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Urinary > 9. H+, K+, Ca2+ And Mg2+ > Flashcards

9. H+, K+, Ca2+ And Mg2+ Flashcards

1
Q

Metabolism of what produced CO2?

A

Carbohydrate and fat.

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2
Q

Metabolism of what produced non-carbonic acids such as ammonium, sulphuric acid and phosphoric acid?

A

Protein.

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3
Q

Why do the kidneys need to re-absorb all bicarbonate before they can excrete excess H+?

A

For each bicarbonate molecule lost in urine, a H+ ion is generated.

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4
Q

What does pH depend on?

A

CO2 + H2O H+ + HCO3-

Net direction depends on the concentrations of reactants and products. pH depends on how much CO2 reacts to form H+.

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5
Q

What is the pH in the descending limb of the loop of Henle and collecting duct?

A

Descending loop of Henle - 6.7 (HCO3- reabsorption).

Collecting duct - variable 4.5-8.

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6
Q

Where is most HCO3- recovered in the kidney?

A

Proximal convoluted tubule.

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7
Q

What is H+ excretion linked to in the proximal convoluted tubule?

A

Na+ entry into the tubular cell.

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8
Q

How is HCO3- reabsorbed in the proximal convoluted tubule?

A

H+ excreted via Na+/H+ exchanger reacts with HCO3- in the tubular lumen, to form H2O and CO2. There are absorbed across the apical membrane by the tubular cell, and converted back to H+ and HCO3- in the cell. The HCO3- is then absorbed across the basolateral membrane via a Na+/HCO3- cotransporter.

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9
Q

What system buffers most of the excess H+ in urine?

A

Ammonia system.

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10
Q

What result does vomiting have on acid-base balance?

A

Loss of H+ and loss of K+.

Metabolic alkalosis.

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11
Q

What result does diarrhoea have on acid base balance?

A

Loss of K+ and HCO3-.

Metabolic acidosis.

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12
Q

How is K+ taken up into cells?

A

Via 3Na+/2K+ ATPase.

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13
Q

What 3 things predominantly increase 3Na+/2K+ ATPase activity and so increase K+ entry into cells?

A

K+ concentration in plasma.
Insulin.
Noradrenaline effect on beta2-adrenoceptors.

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14
Q

Name 1 condition that can inhibit 3Na+/2K+ ATPase activity?

A

Digitalis (foxgloves).

Chronic disease eg heart failure, CKD.

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15
Q

Give 3 things than increase K+ movement out of a cell via K+ channels?

A

High osmolarity.
Acidosis.
Cell damage.
Exercise.

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16
Q

Name 1 thing than reduces K+ movement out of cells by K+ channels.

A

Alkalosis.

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17
Q

Where in the nephron is most K+ reabsorbed?

A

Proximal tubule.

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18
Q

Where in the nephron tubule can K+ excretion be varied?

A

Collecting duct.

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19
Q

What is Liddle’s syndrome?

A

Hereditary disorder involving increased ENaC activity, causing the kidneys to excrete K+ (via ROMK) but retain too much Na+ and H2O leading to hypertension and metabolic alkalosis.

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20
Q

What two things increase K+ secretion?

A

High flow.

Aldosterone.

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21
Q

What is the aldosterone paradox?

A

The ability of the kidney to stimulate NaCl retention with minimal K+ secretion under conditions of volume depletion, and maximise K+ secretion without Na+ retention in hyperkalaemia. (As is able to increase Na+ retention and increase K+ secretion).

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22
Q

Name 2 conditions can a diet high in K+ help protect against?

A

Hypertension.
Stroke.
Kidney stones.

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23
Q

What is the minimum K+ excretion per day (as kidneys are unable to conserve all the filtered K+, unlike Na+)?

A

15 mmol/day.

24
Q

What do the symptoms of hyperkalaemia and hypokalaemia relate to?

A

Their effect on the membrane potential:
Low serum K+, bigger K+ gradient between intracellular and extracellular compartment - membrane depolarised and increased excitability.
High serum K+, smaller K+ gradient between intracellular and extracellular compartment - membrane hyperpolarised and decreased excitability.

25
Q

What affect can hyperkalaemia and hypokalaemia have on the heart? What does this risk depend on?

A

Increased risk of cardiac arrhythmias.

Risk of symptoms depends on degree and rapidity of change.

26
Q

What are the main symptoms of hypokalaemia?

A

Muscle weakness.
ADH resistance leading to polyuria.
Smooth muscle dysfunction leading to constipation.
Arrhythmias.

27
Q

What can cause increased K+ entry into cells, therefore leading to hypokalaemia?

A

Metabolic alkalosis.

Increased beta-adrenergic activity (NA with stress).

28
Q

What can cause increased K+ GI loss, therefore leading to hypokalaemia?

A

Vomiting/NG drainage.

Diarrhoea.

29
Q

What can cause increased K+ urinary loss, therefore leading to hypokalaemia?

A

Increased aldosterone due to volume depletion (diuretics), primary hyperaldosteronism or secondary hyperaldosteronism.
Increased urine flow (diuretics).
Renal tubular acidosis.
Magnesium deficiency.

30
Q

How would you treat a patient with hypokalaemia?

A

Oral K+ supplements and slow IV potassium.

31
Q

What acid-base or electrolyte imbalances can cause hypokalaemia?

A

Acidosis.
Alkalosis.
Hypomagnesaemia.
Hypocalcaemia.

32
Q

What does high calcium in urine increase the risk of?

A

Kidney stones.

33
Q

What state is calcium in in the plasma?

A

Half is protein bound and half is in ionised form.

34
Q

Calcium in what state is filtered by the kidneys?

A

Ionised calcium.

35
Q

What affect does increased parathyroid hormone levels have on Ca2+ levels?

A

Increased parathyroid hormone increases Ca2+.

36
Q

What affect does increases calcitonin levels have on Ca2+ levels?

A

Increased calcitonin decreases Ca2+ levels.

37
Q

What is renal 25-hydroxyvitamin D3 1alpha-hydroxylase?

A

Cytochrome p450 enzyme found in the proximal tubule of the kidney which catalyses the hydroxylation of calcifediol to calcitriol.

38
Q

What affect does increasing calcitriol levels have on Ca2+ levels?

A

Increased calcitriol increases the level of Ca2+.

39
Q

How can Ca2+ levels be increased in the body?

A

Increased Ca2+ uptake from the gut into the blood.
Increased reabsorption of Ca2+ by the kidneys.
Increased mobilisation of Ca2+ from skeleton and soft bones.

40
Q

What area of the kidney nephron does parathyroid hormone and calcitriol act on?

A

Distal convoluted tubule and renal connecting tubule.

41
Q

Give 4 symptoms of hypocalcaemia.

A

Muscular eg fatigue, muscle weakness, paraesthesia (finger tips/lips), tetany, larygnospasm.
Heart - reduced myocardial contractility (long QT).
Neurological - irritability, memory loss, confusion, hallucination, paranoia.

42
Q

Name 3 causes of hypocalcaemia.

A 
Vitamin D deficiency.
Lack of PTH (high phosphate).
Reduced intake.
Malabsorption.
Pancreatitis.
Chronic diarrhoea.
Hypercalciuria.
Hyperphosphataemia.
Hypomagnesaemia (interferes with PTH).
ECF expansion.
Acidosis.
Drugs.
43
Q

Name 2 drugs associated with hypocalcaemia.

A

Loop diuretics.
Drugs containing phosphate.
Phenytoin.
Drugs lowering magnesium levels eg gentamicin, cisplatin.

44
Q

Name 3 functions of Mg2+.

A

Intracellular signalling.
Cofactors for protein and DNA synthesis.
Control of neuronal activity in the brain.
Cardiac excitability.
Neuromuscular transmission.
Osteoblast proliferation and bone strength.

45
Q

How much Mg2+ is usually absorbed by the gut, and how much can this increase to when levels of Mg2+ are low?

A

30-50%.

Increase to 80% of daily intake.

46
Q

What is responsible for the day-to-day fine tuning of Mg2+ levels?

A

The kidney.

47
Q

What proportion of plasma Mg2+ is filtered by the kidneys?

A

70% (other 30% bound to albumin and not filtered).

48
Q

Where in the nephron is most Mg2+ reabsorbed?

A

Thick ascending limb of the loop of Henle.

49
Q

Name two symptoms of hypomagnesaemia with a serum magnesium <0.7mmol/L.

A

Fatigue.
Muscle spasms.
Anxiety/depression.
Headache.

50
Q

Name two symptoms of hypomagnesaemia with a serum magnesium <0.4mmol/L.

A 
Cardiac dysrhythmias.
Hyperreflexia.
Tetany.
Seizures.
Hypokalaemia.
Hypocalcaemia.
51
Q

What percentage of total body magnesium is serum magnesium a measure of?

A

1% of total body Mg2+.

52
Q

Name 5 causes of hypomagnesaemia, one from decreased intake, one a drug, one from GI loss, one from renal loss and one miscellaneous.

A

Decreased intake - malnutrition, prolonged fasting, IV feeding.
Drugs - loop diuretics, thiazides diuretics, proton pump inhibitors, cyclosporine and tacrolimus (transplant), aminoglycosides, cisplatin.
GI loss - malabsorption/short small intestine (resection), chronic diarrhoea, fistulae.
Renal loss - diuretics, polyuria, hyperaldosteronism, diabetes (glycosuria or ketoacidotic states), metabolis acidosis, renal tubule defects.
Miscellaneous - alcoholism, acute and chronic pancreatitis.

53
Q

How would you treat a patient with hypomagnesaemia?

A

Oral magnesium salts (GI side effects).

IV magnesium sulfate (slow infusion, otherwise cardiac arrest).

54
Q

If hypomagnesaemia present with hypokalaemia or hypocalcaemia, which needs to be treated first?

A

Hypomagnesaemia.

55
Q

When can hypermagnesaemia occur?

A

Renal impairment and adrenal insufficiency - but not symptomatic.
Symptomatic - iatrogenic eg IV magnesium, purgatives/enemas, babies born to mothers treated with IV-Mg2+ eh pre-eclampsia.

56
Q

How would you treat a patient with hypocalcaemia?

A

Calcium supplementation and correct underlying cause.

Urinary (14 decks)

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