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Semester 3 - urinary > 9. Regulation of potassium and magnesium > Flashcards

9. Regulation of potassium and magnesium Flashcards

1
Q

What is the main intracellular cation?

A

potassium

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2
Q

What does potassium determine?

A

resting membrane potential

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3
Q

What are the body concentrations of potassium?

A

Total body K+: 3-4mmol/L
• Intracellular fluid: 98%: 150-160mmol/L
• Extracellular fluid: 2%: 4-5mmol/L

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4
Q

What is the effect on resting membrane potential if extracellular K+ rises and falls?

A
  • If extracellular [K+] rises, the resting membrane potential is decreased (i.e. depolarized)
  • If extracellular [K+] falls, the resting membrane potential is increased (i.e. hyperpolarized)
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5
Q

Where in the nephron is potassium reabsorbed?

A

65% in PCT, 20% in TAL

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6
Q

How is potassium reabsorbed in the PCT?

A
  • Passive
  • Through tight junctions (paracellular movement)
  • Via concentration gradient/solvent drag
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7
Q

How is potassium reabsorbed in the TAL?

A
  • Transcellular - Na+K+ ATPase on basement membrane maintains gradient of Na+ by pumping Na+ out of tubular cell to blood and K+ in. Na+K+Cl- cotransporter on apical membrane transport the ions into the cell. ROMK channels and Cl-K+ channels on the basal membrane move potassium and chloride out of the cell into blood
  • Paracellular - ROMK channels on apical membrane also transport K+ out of cell into lumen and the positive charge in lumen repels cations so potassium and other cations move paracellularly to the blood.
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8
Q

Why is there not a lot of reabsorption of potassium in the DCT?

A

K+ reabsorption and leakage back are approximately equal in early DCT

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9
Q

Where does secretion of K+ occur and in which cells?

A

In the late DCT and collecting duct

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10
Q

Describe how secretion of K+ occurs

A

ENaC channels on apical surface move Na into cell. Na+K+ ATPase on basal membrane moves Na into blood and K+ in. the K+ is the then pumped into the lumen through the (ATP dependent) K+ pump

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11
Q

What cells are involved in reabsorption of K+ in late DCt and collecting duct?

A

intercalated cells

• 10-12% reabsorbed if body trying to preserve K+

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12
Q

Describe how reabsorption of K+ occurs at late DCT and CD

A
  • H+ATPase on apical membrane moves H+ into lumen.
  • H+K+ATPase moves H+ into lumen and K+ into cell.
  • on the basal surface, Na+K+ ATPase moves K+ out into blood and Na+ into cell
  • ROMK channels on basal surface also help move K+ into blood
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13
Q

What are the causes hypokalaemia??

A 
• Excess insulin
• Alkalosis 
• Certain catecholamines (beta-2- adrenergic agonists and alpha- adrenergic antagonists
• Insufficient intake
- Anorexia nervosa
- Prolonged fasting
• Too much aldosterone
- Primary aldosteronism
- Compensated heart failure
- Cirrhosis
• Diuretics e.g. loop and thiazides
• Vomiting
• Diarrhoea (lead to metabolic alkalosis)
• Sweat – excessive exercise, hot climate
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14
Q

How does alkalosis lead to hypokalaemia?

A

To lower blood pH K+ moved into cells in exchange for H+

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15
Q

How does increased aldosterone lead to hypokalaemia?

A

aldosterone causes proliferation of carriers on principal cells so increased secretion

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16
Q

What is the pathophysiology behind hypokalaemia?

A
  • Low K+ results in decreased resting potential – nerve and muscle cells are hyperpolarized
  • Less sensitive to depolarizing stimuli and less excitable
  • Less action potentials generated and paralysis ensues
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17
Q

Below which levels does hypokalaemia become symptomatic?

A

Hypokalemia is asymptomatic until K+ concentration falls below 2- 2.5mmol/L

18
Q

WHat are the Clinical effects of hypokalemia?

A
  • Muscle weakness, cramps and tetany (starts in lower extremities)
  • Impaired liver conversion of glucose to glycogen
  • Vasoconstriction and cardiac arrythmias
  • Impaired ADH action causing thirst, polyuria and no concentration of urine
  • Metabolic alkalosis due to increase in intracellular H+ concentration
19
Q

What is the treatment for hypokalaemia?

A

treating underlying cause. Oral or intravenous K+ may also be required

20
Q

What may cause hyperkalaemia?

A 
• Reduced renal excretion
• Increased plasma load 
• Insulin deficiency – Type 1 diabetes
• Transcellular shift of K+ out of cells
• Pseudohyperkalemia, an artifact:
• Certain catecholamines (beta-2- adrenergic antagonists and alpha- adrenergic agonists
• Hypoaldosteronism and drugs which reduce effect of aldosterone (renin inhibitors, ACE inhibitors
etc.)
21
Q

What may lead to reduced renal excretion of potassium?

A

AKI or CKD, mineralocorticoid deficiency (e.g. Addison’s disease), K+ sparing diuretics or renal tubular defects

22
Q

What may lead to increased plasma load of potassium?

A

due to dietary changes, IV infusion or cellular tissue breakdown

23
Q

What may lead to Transcellular shift of K+ out of cells?

A

due to metabolic acidosis, insulin deficiency, exercise or drugs (digoxin)

24
Q

What may lead to Pseudohyperkalemia?

A

due to hemolysis during venipuncture or storage of the sample, a high white cell or platelet count

25
Q

What are the clinical features of hyperkalaemia?

A
  • Can be asymptomatic

* Muscle weakness, cardiac arrythmias

26
Q

How is hyperkalaemia treated?

A

Treatment varies depending on the cause

27
Q

Emergency treatment of hyperkalemia (>6.5mmol/L or ECG changes)

A
  • Calcium gluconate – Ca2+ stabalises 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
28
Q

What are other treatments of hyperkalaemia?

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

29
Q

What are the ECG signs of hyperkalaemia?

A 
> 5.5 mEq/L = peaked T waves
> 6.5 mEq/L = T wave widening and flattening + lengthening PR interval
> 7 mEq/L = Widening QRS
~9 mEq/L = sine wave
> 9 mEq/L = cardiac arrest
30
Q

What is the function of magnesium?

A
  • Controls mitochondrial oxidative metabolism and so regulates energy production
  • Is vital for protein synthesis
  • Regulates K+ and Ca2+ channels in cell membranes
31
Q

What percentages of magnesium are reabsorbed and where?

A
  • 30% PCT
  • 60% LoH
  • 5% DCT
  • 5% excreted
32
Q

What is the effect of increased plasma magnesium?

A

• The Tm for Mg2+ absorption is equal to the concentration of Mg2+ filtered. Therefore an ↑Mg2+ results in ↑filtering which therefore exceeds the Tm. Resulting in an ↑excretion

33
Q

Where is reabsorption of magnesium regulated?

A
  • Regulation of Mg2+ absorption in LoH.
  • If Mg2+ decreases, cell transport of Mg2+ increases
  • PTH increases reabsorption of Mg2+ in the LoH
34
Q

What are the causes of HYPOMAGNESAEMIA?

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
35
Q

What id Hypomagnesaemia commonly associated with?

A
  • Hypokalemia – many conditions cause low K+ concentrations

* Hypocalcemia – Mg2+ needed to make PTH

36
Q

What are the signs and symptoms of Hypomagnesaemia >?

A

• Uncontrolled stimulation of nerves and tetany

37
Q

Treatment of Hypomagnesaemia

A

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

38
Q

cause of Hypermagnesemia

A

• Renal failure – unable to excrete Mg2+
• Ingestion of Mg2+
- Incorrectly prepared IV infusion
- Mg2+ containing medication (magnesium hydroxide, constipation and heartburn)

39
Q

signs and symptoms of Hypermagnesemia

A
  • Reduced muscle contraction
  • High Mg2+ inhabits PTH release. This leads to hypocalcemia (muscle weakness, diminished reflexes, respiratory failure)
  • Very high levels Mg2+ alter the electrical potential across the cardiac cell membrane, lead to cardiac arrythmias
40
Q

treatment of Hypermagnesemia?

A

• Treatment depends on cause. Reduce intake. Calcium gluconate injection (Mg2+ and Ca2+ compete). Furosemide to increase excretion. Hemodialysis in severe cases

Semester 3 - urinary (33 decks)

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