Human phys exam 1 notes

Homeostasis

• Homeostasis is the process of maintaining a constant internal environment.

• Cells maintain a constantinternalenvironment.

• Example: Unicellular Amoeba in freshwater prefers seawater.

• Lysis (bursting of cell) occurs if a cell has lots of ions in it, which results in lots of waste.

• Water moves in or out to maintain osmotic pressure.

• This exchange relies on diffusion.

• Diffusion works because each cell is located very close to environment.

• If there is a longer distance between outside and cells, simple diffusion will not work.

• A circulatory system is used.

• Blood vessels connect cells, are pumped by heart.

• These cells are not in seawater but in their own interstitial fluid or extracellular fluid which consists of interstitial fluid and plasma.

• Feedback loops are necessary since we are not static creatures and our environment changes; our bodies must adapt and change to maintain a reasonably constant state using feedback loops.

Negative Feedback

• Negative feedback limits the range and are called setpoints.

• A disturbance is removed to bring the system back to equilibrium.

• An example is blood sugar: a disturbance is equal to the opposite of the disturbance, leading back to equilibrium.

• Example: In cold weather, the body can't remove the cold, so it produces heat.

• Oscillation can occur when setpoints are too close.

• When sick, sometimes feels cold then really hot.

Positive Feedback

• Positive feedback results in more disturbance, but is usually balanced within negative feedback to go back to equilibrium.

• It anticipates disturbance, so when disturbance does come, the response is faster.

Membranes

• Membranes and potentials are crucial for facilitated diffusion and exchanges.

• The membrane is a fluid mosaic model with two components: lipids and proteins.

• Transport molecules move substances across the membrane.

• $Na^{+}$ doesn't uses ATP directly, but enables movement of two things across the membrane through transport.

• Cotransport (Symport): When two things are going across the membrane in the same direction (e.g., 1 ion $Na^{+}$ and 1 molecule glucose).

• Countertransport (Antiport): Movement of two things across membrane in different directions

Diffusion

• Needs a concentration gradient.

• Pumps: Need pumps to maintain concentration gradient.

• Channels: Specific to certain ions like $Na^{+}$ and $K^{+}$; uses ATP.

Sodium-Potassium Pump

• The $Na^{+}$ / $K^{+}$ pump.

• Moves 3 $Na^{+}$ out and 2 $K^{+}$ in.

• Once channel open, ions will go across.

• Example: Aquaporins channel that only allows water.

Membrane Potential

• $Na^{+}$ pressure high outside, but $K^{+}$ pressure is high inside.

• The inside of cells are negatively charged.

• Em: Membrane potential created by unequal distribution of ions across membrane.

• $Na^{+}$ high outside cell in the interstitial fluid.

• $K^{+}$ high inside cell.

• Proteins have negative charge high inside cell.

• Nernst Equation: If you know the concentration of ions inside and outside cell, you can calculate the equilibrium potential for an ion, i.e., the voltage produced by an ion.

• $E_{ion}$ (Equilibrium Potentials):

  • $Na^{+}$: Low inside, high outside; positive equilibrium potential ($E_{Na+}$).

  • $K^{+}$: High inside, low outside; negative equilibrium potential ($E_{K+}$).

  • $E_{ion} = 595.6 * CT * 60.1$

• Goldman Equation: Uses Nernst equation and adds each of them together adding weight to each membrane permeability.

• Permeability (p) depends on number of channels.

• $Na^{+}$ small p while $K^{+}$ large.

• If you change permeability (p) of a certain ion, the membrane potential (Em) goes toward equilibrium.

• If permeability increases, $E<em>m$ goes toward $E</em>{Na+}$, and $E_m$ increases.

Action Potential

• Cell becomes positive then back to normal (resting state).

  • Depolarized: Less negative.

  • Hyperpolarized: More negative.

• In order to get action potential, need to depolarize membrane to threshold.

• If inject $K^{+}$, going to depolarize membrane closer to threshold, so get a lot of action potentials.

• Voltage-gated $Na^{+}$ channels open, come in cell becomes more positive, more depolarization.

• Stages of action potential include:

  • Rest.

  • Depolarization.

  • Positive feedback depolarizes cell just a little. Not to threshold, not opening all channels.

  • Increase of permeability of $Na^{+}$ depolarizes membrane even more which will open more $Na^{+}$ channels.

  • Voltage-gated $Na^{+}$ channels become inactivated by ball and chain.

  • Voltage-gated $K^{+}$ channels open.

  • $K^{+}$ leaves, hyperpolarizing the cell (negative feedback).

  • $Na^{+}$ opens and closes much faster than $K^{+}$.

Action Potential Thresholds

• When you get to threshold, open voltage-gated $Na^+$ channels, causing an action potential.

• Action potential is the same size and duration of cell.

• Thresholds can change.

Refractory Period

• Period after an action potential has occurred.

  • Absolute Refractory Period: Cannot produce a second action potential because $Na^{+}$ is inactivated (ball and chain is in channel).

  • Relative Refractory Period: Can produce action potential but harder to open $K^{+}$ channels are hyperpolarizing membrane, pulling membrane potential from threshold.

Conduction

• Action potential goes to next, then next, all the way down the axon.

• Myelin helps and accelerates transmission of axon potential.

• Action potential leaps to next region making action potential go faster down axon.

• Nodes of Ranvier: Where action potential occurs where $Na^{+}$ and $K^{+}$ channels are.

• Multiple Sclerosis: Myelin degenerates and goes away, so action potential coordination and strength will be different because this action potential will be at the end of the axon than a normal working axon.

Pain

• Stopping $Na^{+}$ channels from opening means the neuron can't depolarize and can't generate action potentials.

• This stops signal transmission along nerve fiber, preventing pain signals from reaching central nervous system.

• Local anesthetics like Novocaine, Lidocaine, and Xylocaine do this.

Communication

• Communication between cells occurs through synapses.

• Synapses are places where a cell can communicate with another cell.

Gap Junctions (Electrical Synapses)

• Connexin proteins connect two cells forming a hollow tube where ions can pass.

• Nerve axon potential in cell B will produce an axon potential in cell A and vice versa.

• Water, ions, and small molecules can pass through gap junctions.

• Useful if you want groups of cells working together.

Chemical Synapses

• The axon potential goes from nerve to muscle (one way, not in opposite direction).

• Synaptic Cleft: Space between nerve muscle (very tiny).

• Pre-synaptic Cell: The nerve before the synapse.

• Post-synaptic Cell: The next cell that will become excited (muscle).

• Action potential comes down in the pre-synaptic cell.

• Look for vesicles (circles w/ chemicals neurotransmitters) when trying to determine pre-synaptic vs. post-synaptic cells.

• There is a delay in electrical synapses.

Vesicles

• Contain neurotransmitters and a reservoir for storage.

• In resting cell, vesicles are attached to actin by a protein called synapsin.

• Releasable vesicles are attached and docked to membrane by 4 snare proteins (ready to be fused).

Mechanism of Synaptic Release

• Action potential comes down axon to terminal and causes opening of voltage-gated calcium channels.

• $Ca^{2+}$ enters and binds with calmodulin.

• $Ca^{2+}$ calmodulin activates kinase which uses ATP to phosphorylate synapsin protein.

• This causes the vesicle membrane to fuse with the pre-synaptic membrane.

• This action is releasing neurotransmitter into synaptic cleft (exocytosis) via snare proteins.

• Recycling of vesicle membrane occurs because if this were to be left unchanged, the pre-synaptic terminal would get bigger and bigger.

Vesicle Membrane Characteristics

• Vesicle membrane has recognizable proteins on it that cause endocytosis (budding creates coated vesicle proteins fall off creating empty vesicle).

• Vesicle membrane has ATP-dependent proton pump.

  • $H^{+}$ in, transmitter out.

• Now vesicle can connect to actin using synapsin, forming stored or filled vesicles.

Neurotransmitters

• Neurotransmitters act as a ligand and binds to post-synaptic receptors.

• Opens ligand-gated ion channels (mostly $Na^{+}$ but also a little $K^{+}$ and $Ca^{2+}$).

• If these channels were $Cl^{-}$ or $K^{+}$, would hyperpolarize muscle away from threshold, preventing action potential.

Acetylcholine (ACh)

• Slows heart rate.

• Each ACh receptor has 2 receptor sites per each ACh receptor.

• When ACh binds, channel opens allowing $Na^{+}$ to enter, which depolarizes the membrane, leading to an action potential in muscle and muscle contraction.

• If ACh were to remain in the cleft, channels would open again, producing repeated contractions of the muscle, BUT action potential in motor neuron produces single action potential in muscle fiber (single contraction).

• ACh in synaptic cleft is quickly broken down by acetylcholinesterase enzyme (found on muscle membrane) forming choline and acetic acid.

• The body cannot make choline, must eat it but body must recycle to keep it.

• There are choline transporter molecules on pre-synaptic membrane to uptake choline. Now can make ACh in terminal instead of cell body because recycled choline.

• Cholineacetyltransferase + choline + acetyl CoA = Ach.

• This then goes back into empty vesicle.

Toxin Impact

• Action potential produced in nerve ALWAYS produces action potential in muscle.

• Prialt blocks secretion of neurotransmitters released by sensory pain nerve endings; blocks Ca+ channels, so no release of neurotransmitter, no action potential in next cell, gets rid of pain.

• Botox toxin attacks snare protein: no docked vesicles, no secretion of neurotransmitter, no action potential in muscle, no muscle contracting.

• Nerve gases (Sarin gas) inhibits acetocholineesterase: no breakdown of ACh, Ach continuously contracting. Can't breathe out, deadly.

Additional Neurotransmitters

• There are other neurotransmitters other than ACh, each have own specific receptor on post-synaptic membrane, each have channel that allows ions to pass through.

• If it's a $Na^{+}$ channel, it depolarizes cell, if it's a $Cl^{-}$ channel, it hyperpolarizes cell.

• Different effects in post-synaptic cell.

• The dendrites of the post-synaptic cell is where pre-synaptic cell is and where it makes connections and sends signals.

• Axon hillock (trigger zone): First place there are voltage-gated $Na^{+}$ channels; first place action potential occur.

• Stimulation of a nerve causes depolarization of post-synaptic cell; doesn't produce action potential just making cell closer to threshold unless nerve muscle junction.

• If a nerve causes hyperpolarization of post-synaptic cell, then it is away from threshold, ex opening K+ channels.

Temporal vs. Spatial Summation

• Action potentials occur in two ways:

  • Temporal Summation: Same neuron producing EPSP's high frequencies, piggybacking off each other (facilitation) second hump will be larger than first EPSP.

  • Spatial Summation: Different pre-synaptic neurons EPSP's and IPSP's arriving at axon hillock at the same time.

Reasons

• Why AP in presynaptic cell $Ca^{2+}$ comes in, neurotransmitters released.

• If increase frequency of AP, $Ca^{2+}$ stays in cell longer, more vesicles being fused, more neurotransmitter.

Signal and Ligands

• Locked Jaw (epilepsy): Too much EPSP (excitatory postsynaptic potential), not enough IPSP (inhibitory postsynaptic potential).

• Ligand is a chemical that binds to receptor on target cell receptors Neurotransmitters ligands are derived from amino acids.

• Receptors can either be depolarize or hyperpolarize.

Nicotinic ACh Receptor

• Receptor and channel same protein (ionotropic, in neuromuscular junction).

Muscarinic ACh Receptor

• Receptor and channel two different proteins (metabotropic).

Receptor Population Change

• Upregulation: Receptors increase if no lot of neurotransmitters in cleft.

• Downregulation: Receptors decrease if lot of neurotransmitters in cleft.

Common Neurotransmitters

Dopamine

• Pleasure increases when drink alcohol, sex, adrenaline cocaine, blocks reuptake molecules, down regulation of postsynaptic cell.

• Amphetamine: Increases receptor sensitivity increases response.

Serotonin

• Mood depression low concentration in synaptic cleft response in postsynaptic cell is less.

• Anti-depressant drugs (ecstacy): Inhibits reuptake of serotonin in synaptic cleft epstaiythgttefnstapt E1EEYes Tsereceptors decrease back to where was.

• Cell-cell communication more cell communicates another using chemicals gap junction electrical synapse chemical neurotransmitter.

Cell Communication

• Autocrine: Cell secretes chemical and reacts w receptor on same cell membrane in serotonin released in deft then reacts w autoreceptor which maintains homeostasis.

• Paracrine: Chemical secreted in interstitial fluid effecting target cell cell w receptor of that specific chemic.

• Endocrine: Similar to paracrine except goes into blood called hormone not ligand because goes into blood.

Chemical Communication

• Chemical Synapse: Presynaptic postsynaptic cell secretes neurotransmitters neurohormone similar to chemical but neurotransmitter secreted into blood chemical going somewhere.

• Pheromones: Chemicals secreted into air else in body low chemical outside produces change on inside of cell.

• IonotropicReceptor: receptor and channel same protein syn apts hitting funnel is inside but all part of one molecule Tyrosine kinase more later.

Metabotropic Receptors

• Receptor and target protein channel enzyme intermediate often called G protein.

• G protein has 3 components alpha beta gamma GDP GTP can bind to alpha portion G proteins may be excitatory activates the protein or inhibitatory inactivates protein w.io EEE IiiiEE iii iiiiiiiiii.in EE i intercellular 3examples of G proteins Cyclic nucleotides cyclic Amp Amp s gypmessengers protein called Adenylate cyclase when activated ATP CAMP CAMP binds to regulatory unit of protein kinase A PKA PKAsplits and catalytic unit phosphorylates proteins activated proteins can turn glycogen into glucose in fight or flight mode this is what causes high blood sugar levels aquaporins when dehydrated ADH binds to receptor cAMP causes vesicles w aquaporins to fuse w apical membrane upregulation more water absorbed phosphodiesterase inactivates cAMP turns off second messenger activity the phosphorylated proteins still active some people can't drink coffee be cAMP increases heart rate Coffeemethyl Xanthines inactivate phosphodiesterase CAMPhangs around in cell increase heartrate blood pressure Yclic GMP same as cAMP except protein called Guanylate cyclase GTP cGMP iggg.gg ffggy activates PKG not PKA they have different shapes everything else same Prostaglandins enzymecalled phospholipase arachidonic acid PLAZ takes off a fatty acid chain of the phospholipids creates arachidonic acid I c aicipiieiienii.ioYeiiizesitsiaiia'rain'siiéaiidisiiciammat.ms COX1 produces good prostaglandins stomach lining replacement induce blood clotting COX2 bad tissue damage creates inflammation and pain arthritis heart attack Celebrex inhibits COX2 but keeps COXI.

• Non steroid anti inflammatory drugs aspirin Ibuprofen inhibit both Cox enzyme no production of prostaglandins asprin blood clots in blood vesicles women going to brain men going to heart causes strokes heart attacks decreases blood clots IPs and Diacylglycerol protein phospholipase C forms inositoltriphosphate IP 3phosphates on it diacylglycerol IP reacts with receptors on Ca'tchannels on endoplasmic reticulum Ca'tstorage structure Tca s meatenia messengeriii aiessioier.firengiptiiei Y'siii'aseion'aites'sintestinessee me

Nitric Oxide

• Endocrine System: This system is made up of a series of glands thyroid, adrenal, pancreas, ovary, testis, hypothalamus that communicate by endocrine hormone goes through blood vessel neGalled disturbañeEneed to be able to detect this disturbance then communicate w endocrine system.

• Endocrine vs nervous system both secrete hormones from simple specialized nerve cells.

• Simple hormones:

  • Nitricoxide paracrine producedby a cell has effect on target of if.EEifiE a second messenger iinms that doesnotinvolve G protein t.itiiiiiiiiiiii iii mmmm goes through membrane of target cell not binding w receptor on target cell ells outsideneednutrients 02 Oz opensCatchannelsparacrine Catenters ca calmondulin endothelialcellscontract capillary ca calmondulincreates nitric acid synthase Nozgoesthroughlipidbilayer out of endothelialcell Nozenters smoothmusclecell NO binds w guanylylcyclase createsGTP CGMP activatesPKG whichopensK channels hyperpolarizingcell castchannelscloseCapumpactivated decrease Ca Ca moremusclecontractions Ca i relaxmuscle more blood flow when smooth muscle relaxes ifeyqtgimges.gg ow inhibit PDE more PhG Ca i staysdecreased musclerelaxed.

Three Main Types of Hormones

Peptides

• Peptides (3 amino acids, hydrophilic, like water), dissolve in plasma blood and are stored in vessides and have a very small half life, so must maintain secretion for prolonged response

Steroid's

• Steroid'sIEImchaste affirdrompnessEngercAMPthrough G protein steroid hormones made by cell that have enzymes adrenal cortex gonads placenta cannot be stored begostraight through lipid bilayer rate of secretion depends on rate of production steroids bind w proteins stabilizessteriodinblood canlive longer goesthroughentirecircularysystem then dissociates from proteingointocell find receptor most receptors are innucleus some on membrane thesedon'tturn on an enzyme but changes transcription changes proteins inside cell.

GminnessYTamino acids

• GminnessYTaminoacidshydrophobic or hydrophilic tryptophan melatonininpinealgland tyrosine catecholamineshydrophilic thyroid hormones hydrophobic.

Control of Blood Sugar

• The pancreas (both exocrine and endocrine) controls glucose levels in plasma blood.

• Beta cells in pancreas secrete insulin communicates blood sugar levels increase glucosetaken upbygut eating through endocrine blood sugar levels decrease before meals insulin secreted when high blood suggygygy.gl1utstretcoaa sebloodamino acids ask.ae glutose beta taken up by.EEggibutverysiowii tiiuen.cat cannab upregulate glucose uptate i we EE diabetesmellitus not enough insulin secreted high blood sugar levels t Egfr type1 cannot produce insulin because betacells don't work destroyed have togiveshots of insulin type2 insulin produced but receptors broken not there no upregulation of glucosetransporters wheneat lot ofsugarsugarlevelsconstantlyhigh destroys receptor downregulation GLP 1 hormone secretedby L cell causes increasesecretionof insulin decreasebloodsugarlevelsyeig ozempic is a GLP 1 receptoragonist.

• Balance between glucagon insulin other hormones can elevate blood sugar levels epinephrine cortisol BUT insulin is only hormone that decreases blood sugar levels.How brain is connected toendocrinesystemAdrenalMedullasimpleexamplelocated on top ofkidney orangeoutsidereel Enlarges Part of sympatheticautomaticnervous system n ÉstojyI at cancannotcontrolheartrate sympatheticwhenstressed parasympathetic rest ecretes catecholamines epinephrine hormone that goesinto bloodinto many targets part.eeeius braindirectlystimulatingadrenalglandwhichcausessecretionofadrenaline p.FI iytiaiamia'h nYspiinaiam9s patsitianaidpressure were c a Pituitary smallglandhangingfrombrainconnectedbyhypothalamus hypothalamuspartof automaticnervoussystemtaskswedon'tthinkabout hypothalamus area of brain that containcontainsmanygroupsofnervecellbodies FEE Hiii Chemicaltheysecretefromterminals is a hormoneNOTneurotransmitter SteriorPituitary directstimulation cellbodyand axon locatedin hypothalamus axon goesdown terminates onbloodvesside nerve to bloodvessidejunction GPastpiess.isiie5iieieifortionP iiit.hestips.jo Btinsdenuarated ADHbindstoreceptor activatesGprotein activates Adenylatecyclase CAMP vessides w aquaporinsfuse w filtrate upregulation of aquaporins morewatercancomein in hypothalamuscells are sensitivetoosmoticpressureof blood toodehydratedcausethemto secrete Negativefeedbacksystem ADH secretesoxytocin in women childbirth men don't have much nteriorPituitary secretorycellsNotnervecells manyhormonessecretedby this thyroid adrenalcortex hypothalamuscells sentaxondown makesynapses w capillary in anteriorPituitary stimulusdetetetedbybrain hypothalamussecreteshormone goesdownaxon toanteriorpituitary secrete stimulatinghormone goestotargetorganthroughblood targethormonesecretesmorehormones 6releasinghormones stimulating peptide hormones releasinghormones cellsin hypothalamus neurosecretion into capillariesontoanteriorpituitary neurohormone communicationyone grape Thyroidgland locatedat base at neck I in releasinghormones madeup of follicles abunchofgrapes T3 Ty hormones madefromThyrosine w 4 I Tu or 3 I Ts hydrophobic can gothroughlipidbilayer statians target storedin colloidfoundinfollicle Na I symtransporter I frombloodenterfollicularcells.

Systemic Issues:

Hyperglycemia

• High blood sugar levels.

Acidosis

• Less glucose in muscle fat liver cells increase fatty acid metabolism increase production of ketone water loss high level of glucose in kidney peea lot thirsty Glucagon secretedbyalphacellofpancreaticisletswhenbloodsugarlevelslow.

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