B1W1: Physio Flashcards
Na+ conc.
In plasma: 138-146 mM
In cell: 15 mm
Cl- conc.
In plasma: 103-112 mM
In cell: 20 mM
Glucose conc.
In plasma: 75-95 mg/dl
In cell: VERY LOW
Ca2+ conc.
In plasma: 1-1.4 mg/dL
In cell: .0001 mM
K+ conc.
4.4 mM in plasma
120 mM in cell
Ph
- 3-7.5 in plasma
7. 2 in cell
Cystic fibrosis
mutation in CFTR Cl- channel
Lipophillic molecules
resp. molecules (O2, CO2, N2)
organic molecules (alcohols, ketones)
anesthetics
Hydrophillic molecules
Urea, glycerol
What is permeability dependent on?
Px=DB/L
D=ease of mvt within cell membrane; determined by size, shape, charge of solute
B=how easily solute crosses one layer; diff. in force attraction for diffusing molecules within and outside membrane
*when with electrochemical gradient, also dependent on # channels open
B>1 and B<1; B equation
B=[X]i’/[X]i
B>1=lipophillic
B<1=hydrophillic
Vm
sum/net electrical difference across plasma membrane of each permeable ion
–only at steady state, not when ions are at equilibrium
Steady state
When no net change is occurring in cell and it is maintained by energy (not at equilibrium, though!)
Current zero
Equillibrium potential
When ion down diffusion gradient is counteracted by force of electrical potential
Value each ion wants to bring the membrane potential
–would not be under steady state; permeability does not matter
EACH ION WANTS TO DO WHAT IT CAN TO BRING CELL TO EQUILLIBRIUM, even if it means leaving it
Myotonia congenita
Usually Cl- helps repolarize skeletal muscle
BUT Cl- channel inhibited genetically
Cl- not allowed in, prolongued depolarization of flexor muscles, clasped hand won’t relax, abnormal walking gait
Increase in [K+]o
Depolarization of cell
iK outwardly decreases due to less gradient
less K+ leaving, cell stays more positive
Clinical issue with increase in [K+]o
Too much means hyper excitability (huge depolarization), arrythmias, abnormal breathing, loss neural control
Decrease in Pk
depolarization occurs
less K+ is coming out, less separation of + and - charge
Increase in Pk
causes hyperpolarization
Decrease in PNa
little change in cell
In resting cell, PNa small already
Making it smaller does nothing
Increase in PNa
Deplarization large iNa
Increasing permeability in general
pushes membrane towards ion’s equilibrium
Structure of carrier proteins
4 or more membrane spanning protein subunits
Each subunit is 6 segments
Each segment=helical polypeptide sequence
S4 domain
Opens up channels
S5, S6 domain in Na+ channel
inactivates Na+ channel
Terminal intracellular chain of K+ channel
inactivation
3 properties of protein channels
- chemical specificity (D glucose only)
- Saturation
- competitive/noncompetitive inhibition
Ouabain
competitive inhibitor that blocks K+ from binding to Na/K pump
Variables in GHK Current Equation
assumptions are that the cell membrane is homogenous, PM is thin so the electrical field is constant, ions are independent and Px is const.
Vm, [X] and Px of each ion determine current
What are ATPases inhibited by?
Blockers of metabolism because need energy from ATP
i.e. cyanide, dinitrophenol, azide
Steps of binding of facilitated proteins
- Carrier open to outside
- Solute binds
- Outer gate closes
- Inner gate opens
- Solute leaves
Example of facilitated diffusion carrier protein
SLC family of transmembrane glucose transporters (GLUT)
12 sequences connected; 7, 8, 11 make pore
Mobilization by insulin
Na/K pump
Alpha subunit: hydrolyzes ATP and has pore for Na/ (10 polypeptide seg.)
Beta subunit: 1 segment, targets pump to membrane
Cardiac glycosides
Oubain, digoxin and digitalis
Bind to side of alpha subunit of Na/K, causing conformational change that blocks K+
What is the Na/K pump regulated by?
- intracellular ATP
- extracellular K
- intracellular Na
H/K Pump
Primary transport
In gastric glands, kidney
2K+ in, two H+ out
HCl production, acid/base balance
Ca2+ ATPase
Primary transport
aka SERCA
2 Ca2+ into SR from cytoplasm in exchange for 2 H+
Ca2+/Na+ pump
Primary transport
One Ca2+ from cell for one Na+
want low intracellular Ca2+
Ca2+/H+ pump
Primary Transport
1 Ca2+ from cell for one H+
Want low intracellular Ca2+
Na/Glucose pump
Co Transport
In smal intestine epithelium/proximal tubule of kidney
Glucose in cell, Na+ in
Saturation=diabetes
Na/K/Cl Pump
Co transport
In non-epithelial, apical membrane
Cl- and Na+ down concentration gradient inward, K+ up inward
Blockage means increased water loss (water diuresis)
–furosemide water pill blocks channel
Na Ca Pump
Exchange transport
3 Na+ in, down gradient
1 Ca 2+ ion out, up gradient
Raising [Na+]i=depolarization
Cl/HCO3 pump
Exchange transport
Acid base regulation, CO2 transport
In RBC, brings HCO3 out for one Cl- in
Na/H pump
Exchange transport
Calculating osmolarity
Conc. x # particles
What affect does manipulating Na, Ca or Cl have on resting membrane potential?
Little because usually at rest the channels for these ions are closed anyway
A change in K is he only thing that changes resting membrane potential
Isotonic
conc. of cell and outside of cell is equal
No volume change
Won’t increase, decrease in size
isomotic
# of particles inside and outside of cell are equal Won't necessarily stop a hange in size
Hypotonic extracellular solution
ECF concentration is less than that in cytoplasm
Water goes into cell (lysis)
Hypertonic extracellular solution
ECF has concentration greater than cytoplasm
Water goes out of cell (crenation)
Hypokalemia
Decrease in K+ outside causes K+ on the inside to leave, the water following
What direction does water flow from?
Low osmolarity to high osmolarity
The higher value of osmolarity is hypertonic
