potassium balance Flashcards

1
Q

what is the importance of maintaining K+ balance?

A

the kidneys maintain K+ balance in order to maintain plasma [K+] within the narrow concentration range of 3.5-5mmol/L

plasma [K+] within this range is essential for the normal functioning of neurons and muscle, in particular, cardiac muscle

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2
Q

how much K+ do we consume daily?

A

100mol/day with 90mml absorbed through the GIT daily

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3
Q

how is a rise in plasma [K+] after a meal prevented?

A

K+ homestasis maintained by regulation of plasma [K+] in the ECF and regulation of Renal K+ excretion by kidneys to match the dietary K+ intake

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4
Q

regulation of plamsa K+ controlled by?

A
  1. epinephrine
  2. insulin
  3. aldosterone

increase uptake of K+ into skeletal muscle, liver, bone and RBS

increased turnover rate of Na/K/ATPase, Na/K/2Cl, and Na/Cl transporters (acute)

increased quantitiy of na/K/ATPase (Chronic)

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5
Q

What can alter plasma [K+]?

A
  1. acid base balance - metabolic acidosis increases plamsa K+
  2. increase in plasma osmolaltiy causes a release of K+ from cells
  3. cell lysis
  4. exercise
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6
Q

describe K+ excreiton by the kidneys

A
  1. k+ uptake from the blood by the cells of Collecting ducts
  2. K+ is secreted down concentration gradient from these cells into the filtrate and excreted in the urine
  3. secretion is regulated by K+ itself and hormones
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7
Q

describe the regulation of K+ excretion by the DT and CD

A

when plasma [K+] increases

  • hyperkalaemia quickly stimulates K+ secretion -
  • stimulates Na+/K+ pump
  • increases permeability of apical membrane to K+
  • stimulates aldosterone secretion by adrenal cortex (which increases number of Na/K pumps and increases epithelial sodium channels thus increasing permability of apial membrane to K+
  • increases flow rate of tubular fluid
  • ADH- stimulates secretion of K+ by DT and CD but decreases urinary flow rate

hypokalaemia has the opposite effects

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8
Q

what is the overall effect of acute vs. chronic metabolic acidosis?

A

Acute = decreases K+ excretion

chronic = increases K+ excretion- due to associated increase in aldosterone levels

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9
Q

what concentration incidates hypokalemia? What concentration incidates hyperkalema?

A

Hypokalemia < 3.5 mEq/L

due to diuretics, excess aldosterone, metabolic alkalosis, severe diarrhoea, and vomiting

hyperkalemia > 5mEq/L

due to renal failure, adrenal insufficiency, acute acidosis, tissue destruction like burns or trauma

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10
Q

how does severe diarrhoea result in hypokalemia?

A

diarrhoea results in K+ loss via

  1. direct K+ loss via GIT
  2. indirect K+ loss via kidneys - decreases ECF volume, stimulates Aldosterone, cuases excretion of K+ by kidneys

*severe vomitting cuases the same thing to happen*

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11
Q

what are the symptoms of hypokalemia?

A

usually aymptomatic - but if sever

  • weakness of skeletal muscle
  • cardiac arrhythmias- but usually only in those with cardiac disease -

*changes in K+ can have effects of excitable cells- hypokalemia hyperpolarizes the membrane voltage making it more difficult to generate an action potention b/c a larger depolarizing current is needed to reach threshold

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12
Q

why does acute renal failure cuase hyperkalemia?

A

when the glomerular filtration rate falls to about 25% of normal

plasma K+ rises

hyperkalaemia reduces RMP

decreases excitablility of neurons, cardiac cells, and muscle cells, causes cardiac arrest and death

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13
Q

why does hyperkalaemia cause a decrease in excitability of neurons?

A

the membrane potential at the onset of depolarization determines the number of sodium channels activated during depolarization - which in turn determines the magnitude of the inward sodium current and the Vmax of the action potential

as the resting membrane potential becomes less negative (as with hyperkalemia) the percentage of available sodium channels decreases and leads to a decremetn in the inward sodium current (decrease in Vmax)

therefore, as resting membrane potential becomes less negative - Vmax decreases and causes a slowing of impulse conduction through the myocardium and prolongation of membrane depolarization (arrythmia)

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14
Q

why does tissue destruction cause hyperkalemia?

A

when cells lyse and K+ is released into ECF

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15
Q
A
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16
Q

what peak accounts for hyperkalemia on an ECG?

A

tall peaked T wave on ECG

usually seen when K+ is 7mmol/l or higher

17
Q

What do we do with a patient in hyperkalaemic state of emergency?

A
  1. protect the hear - divalent ions Ca2+ depolarizes the threshold potential - when calcium is given, the threshold potential becomes less negative (from -75 to -65) thus the difference between the hyperkalemia-induced resting membrane potential and the calcium induced threhold potential is now back to the normal 15mV and myocyte excitability returns to normal
  2. reduce plasma [K+] - pump it into cells with insulin, glucose,or salbutamol
  3. remove K+ with ion exchange resins in GIT -