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Physiology 1yr

exam 1

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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