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Urinary > 3.1 Regulation Of Potassium And Magnesium > Flashcards

3.1 Regulation Of Potassium And Magnesium Flashcards

1
Q

what ion determines the resting membrane potential?

A

potassium

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2
Q

what is the extracellular concentration of potassium?

A

4-5mmol/L

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3
Q

what happens to the membrane potential if the extracellular fluid concentration of potassium rises/falls?

A

rises : the resting membrane potential is depolarised (becomes less negative)
falls: the resting membrane potential is hyper polarised ( becomes more negative)

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4
Q

describe the movement of potassium in the kidney?

A

PCT: reabsorbs 65%. passive reabsorption by paracellular transport via concentration gradient/ solvent drag
TAL: reabsorbs 20% of potassium through trans cellular and paracellular transport mechanisms
DCT: reabsorption and leakage is equal
late DCT and CD: secretion by principle cells. reabsorption by intercalated cells if plasma levels are too low

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5
Q

describe the channels used in transcellular transport of potassium in the TAL?

A 
Apical surface
-Na/K/2Cl cotransporter for reabsorption
- ROMK for secretion 
basolateral surface 
- NA/K ATPase
- ROMK 
- Cl/K cotransporter 
all reabsorbing potassium
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6
Q

how does activation of the RAAS system affect potassium handling in the kidney ?

A

activation of RAAS increases the secretion of aldosterone by the adrenal glands.
Aldosterone acts a the principle cells to increase the expression of ENAC and ROMK channels. This increases the amount of potassium secreted into the tubular filtrate

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7
Q

How would acidosis affect potassium handling in the kidney?

A

would have greater activation of H+/K+ ATPase in the alpha intercalated cells of the collecting duct. This exchanges H+ ions for K+ ions and therefore we would have increase reabsorption of potassium

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8
Q

what are some of the common causes of hypokalaemia?

A 
excess insulin 
alkalosis
certain catecholamines 
insufficient intake ( anorexia nervosa/ prolonged fasting) 
too much aldosterone 
loop and thiazide diuretics 
vomiting 
diarrhoea (leading to metabolic alkalosis)
diuretics 
sweat - excessive exercise, hot climate
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9
Q

what are some of the causes for too much aldosterone?

A

primary aldosteronism
compensated heart failure
cirrhosis

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10
Q

why can alkalosis cause hypokalaemia?

A

as K+ is moved into cells in exchange for H+ in an effort to decrease the pH

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11
Q

what does hypokalaemia become symptomatic

A

when the potassium concentration falls below 2-2.5mmol/L

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12
Q

what is hypokalaemia?

A

when plasma concentration of potassium falls below 3.5mmol/L

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13
Q

how does hypokalaemia affect the resting membrane potential?

A

as the potassium will tend to move down its concentration gradient, the concentration within the cell will fall, therefore the cell will become hyper polarised and the resting membrane potential will increase

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14
Q

what are the clinical effects of hypokalaemia?

A
  • muscle weakness, cramps, tetany (starts in lower extremities)
  • Impaired liver conversion of glucose to glycogen (raised blood sugar) as insulin requires potassium to work
  • Vasoconstriction and cardiac
    arrythmias
  • Impaired ADH action causing thirst, polyuria and no concentration of urine
  • Metabolic alkalosis due to increase in intracellular H+ concentration
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15
Q

what is the treatment of hypokalaemia?

A

treating the underlying cause

oral or intravenous K+

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16
Q

what commonly causes hyperkalaemia?

A
  • Reduced renal excretion due to AKI or CKD
  • mineralcorticoid deficiency (e.g. Addison’s disease) resulting in less aldosterone and less potassium secretion
  • K+ sparing diuretics or renal tubular defects
  • Increased plasma load
  • Insulin deficiency – Type 1
    diabetes • Transcellular shift of K+ out of cells: due to metabolic acidosis, insulin
    deficiency, exercise or drugs
    (digoxin)
  • Pseudohyperkalemia
  • Certain catecholamines
  • Hypoaldosteronism and drugs
    which reduce effect of aldosterone (renin inhibitors, ACE inhibitors etc.)
17
Q

what might increase the plasma load of potassium?

A

dietary changes
IV infusion
cellular tissue breakdown

18
Q

what is pseudohyperkalaemia?

A

an artifact, not true hyperkalaemia:
due to hemolysis during
venipuncture or storage of the sample, a high white cell or platelet count

19
Q

what are the clinical features of hyperkalaemia?

A

muscle weakness
cardiac arrhythmias
fatigue
- can be asymptomatic

20
Q

why might hyperkalaemia be a medical emergency?

A

due to the effects on the heart
slightly depolarised membrane inactivated some of the voltage gated sodium channels of the heart slowing the upstroke of an AP
- mild hyperkalaemia = increased excitation
- moderate hyperkalaemia = slowed conduction due to inactivation of sodium channels. lengthening of ECG
- severe hyperkalaemia = heart can stop - asystole

21
Q

what is severe hyperkalaemia?

A

a plasma concentration of potassium of greater than 6.5mmol/L

22
Q

what is the emergency treatment for hyperkalaemia?

A

• Calcium gluconate – Ca 2+ stabilises the myocardium, preventing arrythmias
• Insulin – drives K+ into cells to lower plasma concentrations. Given with
glucose to avoid hypoglycemia
• Calcium resonium - Removes K+ by
increasing excretion from the bowels. Only way to remove K+ without renal replacement therapy

23
Q

what ECG changes are seen during hyperkalaemia?

A 
peaked T wave 
P wave flatten / disappear 
PR interval lengthening 
Widening of the QRS complex 
bradycardia 
sine wave pattern (cardiac arrest)
24
Q

what are treatments that may help hyperkalaemia but aren’t first line?

A
  • Salbutamol – Drives K+ into cells when given nebulized or IV. Should not be used in patients with ischemic heart disease or arrythmias
  • Sodium bicarbonate – Correction of acidosis, would also drive K+ into cells. Not used in patients at risk of fluid overload
  • Renal replacement therapy – Dialysis or hemofiltration are used if medical therapies fail to correct hyperkalemia
25
Q

what is the function of intracellular magnesium?

A
  • Controls mitochondrial oxidative metabolism and so regulates energy production
  • Is vital for protein synthesis
  • Regulates K+ and Ca2+ channels in cell membranes
26
Q

what is the normal magnesium plasma concentration

A

2.12 - 2.65mmol/L

27
Q

by what mechanism is magnesium usually reabsorbed?

A

passively through paracellular transport

28
Q

where does the majority of magnesium reabsorption occur?

A

loop of henle (60%)

29
Q

what hormone increases the reabsorption of magnesium in the loop of henle?

A

parathyroid hormone

30
Q

what is hypomagnesaemia commonly caused by?

A

• Decreased intake
• Diarrhea
• Absorption disorder including fat absorption defects
• Renal wasting – intrinsic (Bartters’s syndrome), extrinsic (diuretics e.g.
thiazides)
• Uncontrolled diabetes mellitus – large volume urine flow, carries ions out of
nephron
• Excessive alcohol consumption - ↑renal excretion, poor diet

31
Q

what is Bartter syndrome?

A

rare inherited disease characterised by a defect in the thick ascending limb of the loop of Henle, which results in low potassium levels (hypokalemia), increased blood pH (alkalosis), and normal to low blood pressure

32
Q

what is hypomagnesaemia commonly associated with?

A

hypokalaemia

hypocalcaemia - mg needed to make PTH

33
Q

what are the signs and symptoms of hypomagnesaemia?

A

uncontrolled stimulation of the nerves and tetany

34
Q

what is the treatment of hypomagnesaemia?

A

Treatment depends on cause. Oral supplementation or IV/IM magnesium sulphate

35
Q

what are the common causes of hypermagnesaemia?

A

renal failure - unable to excrete Mg2+

ingestion of mg2+ - incorrectly prepared IV infusion, magnesium containing medication

36
Q

what are the signs and symptoms of hypermagnesaemia?

A

reduced muscle contraction
high magnesium inhibits PTH release. Hypocalcaemia can result (muscle weakness, diminished reflexes, respiratory failure)
Very high levels can cause cardiac arrhythmias be changing the electrical potential across the membrane

37
Q

what is the treatment of hypermagnesaemia?

A

Treatment depends on cause. Reduce intake. Calcium gluconate injection (Mg 2+ and Ca2+ compete). Furosemide to increase
excretion. Hemodialysis in severe cases

Urinary (18 decks)

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