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Physiology > Phys Exam 1 Memory/Terms > Flashcards

Phys Exam 1 Memory/Terms Flashcards

(60 cards)

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1
Q

Depolarization

A

Decrease in membrane potential
Voltage difference between inside & outside of membrane is less

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2
Q

Hyperpolarization

A

Increase in membrane potential
More difference in voltage across membrane

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3
Q

Membrane Potential (Vm)

A

Difference in voltage across membrane

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4
Q

Resting membrane potential (Vr)

A

Voltage across membrane when cell is inactive

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5
Q

Capacitance

A

Membrane’s ability to store charge

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6
Q

Conductance (g)

A

ease of flow

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7
Q

Current (I)

A

Change in ion conductance

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8
Q

Equilibrium Potential of K+

A

-90 mV

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9
Q

Equilibrium Potential of Na+

A

+60 mV

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10
Q

Equilibrium Potential of Ca2+

A

+120 mV

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11
Q

Equilibrium Potential of Cl-

A

-70 mV

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12
Q

Ohms Law

A

V=IxR
Voltage = Current x Resistance

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13
Q

Contractility

A

Cardiac muscle’s ability to change force of contraction w/o changing muscle length

Occurs by change in Ca regulation
Activates sympathetic nervous system for increase of NE release

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14
Q

Gs (type of G protein-coupled receptor)

A

increase AMP | inhibit MLCK | stimulate SERCA
=relaxation

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15
Q

Gi (type of G protein-coupled receptor)

A

decrease cAMP | promote MLCK | inhibit SERCA |
=contraction

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16
Q

Gq (type of G protein-coupled receptor)

A

produce IP3 / DAG | Ca2+ release from SR | activates PKC
=contraction

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17
Q

Contraction Mechanism for Smooth Muscle

A

Ca2+ in | Calmodulin binds to Ca2+ | MLCK activated | phosphorylation of MLC | cross bridge formation | myosin flexibility =contraction

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18
Q

Relaxation Mechanism in Smooth Muscle

A

Ca2+ out of cell | decrease MLCK | dephosphorylate MLC | decrease myosin flexibility
= relaxation

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19
Q

Dystrophin & Role in Muscular Dystrophy

A

Binds sarcomere to outside of cell
Mutation = damage/wasting overtime with stretch (MD)

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20
Q

Order of Motor Unit Recruitment

A

Type I (slow/deep) –> Type II (fast/superficial)

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21
Q

Twitch

A

Muscle contraction from single action potential

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22
Q

Summation

A

combination of EPSPs & IPSPs which can form an Action Potential

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23
Q

Type I Motor Unit

A

Slow oxidative | Low myosin ATPase | Low SERCA | Lots mitochondria | Energy-conservative | Deeper | More excitable
“fine” motor control | fatigue-resistant | small neurons

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24
Q

Type IIA Motor Unit

A

Fast-oxidative | quick shortening | high myosin ATPase | medium SERCA | lots mitochondria

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25
Type IIB Motor Unit
Fast-glycolytic | fastest shortening | high myosin ATPase | high SERCA | low mitochondria | fatigue common
26
Velocity of Muscle Fiber Contraction
Increase Myosin ATPase = increase velocity contraction Determined by alpha motor neuron innervation
27
Power in Muscle Fiber
Greater velocity via Myosin ATPase = greater Power!
28
Force-Velocity Relationship in Muscle
Increase load = Decrease shortening velocity Fastest contraction w/ 0 load
29
Active Force
F produced by actin-myosin cross-bridges
30
Passive Force
F produced by titin & connective tissue (elasticity, wants to go back to resting length) Increase PF = increase muscle stretch
31
Optimal Length (Lo)
Where most active cross-bridges are formed in muscle to produce the maximum force (in middle of how far sarcomere can be stretched)
32
Isotonic Contraction
eccentric (longer fibers) & concentric (shorten fibers) Same load but change length
33
Isometric Contraction
No change in muscle length | Load changes
34
Increase Muscle in Series
Greater speed & shortening
35
Increase Muscle in Parallel
Greater force production
36
Contraction of Skeletal Muscle
Ach release | N1 receptors | Depolarization | Ryanodine pulls Ca2+ channel open | Ca2+ influx | Cross-bridge formation =Contraction
37
Relaxation of Skeletal Muscle
SERCA pumps Ca2+ back into SR | Cross-bridge formation ends =relaxation
38
Cross-Bridge Steps in Skeletal Muscle
Ca2+ binds to Troponin C | Troponin I cause conformational change | ATP binds to myosin | ATP hydrolyzed (at rest) | Myosin binds to actin | Phosphate released | Myosin head cocks = power stroke | ADP released
39
Troponin C
Binds to Ca2+ to uncover myosin-binding sites on actin
40
Troponin I
Causes conformational change so myosin can bind to actin
41
Troponin T
keeps tropomyosin in place
42
Tropomyosin
Covers myosin-binding sites on actin
43
Titin
Allows for elasticity of muscle Stabilizes myosin | causes passive force
44
Tetany
Summation where plateau occurs | muscle cannot relax or "oscillate" at all = sustained contraction
45
Baroreflex Mechanism
BP = Cardiac Output x Peripheral Resistance Up BP --> increase PSNS | decrease SNS = decrease BP
46
SNS (Sympathetic)
"fight or flight" Dilate pupils | Increase HR | Decrease GI | Decrease saliva, Up viscosity Short pregang | Long postgang Thoracolumbar region NT: NE
47
PSNS (Parasympathetic)
"Rest & Digest" Constrict pupils | Decrease HR | Increase GI | Increase saliva, down viscosity Long pregang | Short postgang Craniosacral region NT: Ach
48
Acetylcholine (Ach)
PSNS & SNS | Excitatory (EPSP) Receptors: Nicotinic (ionotropic/NSCC) N1: NMJ - skeletal N2: postganglionic fibers - autonomic neurons Muscarinic (metabotropic) - smooth/cardiac
49
Glycine
Spinal cord | Inhibitory (IPSP) Receptor: ionotropic (ligand-gated) Cl- conductance Location: spinal cord, retina, brainstem
50
GABA
CNS | Inhibitory (IPSP) Receptors: GABAa: ionotropic | Cl- conductance (hyperpolarization) fast GABAb: metabotropic | K+ conductance (hyperpolarization) slow Location: interneurons in brain
51
Jumping Frenchman Disease
Glycine (NT) Receptor mutation
52
Glutamate (Glu)
Brain | Excitatory (EPSP) Receptors: Ionotropic (NMDA | AMPA | Kainate) Na, K, Ca flow | fast Metabotropic (mGluR) Na, K, Ca flow | slow
53
Norepinephrine (NE)
SNS (all postgang) | Excitatory (EPSP) Receptors: a-Adrenergic: metabotropic | more NE than E a1: blood vessels (vasoconstriction) a2: presynaptic terminals B-Adrenergic: metabotropic | more E than NE) B1: heart (up HR) B2: lungs (bronchodilation) B3: fat cells
54
Epinephrine (E)
SNS (adrenal medulla) | Excitatory (EPSP) Receptors: a-Adrenergic: metabotropic | more NE than E a1: blood vessels (vasoconstriction) a2: presynaptic terminals B-Adrenergic: metabotropic | more E than NE) B1: heart (up HR) B2: lungs (bronchodilation) B3: fat cells
55
Receptor Potential
Change in membrane potential at stimulus site
56
Synaptic Potential
Change in membrane potential at synapse when NT released
57
Tonic Receptor
Slow | AP maintained
58
Phasic Receptor
Fast | AP only when stimulus turned on/off
59
Ionotropic Receptor
fast | short | ligand-gated | NSCC | localized
60
Metabotropic
slow | long | G-protein coupled | widespread

Physiology (6 decks)

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