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Physiology Exam I
Answers questions involving the key concepts
Terms in this set (75)
Why is the cell considered the basic unit of life?
Smallest, self-replicating unit of integrated function; The smallest component of an organism that is "alive"; Multicellular organism is made up of different cells
Why do cells have structural and functional similarities and differences?
1. Different expression of genes at different times (or similar genes)
2. Environmental factor influence
Name two examples of a change in gene expression in response to external signals?
1. Mast cell can produce more histamine in response to an allergen binding to IgE on its surface
2. Change in neuron gene expression in response to inflammation. Inflammation -->release of mediators (bradykinin) --> bind to receptors on nerve cells --> upregulates the expression of 156 genes in the nerve cells that innervate the skin
Messenger molecules released from the cell membrane target the endoplasmic reticulum to cause the release of?
Name the 6 functions of the cell membrane.
1. Mechanical Structure: Defines/encloses the cell
2. Selective Permeability
3. Active transport
4. Bulk transport: endocytosis and exocytosis
5. Markers and signaling (cell-cell recognition)
6. Metabolic activities
What are the two types of membrane proteins?
1. Integral proteins - embedded in and anchored to cell membrane
2. Peripheral proteins - not embedded in membrane
Name 6 membrane proteins and function.
1. Ion channels: gate the flow of ions across the cell membrane; establish resting membrane potential, control flow of ions across secretory and epithelial cells, regulate cell volume
2. Transporters: transport of specific substances across the membrane (active and passive)
3. Receptors: communication between cell and outside world; activated by hormones or neurotransmitters (ex: G-protein coupled receptor)
4. Enzymes: rxn typically results in liberation of signaling proteins from membrane or modulation of activity of membrane-resident proteins
5. Cell recognition (ID) proteins: allow immune system to ID cells
6. Linker proteins: interact with cytoskeleton to affect shape of cell and environment
What is potassium's equilibrium potential?
What is sodium's equilibrium potential?
What is Chloride's equilibrium potential?
What is the effect of solute concentration gradient on diffusion rate?
As the concentration gradient increases, the rate of diffusion increases
What is the effect of membrane surface area on diffusion rate?
As the surface area increases, the diffusion rate increases
What is the effect of lipid solubility on diffusion rate?
As the lipid solubility increases, the diffusion rate increases
What is the effect of solute molecular weight on diffusion rate?
As the molecular weight increases, the diffusion rate decreases
What is the effect of membrane thickness on diffusion rate?
As the membrane thickness increases, the diffusion rate decreases
How can electrical charge influence diffusion rate?
Equilibrium potential is the diffusion potential that would have to exist across the membrane to prevent the movement of an ion down its concentration gradient. The ion will favor flowing in the direction that will cause the membrane to become closer to the equilibrium potential.
What are the differences/similarities between simple and facilitated diffusion?
Similarities: passive diffusion
- Facilitated is faster with carrier protein mediation, but has a transport maximum
- Facilitated carrier proteins can become saturated
- Facilitated displays stereo selectivity
- Facilitated exhibits substrate competition
What is the difference between primary and secondary active transport?
Similarities: Active, carrier mediated
- Secondary relies on the Na+ gradient developed by the Na+/K+ pump
- Secondary involves Na+ transported downhill while another solute is transported uphill
What variables determine osmotic pressure?
1.The difference of solute concentration between the 2 compartments (concentration and osmoles)
2. Solute permeability to membrane (reflection coefficient)
3. Temperature, gas constant
What are the basic structural components of neurons?
-Axon: generation and conduction of action potentials
-Axon terminals (synapses)
What is the resting membrane potential of a cell?
Roughly between -65 through -60 mV. This is maintained by active transport of the Na/K ATPase
Which ion can freely flow across the membrane at rest?
Consider a hypothetical cell with a plasma membrane, which is only permeable to Cl-. What would be the membrane potential of the cell?
Equal to the Cl- equilibrium potential
If at rest the membrane is mostly permeable only to K+, then why isn't the resting membrane potential equal to the equilibrium potential of K+?
Na/K ATPase is pumping K+ in an prevents K+ from reaching electrochemical equilibrium.
The flow of K+ ions across the membrane at rest creates what kind of current?
A weak outward current
If the resting potential is -60 mV, opening of chloride channels (ECl=-70mV) results in
Hyperpolarization of the membrane potential
List the steps of an action potential after threshold.
1. Activation of VG Na+ channels
2. Na+ flows in, Vm approaches ENa+
3. VG Na+ channels inactivate, VG K+ channels open
4. K+ flows out, Vm approaches EK+
5. Na/K ATPase restores chemical gradient
Consider a mutation in the voltage-gated Na channel that causes the inactivation gate to close later. How will the shape of the action potential be affected?
The duration will be increased
Explain the mutation that arithromyalgia in the action potential?
Mutation in the Na+ channel, opens at a more hyperpolarized voltage which leads to extreme swelling
Why is propagation unidirectional?
How can time and length constants create a higher conduction velocity?
Small time constant and large length constant
How does myelination effect the the axon resistance?
Myelination increases the membrane resistance of the axon which leads to a larger length constant (increases conduction velocity)
When the neuron is at rest and the K+ leak channels are open, the concentration gradient drives K+ _______ (out of/into) the cell, and the voltage gradient drives K+ ______ (out of/into) the cell. The result is a weak __________ (inward/outward) current.
When suprathreshold depolarization opens voltage-gated Na+ channels and initiates an action potential, the concentration gradient drives Na+ ________ (out of/into) the cell, and the voltage gradient drives Na+ _______ (out of/into) the cell. The result is a strong _________ (inward/outward) current.
When voltage-gated K+ channels are activated during an action potential, the concentration gradient drives K+ _______ (out of/into) the cell, and then voltage gradient drives K+ _________ (out of/into) the cell. The result is a strong _______ (inward/outward) current.
What is the order of events that occur in the presynaptic terminal?
1. Action potential reaches presynaptic terminal
2. Depolarization of presynaptic terminal
3. Activation of VG Ca2+ channels, Ca2+ influx
4. Vesicle fusion
5. Clearance of neurotransmitter
6. Vesicle recycling
What is the difference between ionotropic and metabotropic receptors?
Ionotropic = ligand-gated ion channels
Metabotropic = G-protein coupled receptors to ion channels
What are neuromodulators?
Substances that act on the presynaptic cell to alter the amount of neurotransmitter released in response to stimulation. Alternatively, a neuromodulator may be cosecreted with a neurotransmitter and alter the response of the post synaptic cell to the neurotransmitter
What are neuropeptides?
Synthesized in the nerve cell body. Function as neuromodulators, neurohormones and neurotransmitters. Peptide is delivered to secretory vesicles. Vesicles are moved down the nerve by axonal transport to presynaptic terminal
What is the main excitatory neurotransmitter in the CNS?
How are IPSPs produced?
By opening Cl- channels, hyperpolarizing the membrane. Examples of neurotransmitters that cause this are GABA and glycine.
What is the difference between axodendritic, axosomatic, axoaxonic?
Axodendritic-synapse between axon of one neuron and dendrite of another.
Axosomatic-synapse between axon of one neuron and cell body of another.
Axoaxonic-axon of one neuron in contact with axon of another neuron.
Explain the difference between spatial summation and temporal summation
Spatial summation - stimulation occurs at different sites at the same time.
Temporal summation - stimulation occurs at the same location, but at different times.
Propose an ionic mechanism for achieving presynaptic inhibition.
-Inhibition of VG Ca2+ channels
-Activation of K+ channels to hyperpolarize the cell
-Activation of inhibitory presynaptic ligand-gated channels (GABA)
What is the basic function of muscle?
What is the location of the cell bodies of neurons that innervate skeletal muscle?
In the spinal cord
Describe the sequence of events for neuromuscular transmission.
1. Action potential travels down the motor neuron into the presynaptic terminal.
2. Depolarization of the presynaptic terminal opens Ca2+ channels and Ca2+ enters.
3. ACh is extruded into the synapse by exocytosis.
4. ACh binds to nicotinic ACh receptor on the motor end plate.
5. Channels for Na+ and K+ are opened on the motor end plate
6. Depolarization of the motor end plate cause action potentials to be generated in the muscle
7. ACh is degraded to choline and acetate by acetylcholinesterase
Name and describe two diseases of the Neuromuscular junction.
1. Canine Myasthenia gravis: autoimmune disease, where the body produces antibodies targeted against the acetylecholine receptor on the postsynaptic membrane in the neuromuscular junction --> muscle fatigue and weakness [treated with anticholinesterase inhibitors like neostigmine]
2. Tick Paralysis: produced by a toxin present in the saliva of gravid ticks that has inhibitory effects on the presynaptic release of acetylcholine
Name neuromuscular toxins and describe their mode of action.
1. Pesticides (cholinesterase inhibitors) - bind to acetylcholinesterase and prevent it from degrading ACh; causes spastic paralysis and possible suffocation
2. Botulinus Toxin - blocks ACh release from presynaptic terminals; leads to paralysis of respiratory muscles -->death.
3. Curare - competes with ACh for receptors on motor end plate; leads to Flaccid paralysis (limp muscles) due to curare that competes with ACh
Describe the structure, location and function of thick filaments.
-Structure: Made of heavy and light chains; heads contain ATPase activity, ATP binding and actin binding sites; Tails have alpha helical helixes that associate with other tails to form a thick filament.
-Location: within the A band of a sarcomere, interact with actin on both sides
-Function: Cross bridge cycling with actin
Describe the structure, location and function of thin filaments
-Structure: actin is a globular protein which polymerizes; tropomyosin are paired helices; troponin has 3 sites (T, I, C) which bind to tropomyosin, actin, and calcium; 7 actin to 1 tropomyosin to 1 troponin
-Location: attach to the Z disk scaffolding comprised of alpha-actinin
-Function: engages with myosin for cross bridge cycling
Describe the structure, function and location of T-tubules.
-Structure: plasma membrane extensions, interior is same as interstitial fluids
-Location: invaginate into the muscle cell
-Function: action potentials go through T-tubules; have proteins called "voltage sensors" that interact with ryanodine receptors
Describe the structure, function and location of the sarcoplasmic reticulum.
-Structure: contains storage protein called calsequestrin in terminal cisternae; the Ca2+ channels are ryanodine receptors
-Location: near T-tubules
-Function: primary Ca2+ storage site in skeletal muscles; depolarization of T-tubules triggers Ca2+ release from SR; Ca2+ is reaccumulated into SR via Ca2+-ATPase
Describe the steps of excitation-coupling.
1. Action potential in muscle membrane.
2a. Depolarization of T-tubules
2b. Opens SR Ca2+ release channels (ryanodine receptors)
3. Increase in intracellular Ca2+ concentration
4. Ca2+ binds to troponin C
5. Tropomyosin moves and allows interaction of actin and myosin
6. Cross bridge cycling and force generation
7. Ca2+ reaccumulated by SR
What would be the effect of inhibiting SR Ca2+-ATPase on muscle contraction?
No relaxation, Ca2+ not able to be taken up into the SR.
What would be the effect of an activating mutation in the RyR Ca2+ channel on muscle contraction?
Ca2+ would be released from the SR and there would be cross bridge cycling and muscle contraction. This could lead to constant muscle contraction.
When in the cross-bridge cycle does the myosin ATPase split ATP and when does the myosin head undergo a conformational change?
1. The ATP is split when the myosin head moves towards the positive end of actin.
2. A conformational change occurs when ATP binds to the myosin head and when ATP hydrolysis occurs
What would be the effect of limiting ATP concentrations on muscle contractility?
If ATP cannot bind to myosin as often then the myosin head would be stuck in rigor more often.
Explain the structural basis for the length-tension relationship.
-Ascending limb: Force reduced due to Steric interference
-Plateau: Maximal isometric force
-Descending limb: Force reduced due to reduced overlap
-tension developed by simply stretching a muscle to different lengths
What is the difference between isometric and isotonic contraction?
-Isometric: force generation with no change in length, tension generated by actin/myosin interaction
-Isotonic: shortening against a constant load
What is the difference between summation and tetanus?
-Summation: two stimuli that occur close together in time will produce a greater force than produced during a single twitch.
-Tetanus: sustained contraction of maximum force due to high frequency stimulation
Describe the effect of load on the shortening velocity.
At an afterload of 0, the initial velocity of shortening is at Vmax. As the afterload increases, the velocity decreases. Different preload resting lengths impact how quickly or slowly the velocity decreases with increasing afterload.
Describe the anatomic and functional properties of motor units.
-Anatomic: consists of a motor neuron and the collection of muscles it innervates; smaller diameter=slower muscle speed and vice versa; large diameter cells are white in appearance where lesser sizes are red.
-Functional: fine motor control for small muscle cells to control delicate tasks; load based control involves first small fatigue resistant muscle fibers, the larger muscle cells are added as the load increases, the largest muscle cells are recruited last
Describe the basis of muscle remodeling.
-Hypertrophy results from myofibrils splitting as more thick and thin filaments are synthesized; results due to contractions at maximal force
-Atrophy results from lack of use or denervation
Describe rigor mortis.
When ATP becomes limiting a little bit after death, myosin heads can no longer be released from actin and rigor bonds result.
Describe the relationship between muscle fiber length and the magnitude of force generation.
Muscles in vivo are attached at positions near the joint and have resting lengths close to Lo. At Lo there is a maximum degree of crossbridge overlap which provides potential for maximum force generation.
Name the major sites of smooth muscle in the body.
1. Vascular - regulation of blood pressure
2. Airway - constriction and relaxation
3. GI - peristalsis, segmentation, transit
4. Gallbladder - storage, emptying
5. Uterus - accommodation, delivery
What are the structural characteristics of smooth muscle?
-can be multi-unit or single-unit
-there are actin and myosin filaments
-dense bodies are a focal point for actin filaments
-Gap junctions allow for ion and metabolite flow between cells
-calveolae are involved in the spread of depolarization
-sarcoplasmic reticulum is more scattered and less developed than skeletal
Name and describe the multiple sources of Ca2+ to trigger contraction.
1. Depolarization -->opens VG Ca2+ channels --> Ca2+ induced Ca2+ release from SR
2. Hormones or Neurotransmitters --> opens ligand gated Ca2+ channels --> Ca2+ induced Ca2+ release from SR
3. Hormones of Neurotransmitters --> IP3 -->Ca2+ release from SR
Describe the process from Ca2+ release to Cross-Bridge cycling.
1. Increase in Ca2+ concentration
2. Ca2+-calmodulin complex formed
3. Complex activates myosin-light-chain kinase (MLCK)
4. MLCK phosphorylates myosin light chains
5. Increase in myosin ATPase
6. Phosphorylated myosin binds to actin
7. Cross bridge cycling and tension
What kind of regulation is involved with actin/myosin interaction in smooth muscle?
Cross-bridge activation via Ca2+ release from the SR. Activation of MLCK leads to the phosphorylation of myosin light chains which allows myosin to attach to actin. To relax the muscle, MLCK Phosphatase can dephosphorylate the light chains to inhibit cross-bridge formation. Or, the sarcoplasmic Ca2+ can be lowered through SR Ca2+-ATPase or sarcolemma Ca2+-ATPase.
Name some disorders of smooth muscle.
1. Airway: Asthma
2. Vascular: Hypertension
3. GI: megaesophagus, delayed gastric emptying, intestingal ileus, constipation.
What is the difference between phasic and tonic smooth muscle contractions?
1. Phasic is a twitch
2. Tonic is tetanus
Describe muscle defects with respect to Malignant Hyperthermia.
-After stopping anesthesia, the horse experienced muscle regidity
-After death, the horse experienced rapid rigor mortis
-Alteration in Excitation Contraction Coupling include mutations in the skeletal muscle ryanodine receptor leads to abnormally induced and/or prolonged open state
-MH results from uncontrolled muscle Ca2+ release
-Increased Ca induced Ca release
-Enhanced T-tubule depolarization
-Myoglobinuria - brown colored urine indicating muscle degeneration.
Describe possible treatments for Malignant Hyperthermia with respect to the muscle defects.
Give Dantrolene - muscle relaxant that abolishes excitation-contraction coupling; decreases intracellular Ca likely via ryanodine receptor
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