H, K, Ca & Mg Flashcards
Why does the kidney try to conserve all/generate excess bicarb?
For every bicarb lost in urine an H+ is generated
Therefore need to re-absorb all bicarb before we can excrete excess H+
Acidosis and alkalosis, which can we withstand better?
Alkalosis
The pH is 6.7 at the end of the PCT, why?
Re-absorption of bicarb
The pH in the CD can vary between 4.5-8, why such a large range?
pH will reflex how much acid needed to maintain serum pH
How is the acid-base balance effected in vomiting?
Loss of H+
Loss of K+
Metabolic alkalosis
How is the acid-base balance effected in diarrhoea?
Loss of K+
Loss of bicarb
Metabolic acidosis
K+ intake from food (and therefore serum levels) can be quite high, how is death prevented?
K+ uptake into cells (quick)
K+ excretion in urine (6-8hrs)
What 3 things increase the activity of Na/K ATPase? (Decreasing extracellular [K])
K+ conc in plasma
Insulin
Noradrenaline effect on beta2-adrenoceptors
How is K+ excreted?
Small amounts in faeces and sweat
800 mmol by normal kidneys
What factors increase K+ secretion?
Increased intracellular [K+] = larger gradient (raised by aldosterone)
Increased electro-ve lumen = large pull for K+ (raised by aldosterone)
Increased permeability of the luminal mem (raised by aldosterone)
Decreased luminal [K+]
What is hypokalaemias effect on membrane potential?
Bigger gradient between intracellular and extracellular compartment
Depolarisation lead to increased excitability
Risk of arrhythmias
What is hyperkalaemias effect on membrane potential?
Smaller gradient between intracellular and extracellular compartment
Decreased membrane excitability
Risk of cardiac arrhythmias
Outline the symptoms of hypokalaemia
Weakness
Polyuria = low K causes ADH resistance
Constipation = smooth muscle dysfunction
Arrhythmias
U wave on ECG
What are the causes of hypokalaemia?
Reduced dietary intake
Increased entry into cells = met alkalosis, increased beta-adrenergic activity
Increased GI loss = vomiting, diarrhoea
Increased urine loss = increased aldosterone, increased urine flow, renal tubular acidosis
Ca reabsorption is under what kind of control?
Hormonal and vitD
What inhibits the precipitation of Ca and therefore the formation of stones?
Magnesium
What happens in the presence to hypercalcaemia?
Activation of Ca sensing receptors
Decreased PTH and increased calcitonin release =
1) increased renal excretion
2) less active vit D = decreased calcitriol synthesis = decreased mobilisation of Ca from skeleton and soft tissues
= normal plasma Ca
What happens in the presence of hypocalcaemia?
Inactivation of Ca sensing receptors
Increased in PTH release =
1) decreased in renal excretion
2) more active vit D = increase in calcitriol synthesis = increased mobilisation of Ca from skeleton and soft tissue
= normal plasma Ca
What part of the tubules is under PTH and vit D control?
DCT
What are the symptoms of hypocalcaemia?
Paraesthesia = pins and needles
Tetany
Laryngospasm
Reduced myocardial contractility
Memory loss
Confusion
Hallucination
Outline the causes of hypocalcaemia?
Vit D def
Lack of PTH
Reduced intake
Malabsorption
Hypomagneasaemia = interferes with PTH
Outline the functions of magnesium
Intracellular signalling
Cofactor for protein and DNS synthesis
Control of neural activity in the brain
Cardiac excitability
Neuromuscular transmission
Osteoblast proliferation and bone strength
In the tubule where does the majority of magnesium reabsorption take place?
TAL 50-70%
Name some causes of hypomagnesaemia
Malnutrition
Prolonged fasting
IV feeding
Loop diuretics
Thiazide diuretics
What symptoms occur with hypomagnesaemia?
Fatigue
Muscle spasms
Anxiety
Headache
Cardiac dysrhythmias
Tetany
Seizures
Hypocalaemia
