cell processes

Question 1

overall structure of membrane

Answer 1

thin (~8nm) felxible fluid mosaic - “sea of lipids which proteins float like icebergs)
50% lipid, 50% protein held by H BONDS
cholesterol and glycolipids

Question 2

phospholipids

Answer 2

75% lipid
amphipathic (n-p tails & p heads) –> spontaneous layer
hydroPHOBIC core

Question 3

fluidity and proteins in membrane

Answer 3

composition of leaflet can be asymmetric
tail length (long = less fluid), double bonds (less = less fluid), cholesterol (more = less fluid)
integral proteins (embedded) peripheral proteins (inner/outer surface of mem). receptors, cell identity, enzymes, channels, linkers etc
proteins - since some mol can’t permeate hydrophobic core

Question 4

selective permeability of membrane

Answer 4

PERMEABLE TO:
- n-p uncharged mol. (O2, N2, BENZENE)
- lipid soluble mol (steroid, fatty acid, some vit.)
- small uncharged polar mol (H2O, urea, glycerol, CO2)
IMPERMEABLE TO:
- large uncharged polar mol (glucose, aa)
- ions (charge)

Question 5

diffusion (new info)

Answer 5

rate of diffusion sets a limit on size of cells - ~20μm

Question 6

electrochemical gradient, conc of ions in and out of cell

Answer 6

cells maintain diff of ions inside & out –> electrical gradient
mem store and separate charge
EXTRACELLULAR = HIGH Na+, LOW K+, HIGH Cl-
CYTOPLASMIC = LOW Na+, HIGH K+, LOW Cl-
Na+ in (down conc gradient), K+ out UNTIL electrical gradient even
~30% of resting energy in cells - maintain conc & electrical G

Question 7

osmosis and osmotic pressure

Answer 7

only occurs if mem PERMABLE to WATER, NOT to certain SOLUTES
Pw = Pd + Pf
Pf = aquaporins (9 isoforms –> diff permeability). large, temp independent
Pd = diff through bilayer. small, temp dependant (fluidity)
osmotic oressure = pressure applied to soln –> prevent inward flow of water across mem. DIFF in osmolarity moves water across mem

Question 8

ion channels

Answer 8

rapid (no binding), diffusion
water filled pore - protect ions from PHOBIC core
Hphillic aa lines inside of channel
selectivity - size, charge, harnesses energy stored in gradients
gated channels: gate blocks pore, stimuli (ligand, pH temp, phosphorylation etc) control gate

Question 9

how to measure ion channel function

Answer 9

patch clamp technique
millions of ions flowing per second –> measurable CURRENT (~10^-12amp)
fluctuations = opening & closing channels, conformational changes in channel (gate)

Question 10

carrier mediated transport and different types

Answer 10

uses transport proteins
bind (–> slower) –> change confirmation –> open other side
like enzymes - binding site, inhibition, competition, saturation BUT DON’T CATALYSE - just mediate transport faster than normal rate
TYPES = passive/facilitated, active - primary & secondary

Question 11

transport of glucose (passive/facilitated carrier mediated transport)

Answer 11

direction depends on conc

1. glucose bind to GLUT (tp)
2. change shape –> glucose move across mem
3. kinase enzyme reduce glucose conc inside cell- glucose –> glucose-6-phosphate

Question 12

primary active transport (examples)

Answer 12

directly from hydrolysis of ATP (~30% of energy on p AT)
eg. H/KATPase, Ca/KATPase
Na/KATPase:
1. 3 Na+ bind
2. ATP split , Na+ OUT. (Ph group bind to protein --> shape change so Na+ leave)
3. 2 K+ bind, Ph releases
4. K+ IN
maintains LOW conc. of Na+ and HIGH conc of K+ INSIDE
CONTINUOUS - Na & K leak back into cell
WHY?
- resting potential
- muscle contraction
- maintain steady state cell volume
- uptake nutrients 
- electrical excitability

Question 13

secondary active transport (examples)

Answer 13

energy stored in ionic conc gradient (made by p AT) used (harnessed) in s AP - INDIRECTLY use energy from hydrolysis of ATP
Na+ SYMPORTERS/COTRANSPORTERS: glucose & aa in with Na+ ions
Na + ANTIPORTERS/EXCHANGERS: Na+ IN (passive), energy used –> H+ or Ca2+ OUT

Question 14

tight junctions and role in transepithelial transport

Answer 14

in inter/paracellular space between epithelial cells
barrier - restrict movement through int.cell. space
fence - prevent mem proteins from diffusing in plane of lipid bilayer
apical + basolateral mem

Question 15

paracellular transport (epithelium types)

Answer 15

in space between cell interior
diffusion + tightness of junctions
electrical resistant to ion flow measured - higher resistance = more tight junctions
leaky epithelium = paracellular transport more. PROXIMAL eg. duodenum, PCT
tight epithelium = transcellular. DISTAL eg. colon

Question 16

transcellular transport (‘rules’)

Answer 16

absorption or secretion
p & s AT + ion channels
entry & exit steps
electrochemical gradient (e/es passive or active?)
electroneutrality - movement of ions will attract opposite charge
osmosis - movement of ions –> diff osmolarity –> water flow (if aquaporins)

Question 17

secretion and absorption entry, exit steps + more

Answer 17

entry step = often s AP
exit step = often diff (passive)
primary active transporter SETS up ion gradient.
SECRETION - p AT + entry step basolateral, exit step apical
ABSORPTION - entry step on apical, p AT + exit step on basolateral
+ water + counter ions by diff through TJ

Question 18

glucose absorption in small intestine

Answer 18

relatively leaky epi/TJ

1. (basolateral) Na/KATPase –> low Na+ in cell
2. sodium glucose symporter (SGLT) (apical) - uses energy of Na gradient to move Na+ + glucose inside cell –> more glucose in cell than out
3. GLUT transporter (basolateral) –> glucose into blood
4. sodium in cell removed by pump
5. movement of Cl + H2O PARACELLULAR since charge of Na+ in blood

Question 19

oral rehydration therapy

Answer 19

sugar + little salt soln given to babies w diarrhoea

ability of glucose to enhance absorption of Na+ HENCE Cl

Question 20

glucose-galactose malabsorption syndrome + treatment

Answer 20

mutation to glucose symporter small intestine –> sugar in intestine in lumen –> increase osmolarity in lumen –> water out –> diarrhoea
treatment = FRUCTOSE instead. GLUT5 can transport fructose to epi –> blood. (GLUT 2 exit step)

Question 21

glucose reabsorption in kidney & what could go wrong

Answer 21

sodium glucose cotransporter - g + Na+ into epi cell (secondary AT) –> g passive diffusion into blood
Cl + H2O PASSIVE
if glucose symporter can’t absorb glucose FAST enough (renal threshold* reached) –> diabetes
* transport maximum of SGLT

Question 22

chloride secretion steps + rate limiting steps

Answer 22

1. Na/KATPase (basolateral mem) –> ion gradient
2. NaK2Cl symporter (basolateral, s AT) - 2Cl- (+ Na + K) above its electrochemical gradient in cell
3. Cl leave through chloride channel (apical mem)
4. Cl- secretion –> Na+ + H2O paracellular. same direction
   RLS: Cl channel (CFTR) - Cl can’t leave unless Cl channel open

Question 23

secretory diarrhoea & mechanism of cholera

Answer 23

excessive stim. of secretory cells in crypts of small intestine & colon - secretion of enterotoxin (cholera) OR (less common) high conc of endogenous secretagogues by tumours/inflammation
CHOLERA - irreversibly activates CFTR
1. bind to GPCR (basolateral) –> G protein
2. adenylate cyclase atp –> cAmp
3. p kinase ACTIVE –> phosphorylates CFTR
4. ATP can bind to channel –> open
5. ions move + H2O + Na. dehydration

Question 24

treatment of secretory diarrhoea + crypt & villi cells

Answer 24

crypt secret Cl, villi absorb Na+, glucose, H2O (fluid from crypt cells)
c cells have stem cells divide –> up to villi
oral rehydration therapy - glucose stimulated water influx = TREATMENT

Question 25

cystic fibrosis and management

Answer 25

autosomal recessive - hetero = carries, het + het child has 1/4 chance
mostly affect European
many organs affected - airways, liver, pancreas, small intestine, skin, reproductive tract (all epi)
management = antibiotics, chest percussions,pancreatic enzyme replacement

Question 26

CFTR and cystic fibrosis

Answer 26

regulated by p kinase A dependant phosphorylation of R domain + ATP binding at nucleotide binding domain
CFTR gene defect = no cl secretion –> no H2O + Na+ movement OUT –> dehydrated lumen –> thick mucus = breeding ground for bacteria –> immune response destroy surface of lung
CTFR gene defect ALSO affects Na+ channel - more absorption of Na+ = more dehydrated

Question 27

sweat & cystic fibrosis

Answer 27

normal sweat: primary isotonic secretion by acinar cells, secondary reabsorption (in DUCT) of NaCl (duct cell mem potential depolarised so Cl can enter down electrochemical gradient) but NOT H2O –> hypotonic soln.
CF sweat: CFTR not open in ducts –> accumulation of NaCl in lumen –> salty sweat