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Physiology 1yr
exam 1
| Question | Answer |
|---|---|
| total body water is what % of BW | 60% |
| Intracellular fluid makes up what % of BW | 40% |
| Extracellular fluid; interstitial fluid makes up what % of BW | 16% |
| Extacellular fluid; plasma makes up what % of BW | 4% |
| blood volume percent | 6-8%. 60-80ml/kg BW |
| equivalent | amount of charged solute |
| osmole | number of particles into which a solute dissociates in solution |
| osmolarity | osmoles/L |
| ph expresses H ion concentration | -log10[H+] |
| Major ions in ECF: Cations | Na+ |
| Major ions in ECF: Anions | Cl- and HCO3- |
| Major ions in ICF: Cations | K+ |
| Major ions in ICF: Anions | proteins and organic phosphates |
| why are ion concentration differences important | 1. allows nerve and muscle cells to have resting membrane potentials (K difference) 2.Upstroke action potentials in nerve and muscle cells, and absorption of nutrients (Na difference) 3.Excitation-concentration coupling in muscle cells (Ca2+ difference) |
| Lipid soluble molecules | Co2, steroid hormones, O2 |
| H2O soluble molecules | glucose, protein hormones, ions |
| Simple or facilitated diffusion | down an electrical gradient, no input of energy |
| Against an electrical gradient | primary and secondary transport |
| primary transport | direct input of energy |
| secondary transport | indirect input of energy |
| Carrier mediated transport depends on | 1. Saturation 2.Sterospecificity 3.competition |
| Simple diffusion (non electrolyte) depends on | 1.concentration gradient (driving force) 2.Partition coefficient 3. Diffusion coefficient 4.Thickness of membrane 5. surface area |
| Best conditions for non-electrolytes simple diffusion | small, lipid soluble, thin mem, in non viscous solution travel very quickly |
| non-electrolytes simple diffusion: concentration | large the diff in solute [] increase in driving force |
| non-electrolytes simple diffusion: partition coefficient | based on lipid solubility of solute. more soluble in oil/ lipid. higher coefficient more easily cross over |
| non-electrolytes simple diffusion: diffusion coefficient | based on size of solute and viscosity of solution. smaller solutes in a non-viscous solution have higher diffusion coefficients and easily diffuse |
| non-electrolytes simple diffusion: Surface are | greater surface area= higher diffusion rate |
| Consequences of simple diffusion of electrolytes | 1. potential difference across a mem will change diffusion rate of charged solute 2. creation of diffusion potential when a charged solution diffuses down a concentration gradient (k+) |
| Facilitated diffusion | uses a carrier protein, proceeds faster at low solute [] b/c limited carriers. |
| Examples of primary active transport | Na/K ATPase pump, Ca2+ pump, H+/K+ pump |
| Na/k pump | 3 Na pumped into ECF. 2 K pumped into ICF. Creates a charge separation and potential difference for depolarization and AP. |
| What inhibits Na/K pump | Cardiac glycosides |
| Ca2+ pump | PMCA and SERCA |
| H+/K+ pump | parietal cells of gastric mucosa. pump H+ ions into lumen of stomach |
| Secondary active transport | uses energy by utilizing the Na+ gradient to transport solutes against their [] gradient. Na was directly created using Na/K pump. |
| Example of co- transport systems | 1. Na/glucose co transporter (SGLT) 2. Na/ AA transporter 3.Na/k/2cl |
| example of counter transport | 1. Ca2/ Na exchange 2. Na/H exchange |
| why does osmosis occur | pressure difference. concentration differences of solutes cause difference in osmotic pressure |
| Isosmotic level of cell | 290-300 |
| Osmotic pressure | difference in [solute]. tendency of solution to take in water |
| oncotic pressure | form of osmotic pressure specifically exerted by proteins (albumin) |
| what does oncotic pressure tend to do | pull water into blood vessels because large proteins cant move out of blood vessels |
| oncotic pressure opposes | intersitial colloidal osmotic pressure |
| decrease in oncotic pressure causes what | edema, no longer sufficient to pull water back into capillaries, h2o stays in muscle |
| ion channel gates are controlled by what 3 types of sensors? | 1. voltage gated 2. second messenger 3. ligand gated |
| diffusion potentials help to establish what | resting membrane potentials |
| equlilibrium potential | diffusion potential that opposes the tendency for further diffusion of an ion |
| Nerst equation | used to calculate a concentration difference for an ion into a voltage |
| how is Nerst equation expressed | as intracellular potential relative to extraceullar potential |
| ENa+ | +65 mV |
| ECa2+ | +120 mV |
| EK+ | -85 mV |
| When do ions move across cell membranes | 1. there is a driving force 2. membrane has conductance to ion |
| Greater current flow occurs when | greater the driving force or conductance |
| Resting membrane potential is determined by what ion | K |
| RMP range | -70 to -80 mV |
| How does the Na/K pump help maintain RMP | helps maintain [K] across the mem. Allows K diffusion potential to occur |
| Depolarization | mem potential less negative. Na+ |
| Hyperpolarization | mem potential more neg. |
| Inward current | flow of positive charge into cell. depolarization. Na |
| outward current | flow of positive charge out of cell. K. brief state of hyperpolarization |
| Threshold potential | mem potential at which an AP is inevitable |
| overshoot | portion of AP where mem potential is pos |
| undershoot | portion of AP where mem potential is more neg than RMP. hyperpolarization |
| refractory period | period during which another AP can't be generated |
| Absolute refractory period | overlaps with most of the AP. No stimulus can occur to cause AP |
| Relative refractory period | from end to ARP until through most of hyperpolarization. AP occurs with greater than normal depolarization |
| Time constant | how quickly a mem depolarizes in response to inward Na current. |
| Length constant | how far depolarization current will spread along a nerve. |
| Electrical synapse | current flows between cells via gap junctions. Very fast. ability to stim many cells at once. Important for heart beat. |
| Chemical synapse | gap between presynaptic and post synaptic cells (synaptic cleft). |
| Steps of of action in chemical synapse | 1. AP in presynaptic cell causes Ca2+ channels to open 2. Ca2+ influx 3. Release of NT from presynaptic terminal 4. NT binds receptor of postsynaptic cell |
| Motor neuron | Nerves that innervate muscle fibers |
| Motor unit | single motorneuron and muscle fiber it innervates |
| Events at neuromuscular junction | 1. AP propigated to presynatic terminal 2. Voltage gated Ca2+ channels open 3. Ca permeability increases 4.Ca flows in, causes release of Ach stored in synaptic vessels 5. Ach diffuses to post synaptic mem. 6. Ach binds to nicotinic receptors |
| What happens at neuromuscular junction once Ach binds nicotinic receptors | 1. Channels open 2. Na moves in 3.K moves out 4.End plate potential reached 5.depolar spreads to muscle fiber cell (muscle contraction) 6. EEP stops when Ach degraded by AchE |
| What is the end plate potential | motor end plate depolarizes from -90mv to -50mv |
| A miniature end plate potential is caused by what | A single vesicle of Ach |
| What does acetlycholinesterase do | AchE, degrades Ach which stop EPP |
| Botulinus toxin | blocks release of Ach from presynaptic terminals. No muscle contraction. Paralysis and respiratory failure. |
| AChE inhibitors | prevent degradation of ACh in synaptic cleft. Used to treat Myasthenia gravis: skeletal muscle weakness and fatigue. Ach R blocked by AB therefore need to inhibit AchE. |
| one to one synapses | Neuromuscular junction. Single AP in motorneuron causes single AP in muscle fiber. |
| One to many synapses | found in some motorneurons of spinal cord.Single AP in motorneurons cause many AP in postsynaptic cells |
| Many to one synapses | Very common. Many presynapic cells converge on a postsynaptic cell. Allows input from many neurons to control one area. |
| Excitatory postsynaptic potentials | EPSPs. Depolar cell, open NA and K channels. |
| What molecules cause EPSPs | Ach, NE, Epi, Dopamine, glutamate, serotonin |
| Inhibitory postsynapic potentials | IPSPs. Hyperpolar, opens Cl channels. |
| What molecules cause IPSPs | GABA and glycine |
| Spatial summation | two or more inputs arrive at postsynaptic cell simutaneously |
| Temporal summation | two inputs arrive at post synaptic cell in rapid succession. Additive effect occurs |
| Synaptic fatigue | repeated stim yields a smaller than expected response. |
| What happens if 2 or more excitatory inputs arrive at the same time? | Depolar greater than notmal |
| What happens if 1 excitatory and 1 inhibitory input arrives at the same time? | cancel each other out. nothing happens. |
| What happens if 2 or more inhibitory input arrives at the same time? | inhibit cell. |
| Criteria for Neurotransmitter (NT) | 1. Syn in presynaptic cell 2.released by presynaptic cleft upon stim 3.exogenous app of substance to postsynaptic cleft mimics in vivo response |
| Ach | only NT utilized at the neuromusclar junction. released from ALL preganglionic and most postganglionic neurons in PNS. Released from ALL postganglionic neurons in SNS |
| When enzyme forms ACh | acetlytransferase |
| What enzyme degrades ACh | AChE |
| What is the common precursor of NE, epi and dopamine | Tyrosine |
| What happens when PNMT is present | NE is converted to Epi in the adrenal medulla |
| What enzymes degrade NE, Epi, and Dopamine | MAO and COMT |
| Serotonin | Found in brain and GI. Precursor to melatonin. Syn from Tryptophan |
| Histamine | Syn from histidine |
| Glutamate | Major excitatory NT in CNS (spinal cord and cerebellum). utilizes ionotropic and metabotropic receptors. |
| Ionotropic | form ion channel pore. Direct |
| metabotropic | coupled w/ G protein (2nd messenger). Indirect |
| Glycine | inhibitory NT in spinal cord and brain stem |
| y-aminobutyric acid (GABA) | Inhibitory NT syn from glutamic acid. Utilizes GABAA and GABAB receptors |
| GABAA receptors are linked to what | Cl channels |
| GABAB receptors are linked to what | K channels |
| Neuropeptides | syn in nerve cell body |
| Neuromodulators | Act on presynapic cell to alter amt of NT released. co secreted with NT to alter response of postsynaptic cell |
| Neurohormones | released from neurons into blood |
| Examples of neuropeptides | Substance P and vasoactive intestinal peptide (VIP) |
| NO | inhibitory NT with GI tract and CNS. Diffuses from presynaptic terminal to target cell. |
| Purines | ATP and adenosine are NT in ANS and CNS. |
| What is the result of ATP co secreted with NE | Contraction of smooth muscle |
| excitation contraction coupling | events b/w AP in muscle fiber and contraction |
| Light band | I band. Thin filament. actin. Z disk |
| dark band | A band. thick filament. myosin, |
| Bare Zone | H zone. center of sarcomere. no thin filaments |
| M line | Dark staining protein. Links thick filaments. No contraction happens here |
| Tropomyosin | blocks myosin binding sites |
| Troponin T | attaches entire troponin complex to tropomyosin |
| Troponin C | Ca binding protein. W/O Ca don't get contraction b/c didn't move tropomyosin out of the way |
| Troponin I | inhibit interaction of action and myosin |
| Cytoskeletal proteins | Help align thick and thin filaments |
| Dystrophin | Achors myofibril scaffold to the cell membrane |
| Titin | centers think filaments in the sarcomere |
| Nebulin | sets length of thin filaments |
| Transverse tubules | invaginations in the sarcolemma. next to sarcoplasmic reticulum (SR). extends down into muscle cell. |
| Myofibrils that surround SR. | stores Ca using SERCA pump. Ca bound to calsequestrin in SR. Ca release channel |
| What does the SERCA pump do in a myofibril | move Ca from ICF into SR. |
| At rest why is Ca low in ICF | b/c its in the SR. |
| When is Ca released from the SR | Depolar @ T tubule next to SR |
| What do the T tubules allow for | depolar to travel from motor end plate to interior of cell quickly. |
| Steps of excitation contraction coupling | 1. AP travels down T tubule 2. Conformational change in dihydropyridine receptor 3. Cytosolic [Ca] increase 4.Ca bind Troponin C 5. Conformational change in troponin. 6. Tropomyosin moves away from myosin binding site on actin 7. muscle contraction |
| What does the conformational change in the dihydropyridine receptor cause | a conformational change in the ryanodine receptor causing Ca channels to open and Ca release from SR |
| Ryanodine receptor | Ca release channel |
| Cross bridge cycling | 1. Myosin head attached to actin in 'rigor' position 2.ATP binds myosin head, decreases affinity of myosin to actin 3.myosin release 4.ATP hydrolyzes, myosin moves toward plus end of actin 5.myosin binds new site on actin (power stroke) |
| When does a contraction stop | when AP passes, ryanodine receptors close and Ca reaccumulates in SR via SRCA pump |
| Slow twitch muscle fibers | slow twitch myosin isoform. small diameter, higher oxidative capacity, lower glycolytic capacity. very fatigue resistant. recruited first. red color |
| Fast twitch muscle fibers | fast twitch myosin isoform. Large diameter, high glycolytic capacity, lower oxidative capacity. Easily fatigue. Recruited last. Anaerobic. white color |
| Spatial summation | can increase force of contraction by recruiting more muscle fibers. increase muscle fibers by recruiting more motor neurons. Slow twitch: recruited first, more easily excited. Fast twitch: recruited when more force is needed |
| Temporal summation | can increase force of contraction by repeated stimulation of muscle before it can relax. |
| How does temporal summation result in tetanus | Prolonged elevation of intracellular Ca. Not taking up all the Ca after stimulus. Ca elevated b/c released from SR faster than it can be taken up via SRCA pump |
| Muscle Spindles | run parallel to muscle fibers. responsible for stretch reflex. stretching the muscle causes a reflex of the motor neuron innervating the muscle. Resists further stretch |
| Golgi Tendon organ | low sensitivity. Activated when force on muscle is extreme. In the tendon of the muscle. when activated inhibits stretched muscle. stim opposing muscle. |
| ATP pool replenished with | 1. creatine phosphate pool 2. muscle glycogen stores 3. glucose from blood 4. FA from blood/ stored fat |
| Mechanical junctions in cardiac muscle | fascia adherens and desmosomes |
| Electrical connections in cardiac muscle | gap junctions |
| extracellular Ca mechanism in cardiac cells | 1. enters cell via L-type Ca channels during long plateau. Forms "trigger Ca" |
| L type Ca channels are what receptors | Dihydropyridine receptors |
| What is the role of Trigger Ca | to induce the release of Ca from SR |
| AP relaxation in cardiac cells | 1. reaccum of Ca by SERCA 2. Sarcolemmal 3 Na/1 Ca2+ antiporter 3. Sarcolemmal Ca2+ pump (Ca ATPase) |
| How do you increase the AP force of cardiac cells | Sympathetic nervous system. more Ca uptake b/c phos of more L-type Ca channels |
| How do you decrease the AP force of cardiac cells | Parasympathetic nervous system. decreased Ca flow and amount b/c of Ach. |
| What does smooth muscle have instead of sarcomeres | dense bodies |
| what does smooth muscle have instead of t tubules | caveolae |
| What does smooth muscle lack | troponin and tropomyosin |
| 3 ways to stim smooth muscle contraction | 1. depolar, AP, open voltage gated Ca channels. 2. Hormones/NT, open ligand gated Ca channels 3. Hormones/NT, release Ca from SR via IP3 |
| Smooth muscle contraction steps | 1. release Ca. 2. Ca binds calmodulin 3. Calmodulin binds 4 Ca ions 4. Ca-calmodulin complex activates myosin-light-chain kinase 5. MLCK phos light chain and changes conformation 6. myosin bind actin |
| Smooth muscle relaxation | 1. Hyperpolar 2. inhibit Ca channels 3. inhibit IP3 4. Ca reaccum in SR |
| How does cAMP regulate smooth muscle tone | relaxes smooth muscle by inhibiting MLCK. treat asthma |
| How does cGAMP dependent activation of a myosin phosphatase regulate smooth muscle | NO dependent increase of cGMP relax vascular smooth muscle and increase blood flow |
| How does latch state occur | via dephos of myosin while still attached to actin |
Created by:
ejohnson17
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