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Physiology 1 Test 1
Cell Physiology
Question | Answer |
---|---|
Total Body Water | Accounts for 50-70% of total body weight |
What are the two major body fluid compartments and how much of total body water does each hold | Intracellular Fluid (ICF) 2/3 of total body water Extracellular fluid (ECF) 1/3 of total body water |
What are the components of the ECF and how much of each | Plasma (1/4 of ECF): the fluid circulating in the blood vessels Interstital fluid (3/4 of ECF): The fluid that actually bathes the cells |
How is Interstitial fluid formed | It is an ultrafiltrate of plasma, formed by filtration processes across the capillary wall |
Is there protein in interstitial fluid | NO |
What is the Principle of Macroscopic Electroneutrality | Each compartment must have the same concentration of cations as of anions. Even where there is a charge difference across the membrane, charge balance is still maintained in the macroscopic solution |
What is homeostasis | Stable operating conditions in the internal environment. This is how the body maintains a constant internal environment despite changing external conditions |
Homeostatic control mechanisms | -Sensory receptor cells -Integrators -Effectors |
What is negative feedback | -The body responds in such a way as to reverse the direction of change -Keeps things constant |
What are some factors in the body that are homeostatically regulated | -Nutrients -O2/CO2 -Waste Products -pH -Water, salt, electrolytes -Temperature -Volume and Pressure |
What is positive feedback | -Change occurs in variable, response changes that variable even more in the same direction -EX: Oxytocin |
Composition of Intracellular Fluid | -40% of total body weight or 2/3 of body fluid -Similar in composition from one cell to another and even from species to species |
Major cation in ECF | Na+ |
Major anion in ECF | Cl- HCO3- |
Major cations in ICF | K+ Mg2+ |
Major anion in ICF | Proteins Organic phosphates |
ICF vs ECF acidity | ICF is more acidic |
How do the total solute concentrations compare in ICF vs ECF | They are the same because of the selectively permeable cell membrane |
What is osmosis | Diffusion of H2O from high concentration to low concentration until reaching equilibrium |
What is diffusion | The movement of ions from high concentration to low concentration until ions are equally distributed |
Units for solute concentrations | -Moles, millimoles -Equivalents -pH -Osmolarity |
What are K+ and Mg2+ balanced by | Proteins and Phosphates |
What is Na+ balanced by | HCO3- and Cl- |
What creates concentration differences across membranes | Na+-K+ ATPase Ca2+ ATPase Transporters |
What is Na+-K+ ATPase | A pump that moves Na+ and K+ against the concentration gradient |
What are the transporters that create concentration differences across membranes transporting | Glucose, amino acids, Ca2+, H+ (no ATP is required) |
What is Gibbs-Donnan equilibrium | Electroneutrality across the capillary wall |
What are cell membranes composed of | Phospholipids, cholesterol and glycolipids |
What lipid soluble things cross the cell membrane | CO2, O2, FA, Steroid hormones |
What H2O soluble things cross the cell membrane | Ions, glucose and AA |
What types of proteins are in the cell membrane | Transporter, enzymes, hormone receptors, cell surface antigens, ion and water channels |
What are Integral proteins | Contact both ICF and ECF but anchored to the cell membrane by hydrophobic interactions |
What are Peripheral proteins | -not embedded, not covalently bound, loosely attached -bound by electrostatic interactions EX: ankyrin (cytoskeleton of RBCs to Cl- HCO3- exchanger) |
What is amphipathic | having both hydrophilic and hydrophobic components |
What are some examples of Integral proteins | ligand-binding receptors, transport proteins, pores, ion channels, cell adhesion molecules and GTP-binding proteins |
What is downhill transport and how does it occur | -Transport down an electrochemical gradient -occurs by diffusion, either simple or facilitated (No ATP requirement) |
What is uphill transport and how does it occur | -Transport against an electrochemical gradient -occurs by active transport, either primary or secondary (Needs ATP) |
What is facilitated diffusion | -downhill -Carrier mediated -No energy in required EX: GLUT4 transporter-transports D-glucose into skeletal and adipose tissue |
What is saturation | Is based on the concept that carrier proteins have a limited number of binding sites for the solute. |
What is Transport Maximum | When all binding sites are occupied |
What is Primary active transport | -Uphill -Carrier mediated -Directly uses energy EX: Na-K Pump |
What are the two types of secondary active transport | Cotransport Countertransport |
What is cotransport | -Carrier mediated -Indirectly uses ATP -Solutes move in same direction as Na across the membrane |
What is countertransport | -Carrier mediated -Indirectly uses ATP -Solutes move in opposite direction as Na across the membrane |
Why is the Na-K pump considered electrogenic | -Each cycle 3 Na and 2 K are moved -This means more positive charge is pumped out of the cell than is pumped into the cell -It creates a charge separation and potential difference |
What do cardiac glycosides do | -They inhibit Na-K pumps |
What is osmosis | -Flow of water across a semi permeable membrane due to a difference in solute concentration -Primary method of water movement into and out of body fluid compartment |
What is an isotonic solution | A solution that has the same concentration of non-penetrating solutes as normal body cells |
What is a hypotonic solution | A solution with a lower concentration of non-penetrating solutes |
What happen if a cell is placed in a hypotonic solution | Water enters the cell via osmosis |
What happens if a cell is placed in a isotonic solution | Cell volume remain constant |
What is a hypertonic solution | A solution with a greater concentration of non-penetrating solutes |
What happens if a cell is placed in a hypertonic solution | Water leaves the cell via osmosis |
What is the NaCl concentration in the body | .9% NaCl |
Na equilibrium potential | +65 mV |
Ca equilibrium potential | +120 mV |
K equilibrium potential | -85 mV |
Cl equilibrium potential | -90 mV |
What is the Nersnt Equation | Calculates the equilibrium potential for an ion at a given concentration difference across a membrane |
What is Resting membrane Potential | -Potential difference that exists across the cell membranes of excitable cells -established by diffusion potential |
What is the role of Na-K ATPase in resting membrane potential | It has an electrogenic contribution and maintains concentration gradients for Na and K |
What is the Chord Conductance equation | -Weighs the equilibrium potential of each ion by its relative conductance -At rest the membrane is more permeable to ions like K+ |
What is an action potential | Phenomenon of excitable cells such as nerve and muscle that consists of rapid depolarization followed by repolarization of membrane potential |
What is depolarization | The process of making the membrane potential less negative (more positive) -makes the interior of the cell less negative |
What is hyperpolarization | The process of making the membrane potential more negative |
What is inward current | -The flow of positive charge into the cell -Inward currents depolarize the membrane potential |
What is outward current | -The flow of positive charge out of the cell -outward current hyperpolarize the membrane potential |
What is threshold potential | the membrane potential at which occurrence of the action potential is inevitable |
What is Overshoot | is the portion of the action potential where the membrane potential is positive |
What is undershoot | the portion of the action potential, following repolarization, where the membrane potential is actually more negative than it is at rest |
What is absolute refractory period | a period during which another normal action potential cannot be generated |
What is relative refractory period | a period during which another normal action potential can be generated, however not as strongly |
Steps to Action Potential | 1) RMP, -70 mV, K leak channels fully open 2) Depolarization, -60 - +65 mV, Opening of voltage gated Na channels 3) Repolarization, inactivation of VG Na Channels and activation of VG K channels 4) Hyperpolarization, more negative the RMP |
At rest how are the sodium gates; open or closed | Activation gate is closed Inactivation gate is open |
During Upstroke how are the sodium gates; open or closed | Activation and Inactivation gates are open |
During Repolarization how are the sodium gates; open or closed | Activation gate is open Inactivation gate is closed This is the Absolute refractory period |
What is conduction velocity | Speed at wich impulse travels |
What is conduction velocity dependent upon | Nerve diameter |
What is Saltatory Conduction | Jumping action potential from node to node |
What are the two types of synapses | Electrical and Chemical |
What is an Electrical synapse | Current flow from one excitable cell to the other via low resistance pathways called gap junctions |
What is a chemical synapse | Presynaptic and postsynaptic, in between synaptic cleft |
What is the neuromuscular junction | gap between nerve and muscle |
Are neuromuscular junctions multidirectional | NO Unidirectional |
What are the first 4 steps to Neuromuscular transmission | 1)AP in the nerve 2)Open voltage gated Ca channels (Ca binds to ACh vesicles 3)Exocytosis of ACh vesicles 4)ACh diffuses and binds to nicotinc receptor or motor end plate |
What are steps 5-7 of Neuromuscular transmission | 5)Binding open ligand gated Na/K channels 6)Motor endplate depolarized because of Na and K flow (causes AP in muscle) 7)ACh is degraded by AChE into choline and acetate (choline is transported back to presynaptic terminal) |
Where does synthesis of Acetylcholine happen | In the Presynaptic terminal |
Where does degradation of Acetylcholine happen | In the Postsynaptic terminal |
Describe the Acetylcholine cycle | Choline+Acetyl CoA -> Acetylcholine -> Choline+Acetate |
What enzyme is needed to go from Choline+Acetyl CoA -> Acetylcholine | Choline acetyltransferase |
What enzyme is needed to go from Acetylcholine -> Choline+Acetate | acetylcholinesterase |
Where is acetylcholinesterase located | On surface of motor end plate membrane |
What does acetylcholinesterase do | Terminates acetylcholine activity at neuromuscular junction |
What does Botulinus do | Blocks ACh release Causes weakness |
What does Hemicholinium do | Prevents reuptake of choline Causes weakness |
What does Neostigmine do | Blocks AChE Makes ACH more available and decreases weakness |
What does Curare do | Binds to ACh receptors Causes weakness |
What is spatial summation | Occurs when two or more presynaptic inputs arrive at a postsynaptic cell simultaneously. Inputs combine and the summation determines the output |
What is temporal summation | Occurs when two presynaptic inputs arrive at the postsynaptic cell in rapid succesion. Because the inputs overlap in time, they summate |
What is long term potentiation | Occurs in storage of memorie and involves both increased release of neurotransmitter from presynaptic terminals and increased sensitivity of postsynaptic membranes to the transmitter |
What is synaptic fatigue | occurs where repeated stimulation produces a smaller than expected response in the postsynaptic cell, possibly resulting from the depletion of neurotransmitter stores from the presynaptic terminal |
What are the criteria for something to be considered a neurotransmitter | Formed in presynaptic terminal and has to be degraded after use |
What is degeneration of dopominergic neurons called | Parkinson's disease |
Describe the synthesis of Dopamine, norepinephrine, and epinephrine | Tyrosine -tyrosine hydoxylase-> L-Dopa -dopa decarboxylase-> DOPAMINE -dopamine beta-hydoxylase-> NOREPINEPHRINE -POMT-> EPINEPHRINE |
Is acetylcholine excitatory or inhibitory | EX |
Is norepinephrine excitatory or inhibitory | EX |
Is epinephrine excitatory or inhibitory | EX |
Is Dopamine excitatory or inhibitory | EX |
Is serotonin excitatory or inhibitory | IN |
Where does serotonin act | In brain and GIT |
What is serotonin a precursor to | Melatonin |
Is glutamate excitatory or inhibitory | Ex |
Where is glutamate used | Spinal cord and cerebellum |
What are the types of glutamate | There are four. Three are ionotropic including NMDA and the fourth one is metabotropic which are coupled by G proteins to ion channels |
Is glycine excitatory or inhibitory | IN |
Where is glycine found | In brain stem and spinal cord |
What does glycine do | Increases Cl- conductance of the post synaptic cell membrane and driving the membrane closer to equilibrium potential of chloride, leads to hyperpolarization |
Is GABA excitatory or inhibitory | IN via GABAergic neurons |
What si GABA synthesized from | Glutamate |
What are the two types of GABA | GABAa that is linked to Cl- channel; GABAb coubled via a G protein to a K+ channel |
What disease is associated with GABA | Huntington's disease |
Is Nitric Oxide excitatory or inhibitory | IN but short acting |
Where is Nitric Oxide active | in CNS and GIT, does signal transduction in vascular smooth muscles |
How is Nitric oxide made | Arginine is converted to citrulline and NO |
NO travels uniquely. How? | No packaging, simply diffuses out of presynaptic endplate to the target cell |
What are neuropeptides and Purines | Neuromodulators (alter the amound of NTX release in response to stimulation. ATP acts a neuromodulator with AcH |
What does SKM require in order to contract | 1) action potential 2) Release of Ca2+ 3) Tension |
What is the process of going from action potential to contraction called | Excitation contraction coupling |
What are the two types of tension | Isometric(tension but no change in muscle length) and isotonic(tension and change in muscle length) |
What proteins make up the thin filament | Actin, tropomyosin, troponin |
What proteins make up the think filament | Myosin |
What is the purpose of tropomyosin | Prevents binding of myosin to actin |
What are the types of troponin and what do they do | Troponin C (initiates contraction) Troponin I (inhibits actin/myosin binding) Troponin T (connects tropomyosin to troponin complex) |
What are the scaffold proteins | Dystrophin, titin, nebulin, alpha-actinin |
Basic contractile unit of muscle | Sarcomere |
What does alpha-actinin do | glues actin to z-disk |
What does titin do | goes with myosin |
what does nebulin do | goes with actin |
What is the site of Ca storage in SKM | sarcoplasmic reticulum |
Step by step process of excitation-contraction coupling in SKM | 1)AP->T tubules 2)depolarization of T tubules causes DHP receptor to open ryanodine receptors on sarcoplasmic reticulum 3)Ca released in ICF 4)Ca binds toponin C 5)tropomyosin moves 6)cross-bridge cycling |
What is Ca bound to in the sarcoplasmic reticulum to keep its concentration down | Calsequestrin |
What stores Ca in sarcoplasmic reticulum | SERCA |
Describe Cross-bridge cycling | ATP binds mysoin head -> decreases affinity of myosin/actin -> myosin released -> ATP hydrolysis happens -> myosin head binds new actin site -> Power stroke -> ADP release -> Rigor |
If muscle is stimulated repeatedly there is insufficient time for SR to reaccumulate Ca and Ca concentration never returns to low level. This is called | Tetanus |
Smooth muscle function | produce motility, propel urine along ureter and maintain tension in blood vessel walls |
Where are single unit smooth muscle found | GIT, bladder, uterus, and ureter cells (all use gap junctions as low resistance pathways |
Where are multi unit smooth muscle found | iris, cilliary muscles of the lens, and vas deferens. all are densely innervated by postganglionic fibers of parasymp and symp nervous system |
What are the types of Ca channels in smooth muscle | Voltage gated Ca channel, Ligand gated Ca channel, IP3-gated Ca channel (opens channels on SR) |
Where is Ca stored in Smooth muscle | Extracellularly |
What is used instead of troponin in smooth muscle | Calmodulin |
Tension developed by simply stretch a muscle to different lengths | Passive tension |
Tension developed when a muscle is stimulated to contract at different preloads | Total tension |
Tension that is determined by subtracting passive tension from total tension | Active Tension |
Excitation-contraction coupling in smooth muscle (excitation part) | 1)AP->opens volted gated Ca channels->increase IC Ca concentration 2)Ligand and IP3 gated Ca channels also contribute to increase 3)Ca binds calmodulin->activates myosin-light-chain kinase |
Excitation-contraction coupling in smooth muscle (contraction part) | 4)Phosphorylation of myosin light chain->increase ATPase activity->myosin binds actin 5)relaxation occurs when IC Ca concentration falls |
Is myosin ever not bound to actin | NO, it is just loosely bound during latch-bridge formation |
What is a Dystonia | Excessive, sustained, involuntary muscle contraction/spasm |
What are some types of dystonia | Spasmodic torticollis, blepharospasm, embouchure, writer's cramp |
What is thought to cause dystonia | Imbalance in input to motor neurons; too little inhibitory compared to excitatory |