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SA urinary > S6) Regulation of Ions > Flashcards

S6) Regulation of Ions Flashcards

1
Q

With reference to the CO2 / HCO3- buffer system, explain the control of blood pH

A

pH depends on how much CO2 reacts to form H+:

  • [CO2]dissolved pushes reaction to right
  • [HCO3-] pushes reaction to left
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2
Q

Briefly describe how pH varies along the nephron

A
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3
Q

HCO3- is filtered at the glomerulus but ~ 80% recovered in PCT.

Describe how the renal recovery of bicarbonate occurs

A
  • H+ excretion linked to Na+ entry in PCT
  • H+ reacts with HCO3- in the lumen to form CO2 which enters cell
  • Converted back to HCO3- which enters ECF
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4
Q

Identify the two buffers for H+ excretion in the kidney

A
  • HPO42- (or some titratable acid)
  • NH4+
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5
Q

Illustrate the role of NH4+ in the H+ buffering systems in the kidney

A
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6
Q

Illustrate the role of HPO42- in the H+ buffering systems in the kidney

A
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7
Q

Loss of Cl- and K+ have a synergistic effect on alkalosis.

Explain why this is

A
  • Normally, kidneys respond rapidly to increased HCO3- by excreting the excess
  • Sustained alkalosis occurs when something else disrupts renal regulation of alkali (potassium & chloride)
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8
Q

Distinguish between the acid-base status after vomiting and diarrhoea respectively

A
  • Vomiting: loss of H+ and K+ → metabolic alkalosis
  • Diarrhoea: loss of K+ and HCO3- → metabolic acidosis
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9
Q

Explain how the inhibited Cl- and K+ reabsorption by furosemide contributes to chloride, sodium, potassium and water loss

A
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10
Q

How would one treat a 66 year old man taking furosemide with metabolic alkalosis and a 2 day history of vomiting and diarrhoea?

A
  • Stop furosemide diuretic
  • Replace NaCl
  • Replace KCl
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11
Q

Approximately 98% of total body K+ is found in cells.

Identify 5 organs/compartments where K+ is largely distributed

A
  • Muscle (most)
  • Liver
  • Interstitial fluid
  • Red blood cells
  • Plasma (least)
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12
Q

What is the normal [K+]plasma ?

A

Serum potassium = 4 mmol/L (3.5-5.5)

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13
Q

What is the recommended daily intake of potassium?

A

Average daily intake 40 – 100 mmol / day

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14
Q

What prevents the toxic accumulation of ingested K+ in the extracellular compartment?

A
  • K+ uptake into cells (quick)
  • K+ excretion in urine (6-8 hours)
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15
Q

How much potassium is lost in urine?

A

80-90% lost in urine (remainder in faeces / sweat)

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16
Q

3 Na+ / 2 K+ ATPase facilitates potassium uptake into cells.

Which 3 factors/events increase and decrease its activity?

A
  • Increased by: insulin, β2 receptor agonists, noradrenaline, aldosterone, [K+]plasma
  • Decreased by: digitalis, chronic disease (heart failure, CKD)
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17
Q

Which factors increase and decrease potassium excretion from cells?

A
  • Increased by: high osmolality, acidosis, cell damage, exercise
  • Decreased by: alkalosis
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18
Q

Briefly, describe the renal regulation of [K+]plasma

A

[K+]plasma is regulated by excretion not absorption

kidneys excrete 80% of K

bowels excrete 20% of K

so either need to increase excretion or dialysis to remove potassium

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19
Q

Where in the kidney nephron is potassium reabsorbed?

A
  • 65 – 70% PCT (paracellular)
  • 20 – 25% TAL (transcellular)
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20
Q

Describe the mechanisms driving K+ transport in the DCT

A
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21
Q

Describe the mechanisms driving K+ secretion in CD

A
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22
Q

Describe the mechanisms driving K+ reabsorption in the collecting duct

A
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23
Q

Illustrate the variable K+ excretion based on [K+]plasma

A
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24
Q

How does aldosterone act to increase K+ secretion?

A
  • ↑ [K+]intracellular
  • ↑ electronegative lumen (Na+ reabsorption)
  • ↑ permeability of luminal membrane
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25
Q

What is the aldosterone paradox?

A

The aldosterone paradox is the ability of the kidney to:

  • Stimulate NaCl retention without increased K+ secretion (during volume depletion)
  • Maximise K+ secretion without Na+ retention (during hyperkalemia)
26
Q

What are the benefits of diets high in K+?

A
  • Lower BP
  • Reduced stroke risk
  • Reduced risk of kidney stones
27
Q

What are the effects of hypokalaemia?

A
  • Low serum K+ leads to bigger K+ gradient between intracellular and extracellular compartment
  • Increased excitability (& risk of arrhythmia) and cardiac arrest
  1. Muscle weakness
  2. fatigue
  3. consitpation
  4. High blood pressure:
28
Q

What are the effects of hyperkalaemia?

A
  • High serum K+ leads to smaller K+ gradient between intracellular and extracellular compartment
  • Decreased membrane excitability (& risk of arrhythmias) risk of cardiac arrest
  1. tingiling and numbness
  2. resp failure
29
Q

What are the symptoms of hypokalaemia?

A
  • Weakness
  • Polyuria (ADH resistance)
  • Constipation (smooth muscle dysfunction)
  • Arrhythmias
30
Q

What are the 4 possible causes of hypokalaemia?

A
  • Reduced dietary intake
  • Increased entry into cells (metabolic alkalosis, ↑ β-adrenergic activity)
  • Increased GI loss (vomiting, diarrhoea)
  • Increased urine loss (↑ aldosterone)
31
Q

How does one assess a patient with hypokalaemia?

A
  • History
  • Fluid balance
  • Acid base status
  • Urine K+ excretion (if K+ loss unclear)
32
Q

What is the general treatment of hypokalaemia?

A
  • Oral K+ supplements
  • Slow IV potassium
33
Q

In terms of hypokalaemia, what happens when one electrolyte abnormality present does not respond to treatment?

A

Consider other the effect of other acid-base or electrolyte imbalances:

  • Acidosis
  • Alkalosis
  • Hypomagnesaemia
  • Hypocalcaemia
34
Q

State three functions of calcium

A
  • Strength of bones and teeth
  • Important for nerve and muscle function
  • Concentration determines action potential
35
Q

Briefly, describe how calcium is distributed in extracellular and intracellular spaces

A
36
Q

Outline the mechanisms involved which prevent hypercalcaemia

A
37
Q

Outline the mechanisms involved which prevent hypocalcaemia

A
38
Q

Describe the principles of calcium resorption in different parts of the kidney nephron

A
  • PCT: paracellular
  • TAL: transcellular
  • DCT: transcellular (PTH & vitamin D control)
  • CT: not reabsorbed
39
Q

Point out some neurological and muscular symptoms of hypocalcaemia

A
  • Neurological: irritability, memory loss, confusion, hallucination
  • Muscular: fatigue, muscle weakness, paraesthesia, tetany, reduced myocardial contractility (long QT)
40
Q

Identify 5 causes of hypocalcaemia

A
  • Vitamin D deficiency
  • Lack of PTH (high phosphate)
  • Reduced intake
  • Malabsorption
  • Chronic diarrhoea
41
Q

Identify 4 drugs which are associated with hypocalcaemia

A
  • Loop diuretics
  • Drugs containing phosphate
  • Phenytoin
  • Drugs that lower magnesium levels e.g. gentamicin, cisplatin
42
Q

How can one treat hypocalcaemia due to Vitamin D deficiency?

A
  • Vitamin D supplementation
  • Calcium supplementation
43
Q

Briefly, describe how magnesium is distributed in intracellular and extracellular spaces

A
44
Q

State five functions of magnesium

A
  • Intracellular signalling
  • Cofactor for protein & DNA synthesis
  • Control of neuronal activity in the brain
  • Cardiac excitability
  • Neuromuscular transmission
45
Q

Briefly illustrate how [Mg2+] in the body is maintained through homeostasis

A
46
Q

When GFR normal, up to 2400 mg Mg2+ is filtered per day.

Describe the kidney handling of magnesium

A
  • 10 – 25% PCT
  • 50 – 70% TAL
  • 5 – 10% DCT
47
Q

Hypomagnesaemia is when serum magnesium < 0.7 mmol/L.

What are the symptoms of such?

A
  • < 0.7 mmol/L: fatigue, muscle spasms, anxiety, headache, depression
  • < 0.4 mmol/L: cardiac dysrhythmias, hyperreflexia, tetany, seizures, hypokalaemia & hypocalcaemia
48
Q

Identify 5 causes of hypomagnesaemia

A
  • Decreased intake (malnutrition / prolonged fasting)
  • Malabsorption
  • Chronic diarrhoea
  • Hyperaldosteronism
  • Diabetes (glycosuria / ketoacidotic states)
49
Q

Identify 4 drugs which are associated with hypomagnesaemia

A
  • Loop diuretics
  • Thiazide diuretics
  • Proton pump inhibitors
  • Aminoglycosides
50
Q

Describe the general treatment of hypomagnesaemia

A
  • Oral magnesium salts (GI side effects)
  • IV magnesium sulfate (slow infusion to prevent cardiac arrest)
51
Q

Hypermagnesaemia is uncommon.

When does it occur?

A

Occurs with renal impairment and adrenal insufficiency (asymptomatic)

52
Q

Describe the general treatment of hypermagnesaemia

A
  • Iv magnesium
  • Purgatives / enemas
53
Q

what defines hypernatremia? and what are some causes?

A

>146mmol/L

  1. osmotic diuresis ( excreting too much water)
  2. fluid loss without replacement (vom)
  3. diabetes insipidus (lots of dilute urine)
  4. incorrect IV fluid replacement
  5. primary aldosteronism
54
Q

what defines hyponatremia?

A
  • serum conc of na 140/135 mmol/L
  • normally to do with fluid imbalance
55
Q

what are some causes of hyponatremia

A
  • diuretics (thiazides)
  • GI losses
  • water overload or retention
  • increased ADH
  • increased plasma osmolality
  • diuretics and renal failure → true na loss
  • peritonitis → true Na loss
  • Burns → true Na loss
56
Q

hyponatremia can be caused by 2 main things

A
  • overloaded with fluid
  • fluid depleted
57
Q

what are some consequences of hyponatremia

A
  • nausea
  • vomiting
  • headache
  • confusion
58
Q

how long can insulin decrease K levels for

A

6 hours

59
Q

what happens to resting potential if the extracellular K rises or falls

A
  • extracellular K rises: resting membrane potential is decreased
  • extracellular K drops: membrane potential increases
60
Q

where is the majority of potassium absorbed

A

67% in the proximal convoluted tubule

some in the loop of henely and some in distal tubule

61
Q

what is the emergency treatment of hyperkalemia

A
  • calcium gluconate: Ca stabilises the myocardium preventing arrhythmias
  • insulin: drives K into cells to lower conc
  • calcium resonium: removes K via excretion from bowels

SA urinary (25 decks)

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