Renal physiology - magnesium and potassium - De Zoysa Flashcards
Magnesium
cation, essential for human function
total magnesium content of the human body is ~20mmol/Kg of fat free tissue
Distribution of Mg
99% found in bone (hydroxyapatite), muscle and soft tissue
Intracellular Mg ranges from 5 to 20mmol/L
Extracellular Mg accounts for 1%
Magnesium in physiology
Bone formation Co-factor in > 300 enzymatic reactions - ATP metabolism - Muscle contraction and relaxation - normal neurologic function - release of neurotransmitters Regulation of vascular tone Cardiac rhythm Platelet activated thrombosis
Why is it so hard for Mg to travel into cells?
is always surrounded by heaps of water molecules when in our body, so hard to slip through intracellular channels, so there need to be active processes that strip the water molecules from around the ion
What is normal magnesium homeostasis?
A lot comes from the daily diet, some of this will come from water but this depends on how water is processed
about 100mg excreted through the kidneys each day
Mg reabsorption throughout the nephron
10-20% in PCT (paracellular channel, need Na/KATPase pump)
10% DCT (transcellularly)
60-70% thick ascending limb of the LoH (paracellular through claudin proteins, mutations here can cause low Mg)
In contrast to sodium and calcium reabsorption, a lot of which occurs in the PCT
Assessment of Mg
serum Mg Red cell Mg 24 hour excretion Oral Mg retention test, supplemented by IV retention test Isotope analysis
Causes of hypomagnesamia
- Decreased dietary intake
- GI malabsorption and loss
- Endocrine - hyperaldosteronism, DM, SIADH, “hungry bone syndrome
- Renal loss
- congenital
- Acquired
- Drug induced
Example of drugs that can cause tubular dysfunction –> hypomagnesamia
Amino glycosides
Amphoteriicin B
Cisplatin
Proton pump inhibitors (e.g. omeprazole)
Symptoms of hypomagnesaemia
Weakness and fatigue Fasciculations/cramps tetany/carpopedal spasm Numbness / parasthesia Seizures Arrhythmias
treatment?
IV magnesium (magnesium sulphate) oral used in most cases
Hypermagnesemia
in advanced CKD the compensatory mechanisms start to become inadequate
excessive oral admin of magnesium salts or magnesium containing drugs
Iatrogenic
Potassium
Majority inside cells (a little bit i the skeleton and ECF)
Potassium haemostasis
daily oral intake 1560-5850mg/day
At healthy steady state 90-95% excreted in urine, 5-10% excreted in faeces
Internal balance
- What maintains K+ levels
- Initial changes in extracellular K+ buffered by?
- kidneys
- movement of K into or out of skeletal muscle, regulated by insulin and catecholamines
hyper glycaemia will cause?
K efflux from cell
K reabsorption in nephron
60% in PCT (paracellular, in association with NaKATPase )
30% in thick ascending (active with NaKCl channel and ROMK channel)
Variable in DCT and CD (where regulation occurs: aldosterone and angiotensin)
hypokalemia
serum K <3.5mmol/L Symptoms - muscle weakness - Paralysis - cardiac conduction abnormalities - Cramps - constipation
Hypokalemic periodic paralysis
autosomal dominant (rare) or thyrotoxic Abnormal K+ channels on cell membrane Tigger is often high carb meal (insulin) or SNS activation (beta agonist)anxiety or exercise Excessive movement of K+ into cells extreme weakness
K losses
RENAL hyperaldosteronism - adrenal aldosterone secreting tumor liquorice Diuretics Renal tubular acidosis
GUT Vomiting diarrhoea laxatives Ileostmey
Treatment - hypokalemia
treat underlying problem
Fro mild hypokalemia - use oral
For severe use IV replacement
hyperkalemia
k > 5.0mmol/L symptoms - fatigue or weakness - Parasthesia - Nausea and vom - Dyspnea - Palpitations
Pseudohyperkalaemia
in lab tests due to haemolysed sample
Causes of hyperkalemia
increased intake
disruption of cell intake
- beta blockers
- acidosis
- rhabdomyolysis
Decreased excretion
- renal failure
- hypoaldosteronism
- ACEi/ARB
- Other drugs
Additions disease
opposite of cons tumour
- deficit secretion of adrenal hormones: aldosterone and cortisol
Characteristic hyper pigmented appearance due to excessive ACTH excretion stimulating melanocytes
Symptoms: lethargy, weakness
Weight loss, low BP
hyperkalemia and hyponatremia
Hyperkalemia treatment
stabilise action potential Push K into cells (by giving intravenous calcium) Reduce K absorption Increase elimination Fix underlying problem
Beta agonists
ventolin nebulisers
5mg salbutamol
can do hourly
this also pushes K intracellularly
Insulin
pushes K+ intracellularly
10 units, short acting insulin + 5ml dextrose
starts to work in about 10-20 mins peak effect in a few hours
How to treat acidosis
oral bicarbonate tablets 840mg 1-3bd/tds
In emergency, IV bicarb 8.4%, 50mL over one hours and repeat
medium term: Cation exchange products bind to K in gut and increase decal elimination Calcium resonium can be given orally or rectally
K losing diuretic
Dialysis
- or if rhabdomyalsis
