P Exam 1

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What % of body mass is blood volume?: 8%
What's hematocrit?: % of blood volume occupied by RBC
Increase in sweating leads to an increase or decrease in hematocrit?: Increase
Plasma vs serum: Plasma if it doesn't clot:clotting factors present
Serum if it clots: clotting factors inactive/destroyed in the presence of a clot
[Na]out: 135-145 mEq/L
[Na]in: 10 mEq/L
[K]in: 140 mEq/L
[K]out: 3.5-5 mEq/L
[Ca]in: 0.1microM
[Ca]out: 8.5-10.5 mg/dL
[Cl]in: 5 mEq/L
[Cl]out: 95-105 mEq/L
[Glucose]in: variable
[Glucose]out: 70-110mg/dL
pH of blood: 7.35-7.45
Osmolarity of blood: 280-300 mOsm/kg water
pH formula: pH = -log[H]
What % of body mass is TBW?: 60%
TBW (42L)=: ICF (28L)+ ECF(14L)
ECF=: ISF (10.5 L) + blood plasma (3.5 L) + transcellular fluids (usually ignored)
Temperature depends on?: Heat input and heat ouput via metabolism, conduction, convection, evap, and radiation
Your ability to thermoregulate in the heat depends on?: Sweat rate
Sweat rate depends on?: TBW
avg metabolic rate: 2400kcal/day 100kcal/hr=100W
Which heat exchange is b/n 2 surfaces in direct contact?: conduction
Which heat exchange is from a surface to a gas or fluid?: convection (via air or water)
Ex: lose heat when jumping into cold pool
Which heat exchange is b/n the body and its surroundings by electromagnetic waves?: radiation
When is radiation most important in losing heat?: At rest, and normal ambient temperatures, radiative heat loss is about 50% of the total heat loss
To increase rate of evap, NaCl must be ...: decreased because the presence of NaCl lowers the vapor pressure of water
How do you maintain a constant TBW?: ingest as much water as you sweat
What parts of the body are more important than others in providing cooling thru sweating?: scalp, face, upper torso
What does evap depend on?: air dryness and movement
Humidity decreases evap heat loss
When does heatstroke occur?: when you produce more heat than you can loose therefore increasing core temp
What tells the hypothalamus to change the Tset?: pyrogens/cytokines
Are changes in Tcore or Tsk more important?: Tcore 9x more important
Hyperthermia: Increase in Tcore b/c of exercise
Fever: Increase in Tcore b/c of bacterial toxins
Exertion =: Heat generation
What changes result in acclimatization?: increased sweat rate, decreased NaCl content of sweat, increased ECF volume
Where is BFsk highest?: face, ear, neck, palms
what feature of acclimatization is most important?: increased sweat rate because more evap
which types of proteins are freely diffusable on the surface? and capable of lateral diffusion?: peripheral proteins
purpose of dystrophen-associated protein complex (DPC)?: required for membrane "tightness of fit" to cytoplasm.
The DAPC is thought to play a structural role in linking the actin cytoskeleton to the extracellular matrix, stabilizing the sarcolemma during repeated cycles of contraction and relaxation, and transmitting force generated in the muscle sarcomeres to the extracellular matrix
Mechanism of muscular dystrophy: Lack of dystrophin gene means the sarcolemma is not attached to the cytoskeleton. During contractions, the sarcolemma is not "in sync" with the interior of the cell. Loosness of sarcolemma permits membrane Ca channels to open.
In terms of muscular dystrophy, an increase in [Ca]in does what?: activates proteolytic enzyme, CALPAIN, which acts to digest proteins (contractile) making the muscle weaker
Formula for rate of diffusion.: Rate = KT AD(C1/C2)/X

K=partition coefficient
A=area
D=diffusion coefficient
T=absolute temp
How does temp affect rate of diffusion?: increase temp = increase rate
How does surface area affect rate of diffusion?: Increase area = increase rate
How does distance affect rate of diffusion?: Increase distance = decrease rate
What is the driving force for rate of diffusion?: concentration gradient. The greate the concentration gradient, increase in rate
How does molecule size affect diffusion coefficient?: Increase in molecule size = decrease in diffusion coefficient.
Smaller molecules diffuse faster!
What is the partition coefficient?: measure of a molecule's ability to dissolve (Hydrophobicity). Increase in K=Increase in rate.
K=Cm/Caq
What uses aquaglyeroporins?: water, glycerol,urea
What requires transporters?: large, uncharged polar molecules/ ions/ glucose/ sucrose
What can diffuse through the membrane?: Sterols (very lipid soluble), 02, CO2, N2
Depends on the molecules solubility in LIPIDS
What are some example of factors that cause defects in membranes allowing diffusion of stuff that shouldn't?: Severe stress
Heart attack (severity is determined by the amount of troponin present in plasma that leaked out)
GLUTs are examples of?: Carrier proteins involved in facilitated diffusion.
Uniporters
How many molecules move thru a uniporter at a time?: one molecule at a time
Explain GLUT transporters and how they work: hexose transporters
large integral membrane proteins
12-membrane spanning regions
glycosylated on one extracellular loop
They move sugars by undergoing conformational changes which "flips" the transporter b/n alternate states allowing transport in either direction
Does facilitated diffusion require energy? In what direction do they move molecules?: No additional energy needed for transport
Movement of molecules DOWN their conc. gradient
What are symporters?: Cotransporters involved in transport/diffusion of MORE THAN ONE molecule going in the SAME direction
EX: SGLT1 (Na/Glucose symporter)
SGLT cotransporter: Moves glucose against its conc. gradient
Requires a high conc of Na
Na first binds to neg.charged protein symporter to allow glucose to bind with high affinity.
2 Na/ 1 Glucose move into cell
Examples of Antiporters: Na/H
Cl/HCO3
3Na/Ca
Action of antiporters/exchangers: use energy of one ion (usually Na) to drive another molecule in OPPOSITE direction
What type of tranporter is Na/K/2Cl?: cotransporter located in muscle/kidney turned on by cAMP
What type of transporter is Na/Ca?: exchanger/antiporter
action of Na/K/2Cl (NKCC): to restore normal electrolyte balance in muscle, and kidney reabsorption of Na and water
Where is NKCC mainly? FXN?: musle and kidney
muscle: restore normal electrolyte balane
kidney: reabsorption of Na and water
How do voltage gated channels open?: in response to changes in Em
How do ligand-gated channels open?: in the presence of an extracellular or intracellular ligand
How do mechanically gated channels open?: application of a mechanical force ie. stretch receptors
Purpose of Na/K ATPase?: maintain gradients: Na wants to enter and K wants to leave
Also, maintain [Na] gradient which drives other ions uphill or downhill
3Na out, 2 K in maintaining negative resting Em
When do transporters require energy?: when molecule(s) is moving against its concentration gradient
What are the 3 types of cell surface receptors?: channel-linked R
enzyme-linked R
G-protein linked R
A receptor with a high affinity for a ligand requires a high or low [ligand]?: low ligand concentration
What is the most important channel and how does it work?: Na channels
1. the channel is closed when the gate is closed and ball/chain gate opened
2.the channel is open with gate is open and ball/chain is open allowing Na in
3. channel is locked when ball/chain closes and gate is open
4.both gates close and channel is once again closed
What does a high electric field do to a protein?: changes its shape therefore its activity (shape change causes channel to open due to high voltages)
Activation does what to a channel? Inactivation?: activation opens a channel by voltage changes. inactivation closes a channel by a delayed or slower process
If you are constantly stimulating the channel with voltage, will the channel stay open?: NO, channel will close and reopen if voltage, time are adequate
Are voltage gated or ion gated channels more selective for ions?: v-gated
What toxins block voltage gated Na channels?: TTX (puffer fish)
Saxitoxin (red tide)
What toxins block voltage gated K channels?: Dendrotoxin (black mamba)
TEA
What toxins block Ach receptors or channels?: Tubocurarine, bungarotoxin, cobrotoxin
In comparing pores, channels, and transporters, what is the fastest? slowest?: pores-fastest
transporters/ATPase pumps-slowest
What pump is involved in several pathologic states such as heart disease and hypertension?: Na,K ATPase
Difference b/n primary and secondary transporters?: primary uses ATP directly
secondary uses ATP INDIRECTLY
How does the heart relax?: Ca pumps and Na/Ca exchanger pump free Ca back into stores and out of the cell lowering [Ca]in. The higher [Ca]in persists, the more powerful the heartbeat. If you increase [Na]out the faster the heart will relax
What happens to the force of contraction if the Na/Ca exchanger slows down?: the more powerful the contraction
Effect of digitoxin(cardiac glycosides) on heart?: digitoxin poisons Na/K ATPase therefore increasing [Na]in and lowering the gradient for the Na/Ca exchanger. Heart now beats with more force!
What are some examples of diseases that are connected to impaired fxn of aquaporins?: diabetes insipidus (kidney can't resorb water fast enough leading to polyuria, polyipsia)
congenital cataracts
In the case of diabetes insipidus, where is the mutated aquaporin found w/n the cell?: on the basolateral membrane instead of the APICAL membrane
What causes the insertion of AQP2 into the CT membranes?: Vasopressin, it also INCREASES the activity of those urea transporters w/n 2 min by phosphorylation
What is the action of the antibiotic peptide Gramicidin A produced by soil bacteria?: inserts pores in the cell wall of bacteria that leaks K out and Na in, destroying the Em leading to bacteria death! (When channels can't open or close you die!)
Why is precise control of free [Ca] in essential?: b/c if you increase Ca throughout the cell, it turns on too many chemical rxns and cell dies
What are L-type vs T-type Ca channels?: L-long lived as a group (open for a long period of time)
T-transient as a group (more Ca is let in, but rapidly closed)
What does osmolarity tell us?: The # of PARTICLES of solute in a given volume
more particles=greater osmotic effect
What is tonicity?: the DIFFERENCE in osmotic presure b/n one side of a membrane and the other
What effect will a hypertonic soln have on the cells?: Will draw water out of cells
What effect will a hypotonic soln have on cells?: will force water INTO cells (b/c water can pass freely across cell membranes and solutes cannot)
Concentration gradient has what effect on osmotic pressure?: the greater the conc gradient, the greater the osmotic pressure
What is osmotic pressure?: the pressure needed to push back the water across the semipermeable membrane so that the heights are the same.
A sudden change in plasma osmolarity of more than 1mOsm is very dangerous b/c it takes only 1 or 2mmHg prssure to occulude a capillary
What happens to plasma osmolarity when you sweat?: you lose mainly water in sweat so plasma osmolarity increases and water leaks out of cells...signal is sent to brain saying "im thirsty"
How can you die of water intoxication?: blood become hypotonic and water leaves to enter cells which are hypertonic. cells enlarge until they can no longer expand any more. Increase in fluid in brain which squeezes down on diameter of blood vssls until no more blood flow
What is hyponatremia?: excessive loss of sweat (and production of sweat) due to drinking too much before and during prolonged exercise
Decrease in plasma osmolarity..swelling!
What channel(s) is responsible for the resting Em?: K leak channels which allow K to leak OUT creating a neg resting Em
Voltage gated K channels are responsible for what?: repolarization vs Kleak responsible for resting Em
What does action potential speed depend on?: diameter of axon. increase axon=increase speed of action potential
Effect of increasing [K]out?: depolarize Em b/c gradient decreases
Why is the Nernst eqn not perfect?: it only accounts for one ion at a time...doesn't account for the other ions that also leave
What does LOW [Na]out do to Em?: not much change..b/c resting Em depends on K conc gradient
What does the Goldman-Hodgkin-Katz eqn take into account that the Nernst eqn doesn't?: permeability of Na, Ca, and Cl in addition to K
Besides conc gradient, what must the resting Em also take into account?: diffusion potential.
Few Na allowed to get inside when K leaks out therefore inside cell actually less neg
What is spatial summation?: 2 signals at DIFFERENT spots on neuron leads to reaching threshold
What is temporal summation?: 2 signals at SAME spot on neuron leads to reaching threshold
Action of excitatory inputs on membrane? inhibitory?: excitatory: depol
inhibitory: repol
What is the difference in speed b/n electrical synapes and chemical synapses?: electrical are faster (takes microseconds to reach post-m)
chemical synapses take 0.5 milliseconds-synaptic delay greater in POST-synaptic mem
Electrical has 1 or more gap jxns (connexon channels) that are permeable to small ions
How many R's must be bound w/n post to stimulate a depol?: 30-50! single bound R will NOT stimulat AP
What is a motor unit?: a neuron and all the muscle fibers it innervates (motor unit is what is affected by AP, not just indiv. fibers)
What are the 2 different Ach R's?: muscarinic: transmembrane proteins that interact with G proteins
nicotinic: voltage-gated ion channels
What happens to the Ach after it is used?: reuptake/recycled by V-type H-ATPase channels return Ach to vesicles OR
breakdown by AchE in cleft
Opening of what channels leads to excitatory signals? inhibitory?: excitatory: Na
inhibitory: K, Cl
Where are vesicles and peptide NTs made? How are they transported?: made in golgi/soma
transported in vesicles via tubulin to terminals
Where are NON-petide NTs made?: made at the nerve terminal where they are packaged into vesicles (Ach)
Describe the channels on the post-synaptic membrane.: they are built in receptors that bind NT and cause the channel to open letting ions in
What is happening at the NMJ?: 1. syn of NT, vesicle packaging
2.AP reaches terminal
3.depol. opens N-type VGCC
4.Ca influx
5.vesicles fuse with pre-syn membrane
6.transmitter released into cleft
7.NT binds R on post-syn
8.channel opens
9.Em changes
10.recycling of membrane due to increase area of membrane-need to take up extra membrane to make vesicles
What are the exocytosis proteins present on the inside pre-syn membrane?: syntaxin
SNAP-25
What are the exocytosis proteins present on the outside of synaptic vesicles?: synaptobrevin
synaptotagmin
What exocytosis protein inhibits syntaxin?: n-Sec 1 (in nerve terminal)
Role of synaptobrevin?: interacts w/ synaxin and SNAP-25
Role of synaptotagmin?: binds Ca
Stages of exocytosis of NT?: 1. AP reaches NT
2. n-Sec1 released from syntaxin (by voltage)
3.syntaxin and SNAP-25 form complex on terminal membrane
4.synaptobrevin winds around Syntaxin-SNAP complex forming ternary complex
5.all 3 S's form tight bundle of alpha helices drawing vesicle and presyn membranes closer together (complex contracts)-tightening
6.Ca binds to synaptotagmin-membrane fusion
7.alpha-SNAP and NSF cause dissasembly of SNARE complex w/ ATP
8.SNARE recycled
Name 2 drugs that enhance NT release.: TEA (Tetraethyl Ammonium): K channel blocker prolonging the length of the presyn AP
alpha-Lactrotoxin (black widow):increases NT release by emptying terminals of vesicles
What is omega conotoxin?: neurotoxin that IRREVERSIBLY blocks N-type Ca channels to inhibit exocytosis of NT
abolishes EPPs and EPSPs
What is Botulina toxin?: one of the most potent bacterial toxins
hydrolyzes SNAREs preventing exocytosis
Botulina can cause death how?: by suffocation b/c can't contract repiratory mm
OR
death by flaccid paralysis
High doses of botulina causes what? Low doses?: high: paralysis
low: antispasmotic agent (Botox)
What synapses does botulina act upon?: Most synapses
What is Tetanus toxin?: -one of the most potent bacterial toxins
-proteolytic enzyme that acts to inhibit inhibitory neurons blocking exocytosis of glycine which acts to prevent spontaneous contractions (by hyperpol membrane)
A person with tetanus would have?: spontaneous contractions (due to the fact that glycine release is being inhibited by the toxin
What is the purpose of inhibitory neurons?: to prevent your from using your max strength (inhibitory system inhibited during severe stress)
What happens after tetanus toxin enters through bloodstream?: enters nerve and "back tracks" up through axon until binds to and inhibits nerve terminals of glycine
What do we use for tetanus therapy?: Tubocurarine (decrease m contractions)
oxygen
Antibiotics
What is an example of a non-chemical warefare weapon and what does it cause?: Brucella
fever, drenching sweats, incapacitating headache, backpain
What happens during IPSP?: GABA or glycine release opens Cl channels
influx Cl-hyperpol
outflux K-hyperpol
What happens during EPSP?: Ach release opens Na channels
influx Na-depol
What do inhibitory neurons secrete?: glycine and GABA (open Cl channels)
How specific are ligand gated channels?: 90% specific for that ligand
10% specific for another
When and what inactivates Ach?: after it reaches post-synaptic area by AchE
Where is AchE found?: present in both pre and post synaptic membranes
only want 2 Ach bound to each R, rest is recycled
Why so many Ach molecules/vesicle?: 10000/vesicle
ensures that m. will contract b/c of increased conc. gradient
Describe how Ach R's are postitioned on post-syn membane.: lined up in high density on post across from where vesicles will be released on pre (Ach molecules diffuse 50nm before reaching Rs)
How come Ach causes sk. muscle to contract and heart muscle to relax?: b/c of 2 different Ach R's
1. nicotinic-sk. m Ach release increase Na influx
2. muscarinic-heart Ach release causes K outflux and membrane hyperpolarizes and heart contracts less
What type of channels does PKA open?: Ca and Kvoltage
Describe the AchR in sk. muscle (nicotinic).: 2 Ach activate R by binding to the alpha subunits
beta and gamma won't open channel
How much Ach is needed at motor end plate to get muscle to contract?: 1.3-2 million Ach/stimulus
AchR requires 2 Ach molecules-1 EPP
40-50 simultaneous EPPs needed to depol by 40mv leading to a muscle AP
In a resting cell, what causes spontaneous MEPPs? (pre-syn AP): occasional depol due to spontaneous fusing of vesicles w/ Ach (1 or 2) to membrane releasing contents
-shows the need for inhibitory neurons to block massive secretions of Ach
What is Tubocurarine?: reversible competitive drug of the AchR
-binds to same alpha subunits of R as Ach
What is Pancuronium?: -AchR antagonist used clinically (nicotinic cholinergic blocker)
-used with anesthesia to prevent involuntary or reflex muscle contractions
Effect of Pancuronium on Tetanus patient?: relaxes mm.
What is TTX (Tetrodotoxin)?: -Na channel blocker in NEURON and MEMBRANE
-competitive by mimicking the Na ion
-failure of AP transmission
What are the stges of TTX poisoning?: Immediate: slight numbness of lips and tongue
Stage 1:increase parethesia in face and extremities; headache, nausea, severe ab pain
Stage 2: increase paralysis
Stage 3: CNS dysfxn, complete paralysis, death (50-60% mortality)
What stimulates AchR and what inhibits AchR?: + Ach
+ nicotine
- Tubocurarine
- Bungarotoxin
What inhibits Ach release from vesicles?: Botulinum toxin
Explain myasthenia gravis?: an autoimmune disease in which the body produces antibodies against Ach R's making the R's no longer sensitive to Ach and Na channels don't open
Overall: fewer EPPs, and weakeness of sk. mm
What is the treatment for myesthenia gravis?: increase the duration of EPPs so that they are more likely to reach threshold-use an anti-cholinesterase at low doses (Neostigmine)
What is Neostigmine?: reversible AchEsterase Inhibitor used to treat diseases like myasthenia gravis
Problem with myesthenia gravis? effect on transmisson?: reduces the efficiency of Neuromuscular transmission
transmission rapidly fatigues but can be restored by AchE inhibitors such as neostigmine
-magnitude of APs reduced b/c more and more R's blocked
What do external electrodes measure?: summation of ALL contracting mm
What are vesicants?: chemically burns skin or surface (inside and outside)
What nerve agents are phosphate esters?: GA (Tabun)
GB (Sarin)
GD (Soman)
GF
VX
inhibit AchEsterases
What are the physical properties of phosphate ester nerve agents?: clear, colorless liquids
tasteless, most are odorless
penetrate skin, clothing
Which phosphate ester nerve agent is the most volatile?: Sarin is the most volatile of the nerve agents, which means that it can easily and quickly evaporate from a liquid into a vapor and spread into the environment.
Immediate, but short lived threat
Which phosphate ester nerve agent is the least volatile?: VX-persists b/c it is oily
lethal for months
Units of LD50?: mg/70kg
lethal dose for 50% of population
What is the commone structure of nerve agents?: phosphate double bonded to O
single bonded ester group
Which channels are sensitive to anesthetics?: glycine R's
muscle nicotinic Ach R's
K channels
Na channels
Nerve transmission takes place b/n what?: nerve-nerve
nerve-sk. mm.
nerve-some smooth mm
nerve-exocrine glands
Ach stimulates R site on organ causing the organs to contract
What is the physiology behind nerve agents?: they act to inhibit AchE
therefore less Ach is destroyed causing excess Ach to stimulate organs (channels constantly open and close)--organ overstimulation
Effects of nerve agents on striated sk muscle? exocrine glands?: less effective on sk. m (b/c nictotinic synapses) but still have overstimulation
causes HUGE flow of saliva from exocrine glands
Are nerve agents more potent to muscarinic receptors or nicotinic?: hyperactivity at muscarinic receptors therefore prolonging parasympathetic responses
Only causes little muscle weakness in effecting nicotinic R's
What is the SLUDGE syndrome?: effect of nerve agents on muscarinic R's:
Salivation
Lacrimation
Urination
Defecation
GI Cramping
Emesis
Miosis (small pupils)
What is Atropine?: competitive inhibitor of Ach on muscarinic Ach R's by binding to same place that Ach wants to bind to but does NOT activate them
What is Atropine used as TX for? When must it be administered and how?: used for treating nerve agent poisoning
must be injected immediately after exposure
b/c it is extremely toxic you must only administer 2mg at a time then wait 15 min before giving more
End result: decreases secretions, reverses the spasm or contraction of smooth muscle
medical side effects of atropine?: increased blood pressure, changes in heart rate, amnesia, confusion, excitation
How do nerve agents bind to AchE?: first bind REVERSIBLY to AchEase and inactivate it. Then, after 2-10 min covalent bonds are made and the binding becomes IRREVERSIBLE
What are oximes?: drugs that break the reversible connextion b/n SOME nerve agents and AchE, thus reactivating the enzyme.
Must be given w/n a very few minutes
Used in combo with atropine as therapy
Effect of THC or Marijuana?: reduces or prevents exocytosis decreasing normal nervous transmission
therefore decreasing short term memory, attention span, driving abilty and reflexes
What happens if the same number of same charged ions move in opposite directions across the membrane?: no net change in membrane potential
Is the cell more permeable to Na or K?: K..there are NO Na leak channels
What causes the resting Em?: separation of charges due to K leak channels (more neg inside)...resting Em NOT due to the [K]out versus [K]in
Why is the Em of a resting axon not exactly equal to the Equilibrium of K?: it is slightly less negative than Ek b/c of the small contribution of Na ions that enter the cell
When do Kvoltage gated open?: if membrane is DEpolarized in order to REpolarize the membrane
What happens to the shape of the electronic potential over time after applying a hyperpolarizing stimulus?: decays as a fxn of the distance from the stimulus
What happens to the shape of the AP over time after applying a depolarizing stimulus?: AP remains consistent in magnitude and shape, but the delay b/n stimulus and response increases with distance
What happens to the resting Em when [K]out increases?: more K rushing in--depolarizing Em
What happens to the resting Em when you decrease Na outside?: nothing b/c resting Em depends on K
what happens to the height of the AP when you reduce Na outside?: height of AP decreases
What happens to the height of AP when Na is increased on the outside?: peak ht increases--overshoot
What is the fall in the AP due to?: NOT due to the pumping out of Na..instead due to the exit of K thru voltage-gated K channels
Why is there hyperpolarization?: b/c K channels open too long-more K can leave than Na can enter
Do the Kv channels open before or after Nav channels close during AP?: during.K channels open before Na channel is fully closed
Explain the state of the Na channel gates during resting membrane potential?: the activation gate is closed until cell is depolarized then it opens fast until reaches peak. then inactivation gate slowly closes as AP falls
Why don't we just pump out the Na that entered during AP to return to polarization?: b/c pumps are slower than channels so it makes more sense to open Kv channels
What does reaching threshold depend on?: # of voltage-gated Na channels/area
Not reaching threshold is due to what?: low density of Na voltage channels in area
A low [K]out means what?: low Em (more negative) and less K will enter cell
What is the relationship b/n voltage and distance?: voltage decreases with distance
why does no AP form in the dendrites or soma from local currents?: b/c density of Na-v channels is low and greater depol is reqd to reach threshold than at trigger zone of axon hillock (this is the reason that AP formed at axon hillock proceed forward along the axon)
What is reversed polarization and when does it occur?: as Na enters the cell, the membrane potential is increased towards 0 and keeps going beyond 0mv towards +30 mV (overshoot) b/c of the Na conc. gradient. +30mV is the Na equilibrium potential
What is the absolute refractory period?: period during which a second AP is not possible reguardless of strength or duration of the stimulus
What is the relative refractory period?: period during which a 2nd AP can be generated but at a GREATER VOLTAGE and/or duration
How do strength and duration contribute to reaching threshold?: the greater the voltage you apply, the shorter it takes to reach threshold
What channel types play a role in the cardic AP?: open Nav: peak
open Cav: platea
open Kv: drop
When the inactivation gates are closing what type of refractory period is this?: absolute, b/c the inactivation gates CANT be opened by stimulus and not enough Na channels are available to generate AP.
only activation gates can
What type of refractory period can occur during hyperpolarization when the VGKchannels are still partly open?: relative b/c inactivation gates are open and activation gates are closed
Why can't depolarization spread behind the current AP?: b/c the point behind it is in absolute refractory period
What are 3 factors that influence the speed of conduction?: the diameter of a fiber
temperature
the presence or absence of myelin
What exists b/n areas of myelin on an axon?: Nodes of Ranvier that are UNmyelinated and have high density of Na voltage channels
Why won't areas coated with myelin conduct an impulse?: b/c myelin (fat) acts as an insulator therefore AP's only occur at the nodes and jump over myelin (saltatory conduction)
How does myelin increase the speed of an AP?: b/c w/o myelin, the potential decreases as distance increases. Therefore new AP's are formed at each node
Which is faster: an unmyelinated axon with a large diameter or a myelinated axon that is skinny?: myelinated: speeds up conduction by a factor of 100
Proper fxn of Na channels requires the presence of what?: adequate Ca concentration to bind to Na v channels otherwise they open too easily
Would hypocalcemia increase or decrease nerve excitability?: increase nerve excitability b/c not enough bound to Nav therefore it opens more to increase APs that shouldn't occur (Snowy story)
In terms of the AP, hypernatremia causes what?: overshoot
Height/magnitude of AP depends on what?: both Na and K concentration gradients
Hypo and Hyperkalemia affect what?: resting membrane potential (K concentration)
What is the affect on Em during hyperkalemia?: increased [K]out leads to depolarization b/c K wants to enter
Hypokalemia does what to Em?: cell now requires higher voltage to reach threshold b/c K wants to leave cell hyperpolarizing it
What is an isotonic contraction?: same tension, different length (shortening)
Work done
What is an isometric contraction?: same length, different tension
NO work done
(ex: push against wall)
What is an eccentric contraction?: lengthening of the muscle
slowly lower a heavy load
NEGATIVE work
Which contraction is the most likely to cause injury?: eccentric contraction
can cause rhabdomyolysis
What is the effect of training on muscles?: increases max strength and speeed
What is the purpose of doing warm up exercies before a race?: heat is released when ATP is split, chemical rxns speed up b/c muscle is warmer and muscle develops tension faster
What happens to a muscle when you commence several IDENTICAL stimulations?: tension developed increases over a period of time with stimulus of same strength
Unfused tetanus does what to muscle twitches?: increases frequency of twitches
What is fused tetanus?: double the frequency
reach max. tension
Which contraction produces the greatest tension: twitch or tetanus?: tetanus
contraction of sk. muscle is due to what?: release of Ca from the SR and rise in cytoplasmic [Ca]i
What happens at Z line?: actin attached to Z by alpha-actinin
Describe the polarity of actin and myosin.: opp. polarity
actin points into sarcomere
myosin points outward
What is the bare zone?: region where there are NO myosin heads and NO actin interaction
Fxn of myosin head?: ATPase activity
light chains modify intrinsic speed of m.
Where is titin?: extends from length of Z line to bare zone anchoring think filaments
acts like a spring
Fxn of M protein?: hold the thick filaments in register in the center of sarcomere
I band components?: thin only
H zone components?: thick only
A band components?: thick and thin
each thick surround by 6 thin
each thin surrounded by 3 thick
Which bands/zones of sarcomere shorten with contraction?: H and I
A stays constant
Where do you see double overlap in a sarcomere?: only in heart where thin filaments cross bare zone

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