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NSF > Membranes > Flashcards

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
Q

uniport

1 ATP transporter

A

1 species transported

e.g. Ca2+ATPase

26
Q

symport

A

> 1 type ion/mol transported same direction simultaneously

27
Q

secondary AT

A

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
Q

examples fac diff, 1 AT, 2 AT

A
  • glucose
  • H+ into stomach
  • Na+ - glusose (SGLT) coupled transport
29
Q

cause equilibrium pot

A

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

30
Q

membrane potential

A

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
Q

cause resting mem pot (RMP)

A

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
Q

why is RMP v sim equ pot K+

A

mostly dependent K+
* high conc grad
* most permeable to it

33
Q

what does excitable cell mean

A

changes in mem pot cause ion channels open + close

34
Q

describe a pot

A

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
Q

patch clamp recording

A

isolate small area cell mem + measure currents through individual channels

36
Q

main ion channel properties

A
  1. open + close
  2. sense: voltage, pH, chem, temp, movement
  3. distinguish bet ion types (99% accuracy)
37
Q

structure Na+ + K+ channels

A

4 sub-units

38
Q

what target Na+ channels

A
  • toxins, e.g. pufferfish TTX (tetrodotoxin)
  • local anaesthetics, e.g. lidocaine

physically block = no pass = no a pot = no feeling

39
Q

hyperkalaemic periodic paralysis (HyPP)

A

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
Q

name equ to calc equ pot

A

Nernst

41
Q

neuromyotonia

A

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
Q

dendrotoxin poisoning

A

continuous release ACh = no repolarisation

lungs contract + stay = can’t breathe
diaphragm paralysis bc doesn’t relax

from green mamba

43
Q

Cl- mem facts

A
  • lower inside
  • important for RMP - more in muscles than neurones
44
Q

myotonia

A

mutant muscular Cl- channels - in post-synaptic skeletal muscle inactive
* once contracted stays contracted

congenital anomaly

45
Q

exocytosis

A
  • increase A cell mem
  • add lipids + prots to cell mem
  • release hormones, digestive enzs, neurotransmitters
46
Q

constitutive exocytosis

A

regular growth + renewal cell mem

47
Q

regulated exocytosis

A

stuff stored vesicles cyt + released due stimulus, e.g Ca2+ to release neurotransmitters, water-soluble hormones from endocrine cells

48
Q

phagocytosis

A

macrophage cell mem extends around phagosomes (cont microbes, aged rbcs) + engulf

49
Q

receptor-mediated endocytosis

A

specific ligands (mols) bind mem receptor, whole complex into cell, ligand released + digested lysosomal enzs or recycled to mem

50
Q

transcytosis

A

endocyt 1 side, exo other, e.g. nutrients blood -> tissues

51
Q

what insulin does

A
  1. increase hexokinase expression for more glucose into cell
  2. vesicles cont GLUT4 exocyt = more in mem = more glucose into cell
52
Q

hexokinase purpose

A

convert glucose -> glucose-6-phosphate

maintain conc grad glucose into cell

53
Q

diabetes problem

A

glucose in blood - not taken up skeletal muscle + adipose tissue
* taken up other tissues, like blood vessels + neurones = swell + die

54
Q

adipose tissue

A

connective tissue (fat)

55
Q

hyperglycaema

A

increased glucose in blood

56
Q

Ca-ATPase

A

transports Ca2+ out cell

NSF (22 decks)

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