9. H+, K+, Ca2+ And Mg2+ Flashcards
Metabolism of what produced CO2?
Carbohydrate and fat.
Metabolism of what produced non-carbonic acids such as ammonium, sulphuric acid and phosphoric acid?
Protein.
Why do the kidneys need to re-absorb all bicarbonate before they can excrete excess H+?
For each bicarbonate molecule lost in urine, a H+ ion is generated.
What does pH depend on?
CO2 + H2O H+ + HCO3-
Net direction depends on the concentrations of reactants and products. pH depends on how much CO2 reacts to form H+.
What is the pH in the descending limb of the loop of Henle and collecting duct?
Descending loop of Henle - 6.7 (HCO3- reabsorption).
Collecting duct - variable 4.5-8.
Where is most HCO3- recovered in the kidney?
Proximal convoluted tubule.
What is H+ excretion linked to in the proximal convoluted tubule?
Na+ entry into the tubular cell.
How is HCO3- reabsorbed in the proximal convoluted tubule?
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.
What system buffers most of the excess H+ in urine?
Ammonia system.
What result does vomiting have on acid-base balance?
Loss of H+ and loss of K+.
Metabolic alkalosis.
What result does diarrhoea have on acid base balance?
Loss of K+ and HCO3-.
Metabolic acidosis.
How is K+ taken up into cells?
Via 3Na+/2K+ ATPase.
What 3 things predominantly increase 3Na+/2K+ ATPase activity and so increase K+ entry into cells?
K+ concentration in plasma.
Insulin.
Noradrenaline effect on beta2-adrenoceptors.
Name 1 condition that can inhibit 3Na+/2K+ ATPase activity?
Digitalis (foxgloves).
Chronic disease eg heart failure, CKD.
Give 3 things than increase K+ movement out of a cell via K+ channels?
High osmolarity.
Acidosis.
Cell damage.
Exercise.
Name 1 thing than reduces K+ movement out of cells by K+ channels.
Alkalosis.
Where in the nephron is most K+ reabsorbed?
Proximal tubule.
Where in the nephron tubule can K+ excretion be varied?
Collecting duct.
What is Liddle’s syndrome?
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.
What two things increase K+ secretion?
High flow.
Aldosterone.
What is the aldosterone paradox?
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).
Name 2 conditions can a diet high in K+ help protect against?
Hypertension.
Stroke.
Kidney stones.
What is the minimum K+ excretion per day (as kidneys are unable to conserve all the filtered K+, unlike Na+)?
15 mmol/day.
What do the symptoms of hyperkalaemia and hypokalaemia relate to?
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.
What affect can hyperkalaemia and hypokalaemia have on the heart? What does this risk depend on?
Increased risk of cardiac arrhythmias.
Risk of symptoms depends on degree and rapidity of change.
What are the main symptoms of hypokalaemia?
Muscle weakness.
ADH resistance leading to polyuria.
Smooth muscle dysfunction leading to constipation.
Arrhythmias.
What can cause increased K+ entry into cells, therefore leading to hypokalaemia?
Metabolic alkalosis.
Increased beta-adrenergic activity (NA with stress).
What can cause increased K+ GI loss, therefore leading to hypokalaemia?
Vomiting/NG drainage.
Diarrhoea.
What can cause increased K+ urinary loss, therefore leading to hypokalaemia?
Increased aldosterone due to volume depletion (diuretics), primary hyperaldosteronism or secondary hyperaldosteronism.
Increased urine flow (diuretics).
Renal tubular acidosis.
Magnesium deficiency.
How would you treat a patient with hypokalaemia?
Oral K+ supplements and slow IV potassium.
What acid-base or electrolyte imbalances can cause hypokalaemia?
Acidosis.
Alkalosis.
Hypomagnesaemia.
Hypocalcaemia.
What does high calcium in urine increase the risk of?
Kidney stones.
What state is calcium in in the plasma?
Half is protein bound and half is in ionised form.
Calcium in what state is filtered by the kidneys?
Ionised calcium.
What affect does increased parathyroid hormone levels have on Ca2+ levels?
Increased parathyroid hormone increases Ca2+.
What affect does increases calcitonin levels have on Ca2+ levels?
Increased calcitonin decreases Ca2+ levels.
What is renal 25-hydroxyvitamin D3 1alpha-hydroxylase?
Cytochrome p450 enzyme found in the proximal tubule of the kidney which catalyses the hydroxylation of calcifediol to calcitriol.
What affect does increasing calcitriol levels have on Ca2+ levels?
Increased calcitriol increases the level of Ca2+.
How can Ca2+ levels be increased in the body?
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.
What area of the kidney nephron does parathyroid hormone and calcitriol act on?
Distal convoluted tubule and renal connecting tubule.
Give 4 symptoms of hypocalcaemia.
Muscular eg fatigue, muscle weakness, paraesthesia (finger tips/lips), tetany, larygnospasm.
Heart - reduced myocardial contractility (long QT).
Neurological - irritability, memory loss, confusion, hallucination, paranoia.
Name 3 causes of hypocalcaemia.
Vitamin D deficiency. Lack of PTH (high phosphate). Reduced intake. Malabsorption. Pancreatitis. Chronic diarrhoea. Hypercalciuria. Hyperphosphataemia. Hypomagnesaemia (interferes with PTH). ECF expansion. Acidosis. Drugs.
Name 2 drugs associated with hypocalcaemia.
Loop diuretics.
Drugs containing phosphate.
Phenytoin.
Drugs lowering magnesium levels eg gentamicin, cisplatin.
Name 3 functions of Mg2+.
Intracellular signalling.
Cofactors for protein and DNA synthesis.
Control of neuronal activity in the brain.
Cardiac excitability.
Neuromuscular transmission.
Osteoblast proliferation and bone strength.
How much Mg2+ is usually absorbed by the gut, and how much can this increase to when levels of Mg2+ are low?
30-50%.
Increase to 80% of daily intake.
What is responsible for the day-to-day fine tuning of Mg2+ levels?
The kidney.
What proportion of plasma Mg2+ is filtered by the kidneys?
70% (other 30% bound to albumin and not filtered).
Where in the nephron is most Mg2+ reabsorbed?
Thick ascending limb of the loop of Henle.
Name two symptoms of hypomagnesaemia with a serum magnesium <0.7mmol/L.
Fatigue.
Muscle spasms.
Anxiety/depression.
Headache.
Name two symptoms of hypomagnesaemia with a serum magnesium <0.4mmol/L.
Cardiac dysrhythmias. Hyperreflexia. Tetany. Seizures. Hypokalaemia. Hypocalcaemia.
What percentage of total body magnesium is serum magnesium a measure of?
1% of total body Mg2+.
Name 5 causes of hypomagnesaemia, one from decreased intake, one a drug, one from GI loss, one from renal loss and one miscellaneous.
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.
How would you treat a patient with hypomagnesaemia?
Oral magnesium salts (GI side effects).
IV magnesium sulfate (slow infusion, otherwise cardiac arrest).
If hypomagnesaemia present with hypokalaemia or hypocalcaemia, which needs to be treated first?
Hypomagnesaemia.
When can hypermagnesaemia occur?
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.
How would you treat a patient with hypocalcaemia?
Calcium supplementation and correct underlying cause.
