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Medicine Year 1 Semester 1 - Part 2 > Active transport > Flashcards

Active transport Flashcards

1
Q

Describe the structure and function of the sodium pump

A

The sodium pump is an integral membrane protein which is an enzyme capable of the vectorial transport of Na+ and K+ across the membrane.

The sodium pump has alpha and beta subunits.

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2
Q

Features of the sodium potassium pump

A

The sodium/potassium pump is an Alpha2Beta2 tetramer, MW 270000

Na+ ions bind internally (3 per alpha)
K+ ions bind externally (2 per alpha)

ATP binding sites are intracellular

Most cells have approximately 1 million sodium pump sites.

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3
Q

Where are the ATP binding sites ?

A

Found intracellularly

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4
Q

Where are the cardiac glycoside binding sites ?

A

Found extracellularly
They ONLY inhibit from the extracellular surface

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5
Q

Sodium pump equation

A

3[Na+]i + 2[K+]o <=> 3[Na+]o + 2[K+]I

ATP is hydrolysed to ADP by the enzyme (Na+ + K+)ATPase

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6
Q

Molecular weight of alpha and beta

A

Alpha - 95000
Beta - 40000

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7
Q

Sodium and Potassium concentrations inside and outside

A

OUTSIDE
Na+ : 140mM
K+ : 5mM

INSIDE
Na+ : 10mM
K+ : 140mM

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8
Q

How do cells maintain their steady-state intracellular ionic concentrations ?

A

Passive diffusion :
Na into the cell
K out of the cell

Active transport
3 Na out of the cell
2 K into the cell

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9
Q

Km

A

The concentration of substrate which permits the enzyme to achieve 1/2 Vmax.

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10
Q

Describe an enzyme with a High Km

A

An enzyme with a high Km has a low affinity for its substrate and requires a greater concentration of substrate to achieve Vmax.

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11
Q

What is the rate limiting factor in the sodium pump ?

A

So, intracellular sodium ion conc is rate limiting factor (in normal physiological situation) as usually only about 10mM inside the cell

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12
Q

How can the sodium potassium pump be inhibited and stimulated ?

A

Inhibited by removing [K+]o
Stimulated by increasing [Na+]i

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13
Q

How many times does the sodium potassium pump reaction occur per second ?

A

100 times per second

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14
Q

Cardiac Glycosides

A

Digoxin

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15
Q

Uses of digoxin

A

Used to treat heart failure and arrhythmias

Blocks the Na/K pump

Induces increase in intracellular Na+ that will drive an influx of calcium in the heart and cause an increase in contractility.

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16
Q

What does a decrease in [K+]o result in ?

A

Increased binding between cardiac glycosides and the sodium pump.

Decreased [K+]o leads to increased digoxin binding.

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17
Q

Hypokalaemia

A

Low blood potassium levels

RANGE : Less than 3.5

Moderate : 2.5-3.0
Severe : less than 2.5

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18
Q

Symptoms of hypokalaemia

A

Abnormal heart rhythms
Muscle damage
Muscle weakness / spasms
Paralysis

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19
Q

Norokalaemia

A

Normal blood potassium levels

RANGE : 3.6-5.2

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20
Q

Hyperkalaemia

A

High blood potassium levels

RANGE : More than 5.5

Moderate : 6.1-6.9
Severe : more than 7.0

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21
Q

Symptoms of hyperkalaemia

A

Nausea
Palpitations
Muscle weakness

Over approx 7.0, cardiac arrest

22
Q

How is digoxin toxicity hightened ?

A

By hypokalaemia

As digoxin ends to the K+ site of the Na+/K+ ATPase pump, low serum potassium levels increase the risk of digoxin toxicity.

23
Q

Digoxin feature

A

Has a very narrow therapeutic index

24
Q

Results of hyperkalaemia

A

It diminishes digoxins effectiveness

25
Briefly explain the clinical significance of the interaction between the binding of the cardiac glycosides and the extracellular potassium concentration.
Increased binding between cardiac glycosides and the sodium pump as a result of the decrease in [K+]o. This results in increased digoxin binding, which blocks the Na/K ATPase pump. Induces increase in intracellular Na+ that will drive an influx of calcium in the heart and cause an increase in contractility. (Used to treat heart failure and arrhythmias)
26
Therapeutic index
The dose producing toxicity in 50% of the population --------------------------------------------------------------------------------- The minimum effective dose for 50% of the population
27
Values of therapeutic index
More than ED50 Less than TD50
28
Use of digoxin and therapeutic index
Congestive heart failure 2:1
29
Use of remifentanil and therapeutic index
Patient controlled analgesia (pain relief) during labour Synthetic opioid 33000:1
30
Use of diazepam and therapeutic index
Sedative 100:1
31
Use of ethanol and therapeutic index
Sedative 10:1
32
Explain the difference between primary and secondary active transport
Primary directly couples the hydrolysis of ATP to molecular movement. Secondary uses stored energy e.g. in the Na+ gradient (generated by the sodium pump) to drive molecular transport against the electrochemical gradient.
33
Sodium - potassium pump
Transports Na+ out of the cells and K+ into cells Maintains the Na+ and K+ differences across cell membranes Establishes a negative voltage inside the cell (compared with outside) vital for nerve function and signal transduction.
34
Importance of negative voltage inside the cell generated by the sodium-potassium pump
It is vital for nerve function and signal transduction
35
Describe the sodium potassium pump activation
When 2 x K+ are bound to the external K+ sites and 3 x Na+ to the internal sites ATPase is activated. One ATP is cleaved to ADP + 1 x high energy phosphate bond (Pi) Phosphorylation causes a chemical and conformational change to the carrier protein causing the 3 x Na+ to be extruded across the membrane and the 2 x K+ to be introduced into the cell.
36
Role of the sodium/potassium pump
Maintains cell volume The membrane is not very permeable to Na+ but a small amount does leak through. Na+ must be pumped out of the cell or it would eventually burst.
37
Results of net transfer of ions out of the cell
a) Dilutes the cytosol b) Without this, (too much) water would be pulled into the cell due to osmotic pressure (due to high conc. of osmotically active Na+) and the cell would burst.
38
GLUT1
Basal uptake in placenta and brain
39
GLUT2
Transepithelial transport, Beta cells
40
GLUT3
Basal uptake in the brain
41
GLUT4
Skeletal muscle (insulin dependent)
42
GLUT5
Intestinal absorption of fructose
43
Na+ dependent glucose transporter isoforms
SGLT1 SGLT2
44
SGLT1
Km - 0.8 Affinity - High Na+/glucose ratio - 2:1 Accumulation ratio - 30000:1
45
What uses SGLT1 ?
Intestinal uptake of glucose
46
SGLT2
Km - 1.6 Affinity - Low Na+/glucose ratio - 1:1 Accumulation ratio - 200:1
47
What uses GLUT2 Facilitated diffusion ?
Trans-epithelial glucose transport
48
Diuretics use
They increase urine output by the kidneys Promote diuresis Treatment for : high blood pressure and excessive fluid retention
49
Side effects of diuretics
Loop diuretics such as Furosemide Increased urinary excretion of potassium
50
Cardiac glycoside toxicity and blood potassium concentration
Patients on digoxin (narrow therapeutic index) who start diuretics (furosemide) – may become hypokalaemic. A reduction in competition between K+ and digoxin results in increased digoxin binding to the sodium pump. (though plasma concentration is unchanged) Because of the very narrow therapeutic index, the patient develops digoxin toxicity.
51
Emergency treatment for digoxin toxicity
Administer a digoxin binding antibody Digibind rapidly binds to the digoxin causing it to dissociate from the sodium pump reversing the toxicity associated with the increased sodium pump inhibition caused by the hypokalaemia.

Medicine Year 1 Semester 1 - Part 2 (37 decks)

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