SGU Physiology - Celluar

Created by pdolan 

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Resting Membrane Potential

-90 mV in skel mm, -65 mV in neurons, -40 mV in photoRs (rel high Na+ chans open) and -85 mV in cardiac mm

Na+ equi potential

equi pot: (+)60 mV (slightly higher in mm vs neurons)

K+ equi potential

(-)83mV (lower in skel mm) => > perm => much greater influence on resting memb pot than Na+

tonic control

constantly controlling a var toward the set point, oft referred to ANS SNS/PSNS stim

hiearchy

some feedback loops more important than others

redundancy

multiple homeostatic mechanisms controllling an important parameter

extracellular [Na+]

142 mM

extracellular [K+]

4.4mM

extracellular [Cl-]

102mM

extracellular [protein]

1mM

extracellular osmolarity

290mOsm

intracellular [Na+]

15 mM

intracellular [K+]

120mM

intracellular [Cl-]

20mM

intracellular [protein]

4mM

intracellular osmolarity

290mOsm

diffusion

movement of molecules due to random thermal movement

digoxin

drug for cardiac failure that blocks the Na+/K+ ATPase in cardiac cells => inc [Ca2+]i -> inc contractile F

SGLT

cotransporter of Na+ and Glc

NKCC

Na+/K+/Cl- cotransporter

Dalton's Law

eq: Total Pressure = Sum of Partial Pressures

Henry's Law

eq: []dissolved gas = Ks * Px

Equivalent

Molarity (M) * # of charges

Molarity

[]/liters solvent

Osmolarity

moles of solute particles

Osmolality

Osmolarity/Kg H20

Reflection coefficient

actual/theoretical osmotic pressure

tonicity

how a solution affects cell volume when the cell is placed in to it

excitable cell

any cell that can generate Ap's

depolarisation

phase of Ap that involves opening of volt-gate Na+ chans -> Na+ influx

repolarisation phase

Ap phase involving close of VG-Na+ chans, open VG K+ chans -> K+ efflux

refractory period

Ap phase of around 1ms where neuron can't generate another Ap

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