Axon potential, Muscle, Endocrine Flashcards

1
Q

Flux

A

J = PdeltaC, units of mol/(cm^2*hr)

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2
Q

Permeability coeff

A

P = KD/membrane thickness (X), units of cm/hr

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3
Q

Partition coeff

A

K = solubility in oil : solubility in water

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4
Q

P-type transporter

A

primary AT, E-P intermediate, Ex: Na/K ATPase, Ca ATPase, H/K ATPase

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5
Q

F-type transporter

A

primary AT, H pump run in reverse to make ATP

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6
Q

Cardiac glycosidases

A

Inhibits Na/K ATPase, ex: digoxin, digitoxin

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7
Q

ABC transporters

A

primary AT, MDR and CFTR receptors

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8
Q

Reflection coeff (sigma)

A

= 0 (permeable solute), = 1 (impermeable solute)

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9
Q

Nernst equation

A

[-60/z]*log[Xi]/[Xo]

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10
Q

GHK equation

A

[-60/z]*log(Pk[Ki]+PNa[Nai]+PCl[Clo)]/(Pk[Ko]+PNa[Nao]+PCl[Cli])

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11
Q

Titin

A

connects Z-lines to thick filaments, runs from M-line to Z-line, provides horizontal stability

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12
Q

Nebulin

A

Sets length of thin filaments to 1.05um, important for anchoring capping proteins

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13
Q

Tropomodulin

A

actin capping protein, protects from depolymerization at one end

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14
Q

CapZ

A

actin capping protein, protects from depolymerization at one end, anchors thin filament to Z-line proteins ie alpha-actinin

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15
Q

Alpha-actinin

A

Anchors thin filaments to Z-line

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16
Q

Thick filament

A

3 peptide chains, 1 heavy, 2 light, S1 (ATPase and actin binding site), S2 (neck), and tail region

17
Q

Thin filament

A

double stranded helix of actin monomers, with tropomyosin (extends over 7 actin filaments) and troponin (TnT, TnC, TnI)

18
Q

Cross bridge cycle

A

1) AM (rigor) myosin head bound to actin in 45deg angle
2) A + M-ATP, ATP binds and myosin head is released from actin in 45 deg angle
3) A + M-ADP-Pi, ATP is hydrolyzed, moves to 90deg angle, RESTING STATE
4) AM-ADP-Pi, myosin binds to actin IF Ca++ is present and has bound to TnC and moved tropomyosin out of the way, revealing actin binding site
5) AM, power stroke occurs when ADP-Pi leaves

19
Q

Isotonic

A

Same force, myosin detaches and binds to DIFFERENT actin molecule, shortening occurs

20
Q

Isometric

A

Same length, myosin detaches and binds to SAME actin molecule, force is generated

21
Q

Striated muscle is always turned ?

A

ON! only inhibited by troponin/tropomyosis, turned on when Ca++ binds to TnC of troponin, this is disinhibition

22
Q

T-tubules

A

Extracellular tubular system on invaginations of sarcolemma

23
Q

Sarcoplasmic reticulum

A

Intracellular tubular system which stores Ca++, has longitudinal part with Ca++ ATPase and terminal cisternea which stores Ca-calsequestrin

24
Q

Contraction in skeletal muscle

A

DHR act as voltage-sensor proteins and move foot processes our of the way so RYR can release Ca++ from SR, muscle relaxes through Ca++ ATPase in longitudinal SR which pumps Ca++ out of the cytosol into SR, no extracellular Ca++, contraction is all or none

25
Q

Contraction in cardiac muscle

A

DHR act as voltage-gated calcium channels and respond to AP by letting a little Ca++ into the cell which triggers Ca++ release from the SR via the RYR - Calcium induced calcium release, need both Ca++ ATP for SR and Na/Ca exchanger (secondary AT) to remove Ca++ from the cytosol, contraction is graded, through prolonging plateau phase

26
Q

PKA effects in cardiac muscle

A

1) phosphorylates TnI, increasing relaxation, and decreasing TnC affinity for Ca++
2) phosphorylates phospholamban on SR that increases CaATPase activity, increasing relaxation

27
Q

Force production in skeletal muscle is controlled by what?

A

Neural control

28
Q

How is skeletal muscle graded

A

Twitch, summation of force (repeated APs), tetanus (repetitive stimulation, rarely occurs physiologically)

29
Q

Henneman Size Principle

A

recruitment of motor units within a muscle takes place with recruitment of larger and larger motor units