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ICPP > Session 3 > Flashcards

Session 3 Flashcards

1
Q

What is primary active transport

A

Driven directly by the energy released by hydrolysis of ATP to ADP

Catalysed by the transporter

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2
Q

What type of transporter is Plasma membrane Ca2+-ATPase (PMCA) and what does it do

A

Primary active transporter (drives calcium outside cell against conc grad)

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3
Q

What does ATP synthetase do

A

Uses proton gradient to allow re entry of protons into matrix and drive synthesis of ATP from ADP

Primary active transporter in reverse mode

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4
Q

What is co-transport

A

More than one type of ion or molecule may be transported on a membrane transporter per reaction cycle

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5
Q

What type of pump is the Na+-K+-ATPase

A 
Anti port (3Na+ out and 2K+ in)
Primary active transport 
P-type ATPase
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6
Q

Alpha sub unit of Sodium Potassium pump

A

most important- K+ Na+ and ATP binding sites

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7
Q

How much does sodium pump contribute to the resting membrane potential

A

Very little

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8
Q

What is mainly responsible for membrane potential

A

K+ diffusion through channels

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9
Q

What is secondary active transport

A

Driven indirectly by energy released by hydrolysis of ATP to ADP

Dissipation of gradients formed for another ion or substance provides the energy

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10
Q

What drives the transport of the Na+-Ca2+ exchanger

A

Dissipation of Na+ gradient from sodium potassium pump

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11
Q

Characteristics of primary active transport of Calcium via direct ATP hydrolysis

A

High affinity, low capacity

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12
Q

Characteristics of secondary active transport of Calcium (dissipation of Na+ gradient drives it)

A

Low affinity, high capacity, anti port

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13
Q

What drives the Na+-H+ exchanger

A

Dissipation of Na+ gradient from sodium potassium pump

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14
Q

What drives Na+-Glucose co-transport

A

Dissipation of Na+ gradient from sodium potassium pump

Symporter, brings in glucose against conc grad

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15
Q

Examples of co transport systems

A

Na+-K+-ATPase
Na+-Ca2+-exchange
Na+-H+-exchange
Na+-glucose co-transport (small intestine and kidney)

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16
Q

Transporters in cystic fibrosis

A

Na+ driven transport of Cl-, not possible due to mutated CFTR, Cl- doesn’t pass out of cell so water doesn’t follow

17
Q

Transporters in diarrhoea

A

In gut epithelial cell, Protein kinase A activated CFTR so more Cl- transported out so more water follows

18
Q

Na+-K+-ATPase functions

A

Forms Na+ and K+ gradients needed for electrical excitability

Drives secondary active transport (control of pH, regulation of cell volume, Calcium, Absorption of Na+ in epithelia, nutrient uptake e.g. glucose)P

19
Q

high intracellular calcium is

A

Toxic to cells

20
Q

Cells signal by

A

Small changes in intracellular Ca2+

21
Q

Control of resting Ca2+

A

Na+-Ca2+-exchanger NCX
PMCA
SERCA
Mitochondria Ca2+ uniporters

22
Q

What expels Calcium out of cells and brings it into SR/ER

A 
PMCA out, SERCA in
NXC out (especially during cell recovery)
uniporter into mitochondria (buffer)
23
Q

Characteristics of PMCA and SERCA

A

High affinity low capacity

24
Q

3 types of control of resting calcium concentration

A

Primary active transport
Secondary active transport
Facilitated transport

25
Q

NCX activity is

A

Membrane dependant- depolarised membrane potential reverses mode of operation (Ca2+ in for example in cardiac action potential)

26
Q

NCX in ventricular myocytes

A 
-90 = NCX Calcium out 
\+10 = NCX calcium in 
-90 = NCX calcium out
27
Q

NCX in ischeamia

A

Low oxygen, ATP depleted, sodium pump inhibited, Na+ accumulates in depolarised, NCX reverses, Ca++ in which is toxic

28
Q

Acid extrudes

A

NHE, NBC

29
Q

Base extrudes

A

AE

30
Q

NHE mechanism

A

Exchange Na+ for intracellular H+, regulates pH, 1:1 exchange, activated by growth factors, inhibited by amiloride

31
Q

NBC and AE are

A

Bicarbonate transporters involved in cell volume regulation

32
Q

Cell volume regulation

A

Swell- extrude ions

Shrink- influx ions

ICPP (8 decks)

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