PHYSIO EXAM 2 STUDY GUIDE
PHYSIO EXAM 2 STUDY GUIDE PGY 451LEC
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This 15 page Study Guide was uploaded by Ndidiamaka Okorozo on Friday October 16, 2015. The Study Guide belongs to PGY 451LEC at University at Buffalo taught by Baizer, J S in Fall 2015. Since its upload, it has received 34 views. For similar materials see Human Physiology I in Physiology at University at Buffalo.
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Date Created: 10/16/15
PHYSIO EXAM 2 STUDY GUIDE MEMBRANE POTENTIAL lei Nernst equation Aux RTln Xio ZxFVm where the first group accounts for chemical component AC concentration and the second for electrical component AE l charge Inside Outside AC AE concentratio concentratio n n Glucose 2mM 5mM In None no charge Sodium 12mM 145mM In In Potassium 120mM 4mM Out In Chloride 30mM 105mM In Out cell is at 60mV When there is no net movement the Nernst equation is equal to O the chemical and electrical components equal 615 Xlo At 379C Ex Z log For Na 666mV K 908mV CI 335mV Hyperkalemia high concentration of K in the cell because of kidney malfunction Increases likelihood of heart ring action potential AP Leads to cardiac arrhythmias and cardiac arrest Hypokalemia frequent urination by individuals on diuretics causes loss of K ions decreases likelihood of ring AP causes cardiac arrhythmias and cardiac arrest Resting Membrane Potential the Vm membrane potential where the net current is 0 measured from the inside relative to the outside gt 70mV for a neuron and 90mV for a skeletal muscle cell gt Depends on 0 Ion concentration across membrane 0 Relative conductance of the membrane of different ions Primarily determined by K because it is the most permeable to it gt Ii Vm Ei x gi where Ii is the current El and gi are Nernst potential and conductance for that ion respectively GNa GK GCl I gt Vm ENa 2G Ek ECI E where 26 IS sum of all conductance which 100pS in a normal neuron So GNa 15 10100 015 gt Thus Vm 015 x 666mV 08 x 908mV 005 x 335mV 64325mV Most cells have the highest conductance to K because its Vm is the closest at the RMP so it has 80 of the 26 while Na is 15 and CI is 5 Vm for Na is very high l 65mV and for K is too low l 90mV so Vm is always in between these two values Only a tiny percentage of K needs to diffuse out of the cell to maintain RMP ATPdependent Na K Pump pumps out 3K while pumping in 2 Na ACTION POTENTIAL ATPdependent pump in an axon pumps out 3 Na ions while pumping in 2 K ions to maintain ion concentration across the membrane This pumps contributes about 5mV to the RMP Types of ion channel 1 Voltagegated ion channels open or close in response to membrane potential 2 Ligandgated ion channels open or close when a neurotransmitter ligand binds to the ion channel Nachannels voltage gated 1 pseudo tetramer a subunit has 6 intra membrane cylinders repeated four times and ions bind on a surface Intracellular loop between III and IV block Na from entering after depolarization Kchannels voltage gated tetramer has four subunits with 6 transmembrane regions and allows only potassium passage B subunit only helps with selectivity and regulation Graded potential increase in stimulus strength which produces in amplitude of the depolarization Local or Subthreshold depolarization conducted decrement and doesn t generate action potential AP The depolarizing stimulus doesn t reach the threshold and so is unable to re an AP They are graded and non regenerative and decay over time and distance AllOr None Response either produces a full sized AP or nothing at all In this case amplitude doesn t correlate with stimulus strength because threshold was reached Suprathreshold Response lFiring an AP A stimulus causes the Vm to rise to threshold and as it is reached sodium channels open allowing a massive in ux of sodium into the cell This causes a rapid up stroke of the AP which is referred to as depolarization because its moving the Vm closer to zero However the in ux of Na is too rapid that the AP reaches up to 50mV The area above OmV is called overshoot Meanwhile the potassium channels are increasingly opening because the Vm is being moved far away from their membrane potential 90mV At 50mV the peak of the AP sodium channels close and K channels start pushing out K which repolarizes the cell as it takes it back to the negative membrane potential The force of pushing K is too fast because of both electrical and chemical forces that the AP falls below the RMP 70mV which is called afterhyperpolarization before the K channels close and the membrane potential returns to rest Total period of ring AP lasts for about 34 msec o Rising phase of AP opening of the voltage dependent NA channels and depolarizing action of Na current 0 Falling phase of AP reduction in gNa and increase in gK Positive feedback loop in Na when threshold is reached gNa Na conductance increases as massive entry in to the cell occurs l Na activation So as Vm increases more Na channels open and more Na ions enter and the Vm increases even more till at 50mV when the sodium channels close Closing of Na channels starts repolarization while gK helps complete it Right at the peak of AP 0 Na AE is going out and AC is going in opposite K same both AE and AC are going out so K has a great driving force 5i I nsPeak overshoot value 3 1 Il Hypo polariT39 an zatlon Repularlzatlon Afterhyperpnlarizatinn will sm w w w w w w w w w w w w w m m m an Membrane PotentialI m ll39 Time rusez Absolute Refractory Period Na channels are inactivated and cannot be reopened till the membrane is repolarized This consists of the rapid rising and falling phases Parallel with Na activation and inactivation About 1msec in an axon Relative Refractory period cell is able to re a second AP in the later part of the rst AP but a stronger than normal stimulus is required Consists of the latest part of repolarization and afterhyperpolarization Parallel with changes in gK About 34msec in an axon Refractor period limits the frequency of AP if RF period 4msec the max freq 250Hz because max freq 1000 spikes per second AN ESTH ETICS Cocaine rst anesthetic discovered block Na channels from outside of the membrane to prevent Na from coming in when threshold is reached Poisons 1 Tetradotoxin 39ITX Block Na channels from outside prevent generation of AP 2 Saxitonin STX blocks Na channels from outside prevent generation of AP 0 They don t work on the heart because it has an amino acid that prevents the blockage Propagation of AP AP is generated at the axon hillock where there is an abundance of Na which lowers the threshold and makes it easier to propagate an AP Conduction of AP back propagation doesn t occur because the threshold there is high and the Na channels are inactivated afterjust receiving an AP refractory period so propagation moves forward to the activated Na channels waiting for propagation Unidirectional Length Constant 37 1e how long AP can go without disappearing A LC correlates with radius of axon larger lionger LC amp slower the decay and membrane resistance Rm aRm I I 2R1 RI intracellular reSIstance Unmyelinated axons support conduction but AP has to be generated all the time to propagate so it uses a lot of energy and conduction velocity is slow CV Therefore the freq of AP depends on how big the LC is o Axon diameter l LC l Conduction Velocity of AP Myelinated axons Schwann cells in Peripehral Nervous System and Oligodendrocytes in Central Nervous System Increase membrane resistance greatly Increase insulation of axons l prevents leaking I increases Rm amp LC 0 Don t have refractory periods and hyperpolarizing after potential because there are no K channels at the nodes so less energy is used Nodes of Ranvier no K channel concentrated amount of Na channel AP is generated without fail l higher CV A much smaller myelinated axon is better than a big unmyelinated axon Saltatory Conduction AP appears to jump from node to node Permits re ex lnternode insulated areas aren t involved in propagation and generation of AP Occurs only in myelinated axons Myelination l lowers energy expenditure l generate AP fewer times generate higher CV Multiple Sclerosis demyelinating disorder patches of demyelinated axons in the CNS Loss of motor control because axons fail to re AP because of demyelination which cause loss of current NEUROMUSCULAR JUNCTION NMJ Junction between a the axon terminal of an alpha motor neuron and a skeletal muscle cell ber One NMJ per muscle ber and it s located near the middle of the muscle bercell One a motor neuron I one axon l different axon collaterals innervating different muscle bers RMP of a muscle ber 90mV End Plate Potential EPP potential of the muscle ber which increases in response to the presence of Ach Ach are synthesized and packaged in the synaptic vesicles which are aligned with the acetylcholine receptor AchR to generate the greatest response Depolarization is produced by increase of gNa and gK in the AchR on the end plate EP 0 Outside of the EP region it is propagated by local current ow which decreases with distance Ach Synthesis Neurotransmitter NT vesicles are made in the cell body and transported to the terminal Ach are synthesized and packages in these vesicles Cholineacetyltransferase ChAt catalyzes the production of Ach from choline and acetyICoA A proton pump pumps protons into the vesicle creating an acidic environment Another pump pumps out the proton whie pumping in Ach into the vesicle Process AP arrives at the presynaptic terminal and depolarizes it thus induces the in ow of Ca2 into the nerve cell from the voltagegated channels Presence of calcium causes the fusion of the vesicle with the membrane and releases the contents of the vesicle Ach Ach now in the synaptic cleft bind to receptors on the postsynaptic cells which open up and lead to changes in the Vm of the cell by allowing the in ow of Na K and Ca2 This produces EPP and it ALWAYS res an AP Ach is retaken up from the synaptic cleft by acetylcholine esterase AchE and recycled Ach Receptor nonselective cationic ligand gated channel has 6 subunits and the two a ones allow for Ach to bind Opens when two Ach are bound to it allow for only cations to enter In ux of positive ions brings the Vm closer to OmV which depolarizes the motor end plate Ina normal muscle cell Na AC and AE are pushing Na in o K AC is pushing out and AE is pushing out Curare prevents Ach from binding to Ach receptors so no AP is produced gt But EPP always produces an AP suprathreshold 40mV is suprathreshold in a healthy person Graded potential the amplitude of the AP is dependent on the amount Ach released and amount of AchR it activated not allornone principle Myasthenia Gravis severe muscle sickness An autoimmune disease where antibodies bind to and destroy AchR It decreases the amplitude of EPP to below threshold thereby preventing the generation of AP Causes sickness andfaUgue Treatment introducing physostigmine to the synaptic cleft inhibits acetylcholine esterase and prolongs the presence of Ach in the cleft Also drugs that suppresses the immunes system to stop the production of the antibodies and lastly surgical removal of the thymus gland Some agents at the NMJ Skeletal Na channel blockers tetradotoxin saxitoxin and u conotoxin K channel blocker dendrotoxin Ach release blockers tetanus and botulinum toxins AchE blockers physostigmine and DFP AchR blockers dtubocurarine succinylcholine and alphabungarotoxin binds to same a subunit as Ach 6 Ca2 channel blocker in axon terminal l w conotoxin SYNAPTIC TRANSMISSION U39lbUUNH Types of Synapses 1 Electrical Synapse has gap junctions low resistance pathway and allows exchange of small molecules in addition to ions permeable to up to 1kDA Occurs between glial cell and neurons Fast and bidirectional can be regulated 2 Chemical Synapse involves neurotransmitter and does majority of interactions between cells Fast and unidirectional Focused more on for this class Chemical Synapses 1 Anatomical categorization axosomatic inhibitory axodendritic excitatory axoaxonal regulates release dendrodendritic and dendrosomatic not common 2 Functional categorization a Excitatory postsynaptic density PSD b Inhibitory symmetric no PSD c Modulatory GPCR Neuron doctrine neuron are the information processing units of the nervous system Neurotransmitters according to impact on AP ring 1 Excitatory a Glutamate ligandgated channels i NMDA receptors ii AMPA receptors iii Kainate receptors b Acetylcholine nicotinic receptors 2 Inhibitory ligandgated channels a GABA GABAA receptors also GABAC b Glycine receptors 3 Modulatory or metabotropic GPCRs a monoamines dopamine serotonin etc b acetylcholine muscarinic c glutamate metabotropic glutamate receptors d GABA GABAB Fast NTs act on ligand gated channels and mediate synaptic transmission Slow NTs modulate ligand gated or voltage gated channels Modulate synaptic transmission EPSP receptor channels opened by glutamate Na in and K out At resting potential EPSP is caused by Na in ux There is an increase in gNa and gK but because the Vm is further from ENa there is a greater inward movement of Na than the outward movement of K Amplitude is dependent on holding potential Increases probability of ring AP by bringing the Vm closer to threshold IPSP receptor channels opened by GABA allows CI in Increase in gCl allows it to go in and hyperpolarizes the cell Also gK can also hyperpolarize cell in certain cases where there is increase in gK and K ions leave the cell Decreases probability of ring AP by moving the VM farther from the threshold ONLY ionotropic ligandgated ion channels result in EPSPs and lPSPs gt They are graded potentials and are conducted with decrement Summations a Temporal summation if synapses occur within a short amount of time they are summed up and could produce AP b Spatial summation synaptic potentials generated in soma and dendrites interact Different neurons can produce EPSPs and lPSPs at the same time so their some is taken Amplitude of an AP does NOT provide information about the strength of the stimulus because of allornone response only the STRENGTH provides this information Refractory period limits the max frequency of AP because if total refractory 1000 msec period is 4msec you can only generated 250APsec 4msec But more large myelinated axons can do up to 100APsec Clearance of NTs from Synaptic Cleft After NTs has been released by presynaptic neuron into the cleft it has to be terminated to create the AP This is done by a Reuptake the NTs are taken up from the cleft by plasma membrane NT transporter wither on presynaptic or postsynaptic neurons It is usually cotransported with Na Cl and H ions b Degradation by NT degrading enzymes like choline esterase for Ach and COMT for dopamine c By diffusion down the concentration Synthesis Glutamine is converted to glutamate by glutaminase gt Glutamine is converted to GABA by glutamate decarboxylase gt Tyrosine is converted to LDOPA by tyrosine hydroxylase and LDOPA is converted to Dopamine by AADC Sequestration of the NTs into the vesicle is done by NT transporter and driven by proton gradient across the vesicle membrane Neurotransmitters 1 Smallmolecule neurotransmitters packaged in vesicle released in cleft and terminated a Acetylcholine b Amino acids i Glutamate major Excitatory NT in CNS ii GABA in GABAergic Neurons Major inhibitory NT iii Glycine modulate NMDAmediated synaptic transmission c Biogenic Amines i Catecholamines dopamine epinephrine norepinephrine ii Serotonin made from tryptophan iii Histamine made from histidine d Purines 2 Neuropeptides a synthesized as precursors in cell body just like proteins b Carried from cell body to terminal via the axon c sequestered in large electron densecore vesicles d release can be nonsynaptic and only with large freq of stimulation 3 Gaseous neurotransmitter NO and CO a highly permeable diffuse everywhere and not in vesicles b release upon synthesis which is triggered by Ca2 in ux no reupta ke Difference between nonpeptide and peptide NTs NonpepUde Peptide Synthesized amp packaged in terminal Synthesized amp packaged transported to terminal Synthesized in active form Active when fused with larger polypeptide In small and clear vesicles In large electron dense vesicles Released in the synaptic cleft and has short latency and duration Could be released a bit far from postsynaptic cell long latency and duration is seconds Terminated by reupta ke Terminated by proteolysis or diffusing Receptors for Classic Neurotransmitters 1 Acetylcholine Nicotinic pentameric nonselective cationic channels gated by Ach Muscarinic ve different GPCRs two classes M135 coupled to Gq M24 coupled to Gi 2 Amino acids Glutamate lonotropic tetrameric nonselective cationic channels gated by Glu Cocentrated at postsynaptic densities PSDs NMDA Receptors NR1 and NR2ABCD l acts as quotcoincidence detectorquot Mg2 blocks NMDA at resting Vm depolarization removes it Involved in regulation mental and cognitive attributes AMPA Receptors GluR14 l mediate fast synaptic transmission Kainate receptors GluR57 KAR12 Metabotropic 8 different GPCRs Group I mGluR15 Group II mGluR23 Group III mGluR467 GABA 8 lonotropic GABAA concentrated at soma and proximal dendr esL GABAc pentameric Cl channel gated by GABA Metabotropic GABAB GPCR Glycine ionotropic pentam eric Cl channel gated by glycine 3 Biogenic Amines Except 5HT3 all GPCR Many subtypes for each dopamine epinephrine norepinephrine serotonin histamine 4 Purines receptors for ATP onotropic P2X 7 subtypes nonselective cationic channels distinct form others Metabotropic P2Y 10 subtypes NT Receptors 1 Ligandgated channels ionotropic Receptors act on EPSP or IPSP directly gt Two types generally Cys loop family channels Ach GABAA Glycine and Seratonin AND glutamate channels NMDAR AMPAR and KAR 2 Gprotein Coupled Receptors modulate EPSP or IPSP indirectly PentoBarbital enhances IPSP s gt Other agents that enhance IPSPs by binding to GABAAR are Benzodiazepines increase the freq of Cl channels opening Barbituates increase the duration of Cl channels opening 0 Enhanced inhibition l sedation gt Have same effects but bind to different sites progesterone amp corticosterone SENSORY TRANSDUCTION Vision photons Hearing mechanical via air compression Taste chemical Smell chemical Touchpressure mechanical Proprioception mechanical Paintemperature mechanical thermal All these are converted to generator potentials which produce AP s Coding of AP s done by frequency of ring temporal patterns periodicity and consistency Process of sensory transduction a single axon from the sensory organ transmits AP to the next neuron in the spinal cord For example stretch of muscle spindle generates AP which is sensed by mechanosensitive receptors and transmitted to the spinal cord and releases Glu Glu elicits EPSP on the alpha neuron which releases Ach on the muscle and it contracts The stretch on the muscle spindle is interpreted by the sensory neurons into patterns of AP Motor Unit an alpha motor neuron and all the muscle bers it innervates The number of bers innervated by a motor neuron is dependent on the neness of control higher of bers l less ne control while lower of bers l more ne control Muscle Unit all the muscle bers innervated by one motor neuron Always belong to the same type slow or fast twitch Dermatome area innervated by a dorsal root ganglion neuron Shingles reactivation of herpes zoster virus lies dormant in the DRG after chickenpox Re ex predictable involuntary and stereotyped response to a stimulus Re ex arc basis circuit that mediated a re ex has three components afferent imb carry info to brain central component synapses on interneurons in CNS and efferent imb cause motor response IA Fibers carries AP to spinal cord and synapse on the motor neuron in the spinal cord Stretch Re ex tendon tap Muscle spindle stretches which produces a generator potential GP and creates an AP on the IA sensory axon Transient Receptor Potential TRP Channels are involved in temperature sensing gt Hair cells have mechanosensitive TRP channels Types of Ion Channels 1 Voltagegated Na and K channels for AP in axons and skeletal muscles 2 Voltagegated Ca2 channels in axon terminals heart and smooth muscle 3 Ligandgated ionotropic Na K and Cl channels EPP EPSP IPSP 4 Stretchactivated ion channels in sensory receptor sensitive to mechanical stimuli GP 5 Gprotein activated metabotropic ion channels in special senses smooth muscle glands etc Mechanoreceptors in the skin FA fastadapting to change in stimuli l senses change SAslow adapting only tell when you re touching something pressure FA1 and SA1 shaow in skin sense direct pressure and small receptive eld FA2 and SA2 deep sense broad contact and large receptive eld Homunculus topographical correspondence between motor cortex and body parts For better 2point discrimination small receptive elds high density of touchpressure receptors and large cortical representation Vision Retinal neural processing retina converts photons to AP sent to the brain for interpretation GP produced by photoreceptors are processed to AP in optic nerves Cones day vision color less sensitive concentrated in fovea less numerous Rods night vision detects luminescence more sensitive and more numerous gt Ampli es signals one photon causes membrane potential alteration by 1mV Rhodopsin GPCR Light enters l Rhodopsin contained in disc increases l PDE increases l cGMP decrease l cGMPgated decreases l Vm decreases Release decreases cGMP gates the channel and when it is destroyed channel opens less and Na enters less decreasing the Vm leading to less NT release Taste Sweet sucrose energy Salty NaCl minerals Sour HCI bad Bitter quinine bad Umami monosodium glutamate meat gt Receptor cells are specialized epithelial cells not neurons that convert taste to NTs which are sensed by the cranial nerves then generate GP which might generate AP To elicit GP there are three different pathways a Na and H which are have high concentrations outside go in and changes Vm D depolarization D generate GP D Ca2 in ux D increase NT release b Changes make channels open l goes in l increase Vm NT release c BitterSweetUmami bind to GPCR l intracellular pathway l Ca2 in ux Smell Olfaction Odor receptors GPCRs activate Golf GProtein is activated l increase cAMP lactivated cAMPgated channels Na and Ca2 in ux l Cl out ow l depolarization l produce GP Odorants receptor cells regenerate every 60 days A single smell can activate may different receptor proteins and the convergence of their AP s determine what you smell AUTONOMIC NERVOUS SYSTEM a Does NOT control skeletal muscles b Controls smooth muscles cardiac muscles and glands of the internal organ viscera c Helps in maintaining homeostasis d Coordination of responses to external stimuli ght or ight 3 Major Divisions a Sympathetic NS ThoracolumbarT1L3 division of ANS mobilization of body quot ghtor ightquot response One preganglionic neuron innervates a few postganglionic neurons Wide spread and greater divergence in effect Sensory input on short preganglionic neuron l releases Ach on long postganglionic neuron l releases Ach on muscarinic receptor on organ b Parasympathetic NS craniosacral division of ANS Concerned with the Resting response One preganglionic neuron innervates many postganglionic neurons Discrete and short spread response which is localized The postganglionic neuron is short and is very proximal to the organ c Enteric NS oldest part of ANS controls GI tract pancreas gall bladder to help in digestion Doesn t require inputs from other parts on the nervous system Sympathetic Parasympathetic Locations of preganglionic thoracic Tl12 brainstem soma upper lumbar Ll3 sacral S24 Length of preganglionic ber short Long Locations of postganglionic paravertebral close to target soma ganglia prevertebral organ gangHa Length of postganglionic ber Long Short Ratio of prepost bers 110 13 divergence Functions Both systems act in coordinated manners to maintain homeostasis Neurotransmitters Ach Ach preganglionic Neurotransmitters Norepinephrine Ach postganglionic Muscarinic receptors that the postganglionic Ach from parasympathetic neuron binds toquot M1 class couple with Gq to increase Ca2 M2 class with 61 to inhibit PKA gt Atropine blocks all muscarinic receptors Agonists carbachol muscarine oxotremorine help with Ach binding to receptors Because all postganglionic parasympathetic neurons release Ach to act on muscarinic receptors on effector cells the nonselective antagonist atropine blocks the action of parasympathetic neurons effectively Eg resuscitation with atropine injection in bradycardia to inhibit the parasympathetic vagus nerve which slows heart beat
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