9.22) |
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Definition
i) resting fibre length optium ii) Fibre is shorter than resting when stimulated i) Fibre stretched when stimulated
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Term
i) resting fibre length optium |
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Definition
- max of crossbridges can be attached on stimulation therefore max tension |
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Term
ii) Fibre is shorter than resting when stimulated |
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Definition
--> thin overlaps and interferes with cross bridge attachment. Therefore few cross bridges would attached and you would have decreased tension. - Minimum of length is 70% of optimal |
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Term
iii) Fibre stretched when stimulated |
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Definition
- Not all myosin heads are near actin binding sites, therefore fewer cross bridges attachà decreased tension - Max length is 130% optimal |
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Term
c) Size of the fibre tension |
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Definition
- the thickness means that you have more myofibrils/fibre - larger = more tension (ex. Exercise) |
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Term
Factors affecting tension in a whole muscle |
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Definition
a) Number of fibres contraction i.e. number of active motor units - More units = increase in whole muscle b) Number of fibres/moto units - One neuron à 10 fibres à delicate contractions - One neuron à 5000 fibres à strong contraction · Large muscle will have potential for more of A=B, therefore can contract more strongly than a small muscle c) Fatigue |
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Term
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Definition
- At any given time, a few fibres develop low tension - Different motor units are stimulated over time, but the tone remains relatively constant - Gives firmness to muscle |
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Term
Types of Skeletal Whole Muscle Contractions (fig 9.19 p.301) |
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Definition
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Term
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Definition
- Muscle changes length - Tension is relatively constant during the contraction - Tension exceeds the resistance of the load lifted - Used for body movement and moving objects - Ex. Flexion of the elbow |
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Term
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Definition
- Muscle length condensing - Tension increases – cross bridges attach but no shortening - Tension less than that required to move load - Used standing, holding book in place - Ex. You lift a book to read using your biceps brachii, you will have isotonic contraction to lift it and isometric to hold it in place. |
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Term
Muscle Metabolism During resting conditions |
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Definition
- Fatty acids used to produce ATP (aerobic) - Storage of glycogen - Creatine phosphate (a way to store ATP, without actually storing ATP) - Little ATP ATP+ Creatine à ADP + creative phosphate (C~P) |
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Term
muscle metabolism During short term exercise (less than one minute) |
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Definition
- Primarily anaerobic a) Creatine phosphate used to form ATP C~P + ADP à ATP + creatine C~P lasts for about 15 secs b) Muscle glycogen à glucose à pyruvic acid à anaerobic pathway à lactic acid (lasts about 30 secs) |
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Term
muscle metabolism during Long term exercise (1 minute to hours) |
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Definition
- Glucose ( from the liver) - Fatty acids – used more as exercise continues - ATP – from aerobic pathway O2 from – haemoglobin – myoglobin |
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Term
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Definition
- Not completly understood - Inability to maintain tension - Fatigue is a decrease in ATP use, therefore it is protective (ATP only to 70% of resting – If too little, cross bridges can’t release |
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Term
Muslce fatigue is due to: |
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Definition
a) Depletion of energy supplies ex. Glycogen b) Build- up of end products ex. H+ from lactic acid ( muscle contraction compresses) blood vessels - O2 to muscles decreases, therefore you might have to go anaerobic for short periods - Phosphate (from ATP à ADP + P) c) Failure of APS è Concentration of especially rapid stimuli (?) è In small space of T-Tubules è Long term: neuron runs out of Ach |
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Term
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Definition
- Failure of CNS to send commands to muscles |
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Term
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Definition
recovery O2 consumption a) To replenish stores of glycogen, C~P, O2 in haemoglobin/myoglobin b) Convert lactic acid – to pyrivic aicd -to glucose in liver Also increase in body temp from exercise = increase O2 demand, deep rapid breathing until body returns to resting state |
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Term
this is it for the mid term! |
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Definition
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