Membranes Flashcards
what goes through fluid phospholipid bilayer w/o specific pathway
lipid soluble mols, e.g. steroid hormones, fatty acids, O2, CO2
plasma mem structure
fluid phospholipid bilayer into which prots are embedded
what is interstitial fluid
fluid bet cells, subset ECF
relative [NA+]
extracellular high (145), intra low (10)
mM
relative [Ca2+]
extracellular low (2.5), but intra v. low (0.00007)
mM
relative [K+]
extracellular low (5), intra high (120)
measured mM (milimoles)
relative [Cl-]
extracellular high (120), intra low (3)
define simple diffusion
continuous random, passive movement mols until evenly distributed
differneces bet simple + facilitated diffusion
facilitated:
* specific
* transport capacity limited by no. prots
* affected competitive inhibition
* still PASSIVE bc no ATP
basic how carrier prot works
mols binds, prot changes shape, mol exposed to cytosol fluid, bonds breaks + mol moves away
define osmosis
movement water across mem down conc grad
aiming even sol conc
define osmotic press
press exerted by inorganic mols to draw in water + cause/stop osmosis
hypo/hyper/iso-osmotic refers to this
osmolarity?
no particles solute per litre solvent
Osm/l = mosmolL-1 = no. osmoles/L
osmolality is?
no particles solute per kg solvent
Osm/kg
difference osmolarity + tonicity
osmolarity compares 2 sols, tonicity comps sol + cell (usually w ref to blood) - no units as comparative term
hypotonic = low solute conc = high water conc
factors affecting RATE mem passage
- SA
- mem thickness = diff dist
- conc grad
- mem permeability
* lipid solubility
* transport mechanism
* size of mol = molecular weight
* lipid composition of mem
last 2 less important
effects pneumonia
oedema alveolar walls (= swell) due exudation (fluid leaks out blood vessels into tissues
swelling = greater diff dist….
results hypoxia = O2 not available sufficient amounts in tissues
if there were no ion pumps in cell mem
enzs etc neg charge = transmem voltage grad = + ions attracted in = water in by osmosis = more pos ions than neg = water by osmosis etc + cell swells + swells until bursts.
ions also entering on conc grads
so ion pumps move ions out to maintain osmotic press
differences bet channels + carriers/pumps
- channels opened or closed w movement passive down conc grad
- pumps specific, require E, graded + set up ion grads
- for channels more conc grad = goes faster but pumps saturate - transporter working max rate
- pumps also have competition
how voltage-gated channels work
changes in mem pot cause electrostatic forces move electrically charged gate structure
* muscle contraction
* propogating nerve impulses
how ligand-gated channel prots work
controlled signal mols in ECF or IC signal pathways
* nerve synapses
* neuromuscular junctions
how mechano-gated channel prots work
affected deformation cell mem, e.g. stretch, press
* activation pain
primary AT
move substances against conc grad using carrier prot + E - direct ATP hydrolysis
antiport
1 AT transporter
2 species transported opp directions
e.g. Na+K+ATPase
uniport
1 ATP transporter
1 species transported
e.g. Ca2+ATPase
symport
> 1 type ion/mol transported same direction simultaneously
secondary AT
uses potential E from movement ions
ATP used create conc/electrochem grad (typically Na+) then substance diffuses, releasing E - used by carrier prot
E = potential E stored in ion conc grad
examples fac diff, 1 AT, 2 AT
- glucose
- H+ into stomach
- Na+ - glusose (SGLT) coupled transport
cause equilibrium pot
diffusion pot causing ion movement one direction equal electrical pot other direction - takes while to reach
Ek = equ pot K+
bet -100, +100mV any ion
membrane potential
result combination equ pots all ions, relative to how permeable mem is to them
diff in charge bet inside + outside cell
harder + harder ions move until reach equ pot
cause resting mem pot (RMP)
AT REST mem most permeable K+ = diffs out down conc grad, but large anions stuck in (selectively permeable mem) = imbalance charge across mem
Na-K-ATPase = 3K+ out, 2Na+ in
-60mV
why is RMP v sim equ pot K+
mostly dependent K+
* high conc grad
* most permeable to it
what does excitable cell mean
changes in mem pot cause ion channels open + close
describe a pot
if depolarisation reaches threshold (-30mV) v-gated Na+ open = loads Na+ in, then slower v-gated K+ channels open + Na+ tired + close = K+ out = repolarisation, then hyperpolarisation then to resting
mem pot moves towards Na+ then back towards K+
patch clamp recording
isolate small area cell mem + measure currents through individual channels
main ion channel properties
- open + close
- sense: voltage, pH, chem, temp, movement
- distinguish bet ion types (99% accuracy)
structure Na+ + K+ channels
4 sub-units
what target Na+ channels
- toxins, e.g. pufferfish TTX (tetrodotoxin)
- local anaesthetics, e.g. lidocaine
physically block = no pass = no a pot = no feeling
hyperkalaemic periodic paralysis (HyPP)
mutation v-gated Na+ = open too easily
* normal exercise + releases K+ blood
* normal small depolarisation muscle then Na+ open, more K+ in pos feedback loop
* neurones going loco = can’t transmit to muscles = paralysis
eventually recover but bad
name equ to calc equ pot
Nernst
neuromyotonia
antibodies directed against v-gated K+
= a pot no come back down easily
= muscle contracted stays contracted
phenytoin maybe for treatment - blocks Na+ channels
dendrotoxin poisoning
continuous release ACh = no repolarisation
lungs contract + stay = can’t breathe
diaphragm paralysis bc doesn’t relax
from green mamba
Cl- mem facts
- lower inside
- important for RMP - more in muscles than neurones
myotonia
mutant muscular Cl- channels - in post-synaptic skeletal muscle inactive
* once contracted stays contracted
congenital anomaly
exocytosis
- increase A cell mem
- add lipids + prots to cell mem
- release hormones, digestive enzs, neurotransmitters
constitutive exocytosis
regular growth + renewal cell mem
regulated exocytosis
stuff stored vesicles cyt + released due stimulus, e.g Ca2+ to release neurotransmitters, water-soluble hormones from endocrine cells
phagocytosis
macrophage cell mem extends around phagosomes (cont microbes, aged rbcs) + engulf
receptor-mediated endocytosis
specific ligands (mols) bind mem receptor, whole complex into cell, ligand released + digested lysosomal enzs or recycled to mem
transcytosis
endocyt 1 side, exo other, e.g. nutrients blood -> tissues
what insulin does
- increase hexokinase expression for more glucose into cell
- vesicles cont GLUT4 exocyt = more in mem = more glucose into cell
hexokinase purpose
convert glucose -> glucose-6-phosphate
maintain conc grad glucose into cell
diabetes problem
glucose in blood - not taken up skeletal muscle + adipose tissue
* taken up other tissues, like blood vessels + neurones = swell + die
adipose tissue
connective tissue (fat)
hyperglycaema
increased glucose in blood
Ca-ATPase
transports Ca2+ out cell
