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Membranes Flashcards

1
Q

what goes through fluid phospholipid bilayer w/o specific pathway

A

lipid soluble mols, e.g. steroid hormones, fatty acids, O2, CO2

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2
Q

plasma mem structure

A

fluid phospholipid bilayer into which prots are embedded

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3
Q

what is interstitial fluid

A

fluid bet cells, subset ECF

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4
Q

relative [NA+]

A

extracellular high (145), intra low (10)

mM

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5
Q

relative [Ca2+]

A

extracellular low (2.5), but intra v. low (0.00007)

mM

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6
Q

relative [K+]

A

extracellular low (5), intra high (120)

measured mM (milimoles)

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7
Q

relative [Cl-]

A

extracellular high (120), intra low (3)

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8
Q

define simple diffusion

A

continuous random, passive movement mols until evenly distributed

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9
Q

differneces bet simple + facilitated diffusion

A

facilitated:
* specific
* transport capacity limited by no. prots
* affected competitive inhibition
* still PASSIVE bc no ATP

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10
Q

basic how carrier prot works

A

mols binds, prot changes shape, mol exposed to cytosol fluid, bonds breaks + mol moves away

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11
Q

define osmosis

A

movement water across mem down conc grad

aiming even sol conc

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12
Q

define osmotic press

A

press exerted by inorganic mols to draw in water + cause/stop osmosis

hypo/hyper/iso-osmotic refers to this

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13
Q

osmolarity?

A

no particles solute per litre solvent

Osm/l = mosmolL-1 = no. osmoles/L

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14
Q

osmolality is?

A

no particles solute per kg solvent

Osm/kg

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15
Q

difference osmolarity + tonicity

A

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

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16
Q

factors affecting RATE mem passage

A
  1. SA
  2. mem thickness = diff dist
  3. conc grad
  4. mem permeability
    * lipid solubility
    * transport mechanism
    * size of mol = molecular weight
    * lipid composition of mem

last 2 less important

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17
Q

effects pneumonia

A

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

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18
Q

if there were no ion pumps in cell mem

A

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

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19
Q

differences bet channels + carriers/pumps

A
  • 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
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20
Q

how voltage-gated channels work

A

changes in mem pot cause electrostatic forces move electrically charged gate structure
* muscle contraction
* propogating nerve impulses

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21
Q

how ligand-gated channel prots work

A

controlled signal mols in ECF or IC signal pathways
* nerve synapses
* neuromuscular junctions

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22
Q

how mechano-gated channel prots work

A

affected deformation cell mem, e.g. stretch, press
* activation pain

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23
Q

primary AT

A

move substances against conc grad using carrier prot + E - direct ATP hydrolysis

24
Q

antiport

1 AT transporter

A

2 species transported opp directions

e.g. Na+K+ATPase

25
uniport | 1 ATP transporter
1 species transported | e.g. Ca2+ATPase
26
symport
>1 type ion/mol transported same direction simultaneously
27
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
28
examples fac diff, 1 AT, 2 AT
* glucose * H+ into stomach * Na+ - glusose (SGLT) coupled transport
29
cause equilibrium pot
diffusion pot causing ion movement one direction equal electrical pot other direction - takes while to reach | Ek = equ pot K+ ## Footnote bet -100, +100mV any ion
30
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
31
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
32
why is RMP v sim equ pot K+
mostly dependent K+ * high conc grad * most permeable to it
33
what does excitable cell mean
changes in mem pot cause ion channels open + close
34
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+
35
patch clamp recording
isolate small area cell mem + measure currents through individual channels
36
main ion channel properties
1. open + close 2. sense: voltage, pH, chem, temp, movement 3. distinguish bet ion types (99% accuracy)
37
structure Na+ + K+ channels
4 sub-units
38
what target Na+ channels
* toxins, e.g. pufferfish TTX (tetrodotoxin) * local anaesthetics, e.g. lidocaine physically block = no pass = no a pot = no feeling
39
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
40
name equ to calc equ pot
Nernst
41
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
42
dendrotoxin poisoning
continuous release ACh = no repolarisation lungs contract + stay = can't breathe diaphragm paralysis bc doesn't relax | from green mamba
43
Cl- mem facts
* lower inside * important for RMP - more in muscles than neurones
44
myotonia
mutant muscular Cl- channels - in post-synaptic skeletal muscle inactive * once contracted stays contracted congenital anomaly
45
exocytosis
* increase A cell mem * add lipids + prots to cell mem * release hormones, digestive enzs, neurotransmitters
46
constitutive exocytosis
regular growth + renewal cell mem
47
regulated exocytosis
stuff stored vesicles cyt + released due stimulus, e.g Ca2+ to release neurotransmitters, water-soluble hormones from endocrine cells
48
phagocytosis
macrophage cell mem extends around phagosomes (cont microbes, aged rbcs) + engulf
49
receptor-mediated endocytosis
specific ligands (mols) bind mem receptor, whole complex into cell, ligand released + digested lysosomal enzs or recycled to mem
50
transcytosis
endocyt 1 side, exo other, e.g. nutrients blood -> tissues
51
what insulin does
1. increase hexokinase expression for more glucose into cell 2. vesicles cont GLUT4 exocyt = more in mem = more glucose into cell
52
hexokinase purpose
convert glucose -> glucose-6-phosphate maintain conc grad glucose into cell
53
diabetes problem
glucose in blood - not taken up skeletal muscle + adipose tissue * taken up other tissues, like blood vessels + neurones = swell + die
54
adipose tissue
connective tissue (fat)
55
hyperglycaema
increased glucose in blood
56
Ca-ATPase
transports Ca2+ out cell

NSF (22 decks)

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