Physiology: Membranes And Transport Ii

Front 1

Facilitated Diffusion - what substance should we immediately think of? How does it work?

Back 1

Glucose in muscle/fat (insulin dependent) - only works in the direction of a gradient.

Binding of glucose to receptor causes receptor to change confirmation and drop glucose into the cell.

This is called Glut-4

Front 2

Active transport - what kinds are there?

Back 2

Two: Primary and Secondary.

Both allow transport against a gradient and require energy to run.

Front 3

Primary active transport - go

Back 3

Primary Active Transport example is the Na/K ATPase pump, the Ca++ ATPase pump. Transport against a gradient, 3Na+ out, 2K+ in

Front 4

Secondary Active Transport - Go

Back 4

This is where you have coupled transport - the movement of two solutes.

If they go the same direction = SYMPORT (think glusose and Na in the intestines).
Also have ANTIPORT (movement in opposite directions - think of the Na-H exchanger for pH maintenance).

Front 5

Go through one good example of primary active transport:

Back 5

Na/K pump. Intracellular Na binds to receptors on the inside of the transporter - this induces ATP to phosohorylate the transporter, which changes its confirmation and exposes Na to the outside world.

K+ binding sites are revealed to the extracellular space, they bind. Their binding kicks off the phosphate that was added earlier, which reverses (again) the confirmation and exposes K on the inside of the cell.

Front 6

Go through one good example of secondary active transport:

Back 6

Intestinal glucose/Na transport.

Need both glucose and Na to bind to allow movement into the cell. Depends on concentrations of both.

This means that it actually depends on the Na/K pump discussed earlier to keep a sufficient supply of Na outside the cell for binding/glucose transport.

Front 7

Glucose transport in the gut vs. the muscle/fat cells. What styles of transport are going on?

Back 7

facilitated diffusion is happening in muscle/fat cells (glut 4), insulin sensitive.

in the gut, have secondry active transport - symport with Na+, the gradient for which is set up by the Na/K transporter

Front 8

Describe what happens in cerebral ishemia in regards to Na and Ca++

Back 8

Normally, Ca++ is exported from the cell in exchange for 2 Na++ (secondary active antiport).

With ischemia, this begins to breakdown - the neuron becomes more permeable to Na and K, so the intracellular concentration of Na+ goes up.

When this happens, it can bind to the inside of the Na/Ca++ transporter and get sent outside of the cell - the antiport still works and forces Ca++ in, killing the cell.

Front 9

In CF, what's up with sweat and lungs?

Back 9

It's a problem with Cl- transporters. In the lungs, Cl- can't be excreted. Usually, water follows the Cl- solute, so your mucous ends up all gunky.

In sweat, the produced fluid is isotonic - it then travels through a reabosptive duct, leaving sweat hypotonic.

if cl- isn't working, sweat remains isotonic (has more salt than normal, though).

Front 10

What happens faster - diffusion of facilitated diffusion?

Back 10

facilitated (carrier mediated) happens faster.

Front 11

Is the Na/K pump electrogenic?

Back 11

yes! it results in a net movement of charge (3na out, 2k in).

Front 12

paracellular pathway - go

Back 12

gap junctions, leaky

Front 13

cellular pathway - go

Back 13

tight

Front 14

Epithelial transport of sodium - what's going on in the cells? What drug blocks this?

What organs have weird transport?

Back 14

usually a Na/K pump at the baso/lateral side to lower the Na inside, creating a gradient.

Often use SIMPLE DIFFUSION through channels.

Ameloride blocks this!!!

note -

Front 15

what cells must have some kind of active NaCl transporter going on?

Back 15

galbaldder, proximal tubules, small intestines. - note- ameloride doesn't block NaCl transport here!

Front 16

provide examples of leaky and tight epithelia:

Back 16

leaky = proximal tubule and small intestines.

tight = collecting duct and salavary gland.