Membrane transporters Flashcards

1
Q

Primary active transporters derive their energy from:

A

directly from the splitting of ATP

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2
Q

Other than the _____, there are no other ubiquitous primary active transporters in the plasma
membrane of cells

A

Na/K pump

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3
Q

Inside mitochondria is a very special proton pump that, when running backwards, lets

A

(the F1-ATPase)

protons leak across a membrane and synthesizes, rather than hydrolyzes ATP

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4
Q

Secondary active transport Energy to do the work of pumping comes from

A

not from metabolism (ATP), but from a secondary source

• Usually this energy source is the ‘downhill leak’ of Na+ into the cell.

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5
Q

Secondary active transport is

A

Mechanism by which most substances are pumped.

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6
Q

There are two basic types of secondary active transporters:

A

Cotransport:

Antiport or Exchange:

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7
Q

Cotransport:

A

those that move different solute species in the same direction

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8
Q

Antiport or Exchange:

A

those that move solute in opposite directions

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9
Q

Secondary active transport For example,cells can accumulate amino acids
This active uptake is dependent on ______

A

against their energy gradients

external Na+; if external Na+ is removed, amino acid
uptake is abolished

Conversely, removing the amino acid reduces the entry of Na+

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10
Q

Secondary active transport The carrier ingeniously captures the energy released by

A

the inward leak of Na+ and instead

of letting it escape as heat, uses it to pump the amino acid into the cell.

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11
Q

Secondary active transporters do not necessarily.

A

always run in the same direction

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12
Q

All secondary transport mechanisms depend ultimately on the ______

A

Na+/K+ pump (and therefore on ATP).

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13
Q

Some secondary active transporters are

A

electrogenic in that one cycle produces a net charge transfer across the membrane.
o

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14
Q

Other secondary active transporters are

A

non-electrogenic.

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15
Q

The main feature of electrogenic secondary active transporters is that their activity is

A

governed by the membrane potential.

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16
Q

Secondary active transporters The will always tap the ____, because of this, they can _____.

A

bigger leak to drive the smaller pump.

reverse direction sometimes

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17
Q

example of secondary active transporters moving in reverse

A

the sodium-calcium exchanger, which reverses direction in heart muscle cells every time the heart beats.

18
Q

Electrically silent transporters could not care less about

A

membrane potential

19
Q

if the Na+/K+ pump is blocked, cells fill up with Na+, and thus the ______ is reduced. Because this is the energy source for ______

A

Na+ electrochemical gradient

secondary active transport, all of these transport mechanisms suffer.

20
Q

For example, Na+/ amino acid transporters are electrogenic, because

A

one cycle transfers a net positive charge (Na+) into the cell.

21
Q

An example of non-electrogenic. is the

A

Na/K/2Cl cotransporter, which a ch cycle moves one sodium ion,one
potassium ion, and two chloride ions into the cell.

22
Q

Cotransport:

A

secondary transporters that move different solute species in the same direction

23
Q

Exchange:

A

secondary transporters that move solute in opposite directions

24
Q

A non-electrogenic secondary active transporter is one in which

A

no net charge is moved across the membrane.

25
Q

Driving Force =

A

Vm-E

26
Q

as Vm becomes more positive, the net driving force will

A

continue to decrease.

27
Q

reversal potential (Vrev);

A

it’s the value of Vm at which there will be no net movement via this exchanger.

28
Q

Vrev = Vm at which

A

there is no net movement

29
Q

At values of Vm more positive than Vrev, the exchanger will run

A

in the other direction: moving H+ into the cell and pumping Na+ out of the cell.

30
Q

infusing K+ causes _____, and infusing acid causes _____

A

acidemia (the K+ is taken up by cells ‘in exchange’ for H+)

hyperkalemia

31
Q

hyperkalemia will cause _____. Hyperkalemia also will ____ cells (by shifting EK in a positive direction), and the change in membrane potential can affect ____

A

extra K+ uptake via the Na/K pump.

depolarize

the rate of activity of electrogenic transporters.

32
Q

facilitated diffusion.

A

Some transporters act like ion channels, shuttling a single solute species in either direction.

33
Q

How, then, do cells concentrate glucose? ]

A

The answer is that as soon as a glucose molecule gets into the cell, it is phosphorylated to Glucose-6-Phosphate.

34
Q

How to treat Hyperkalemia

A
C BIG K
C: calcium
B: Bicarbonate
I: insulin
G: glucose
K: kayexalate
35
Q

Hyperkalemia is very dangerous because it can lead to

A

heart arrhythmias.

36
Q

Increased extracellular potassium levels result in ______ of the membrane potentials of cells. Which results in _____

A

depolarization

This depolarization opens some voltage-gated sodium channels, but not enough to generate an action potential.

the open sodium channels inactivate and become refractory, increasing the threshold needed to generate an action potential.

This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems.

37
Q

Biggest concern in hyperkalemia

A

the impairment of cardiac conduction which can result in ventricular fibrillation.

38
Q

Hyperkalemia treatment with calcium

A

Ca+2 ions bind to the outside surface of cell membranes.
they trick the Na+ channels into thinking the membrane has been hyperpolarized. This increases threshold potential and restoring normal gradient between threshold for an action potential,

quieting down the aberrant, spontaneous depolarization of individual cardiac cells.

VERY LOCALIZED EFFECT!

39
Q

Hyperkalemia treatment with bicarbonate

A

The presence of excess bicarbonate ions will stimulate an exchange of cellular H+ for Na+, thus
leading to stimulation of the sodium-potassium ATPase which will stimulate uptake of K+ into the cell.

40
Q

hyperkalemia treatment with insulin and glucose

A

stimulates the Na+/K+ pump, drawing K+ into the cell from the blood

41
Q

Hyperkalemia treatment with Kayexalate

A

Ionic species in which Na+ is bound to a large, negatively charged kayexalate ion

Kayesalate prefers to bind to K+, so when introduced into K+ saturated blood, Kayexalate will exchange Na+ for K+ and sequester free K+ ions.

This is usually a longer-term treatment, so must be combined with the other short term ones to actually work (patient could die before Kayexalate would have an effect).