Renal Physiology: Salt and water Flashcards
More adept breakdown of ECF
note 70kg male, 60% water (42L) so 2/3 ICF, 1/3 ECF
IF, transcellular, intravascular
Transcellular (CSF, aqueous humour, synovial fluid, pericardial/pleural). Formed from transport activities of cells.
Key electrolyte concs
ECF: high sodium, low potassium
ICF: low sodium, high potassium
Maintained by Na+/K+ ATPase
What is plasma osmolarity maintained between, and what is it regulated by
NB tonicity
285-295 mOsmol/L
Regulated by salt and water
Hyperosmolar is too much cation, too little water
Hypo-osmolar is too little cation, too much water
effect a solution has on a cell, e.g hypertonic, cell shrinks
Brief definition of what occurs at each part of nephron Glomerulus PCT LoH: A+ D DCT CD
note on filtrate osmolarity at different points
Glomerulus: free filtration of water and salt
PCT: 65-75% of water and sodium reabsorbed, slight filtrate concentration to 300mOsmol/L
LoH, descending: Active water reabsorption
LoH, ascending: Active Na+ reabsorption, 15-20%
(At bottom, 600mOsmol/L, by top 400)
DCT: 5% Na+
CD: 5% Na+
brief diuretics, thiazides and loop
Thiazides, in DCT inducing natriuresis (sodium, chloride symport)
Loop, acting at LoH (NKCCl)
Amiloride, ENaC ?
When is ADH secreted
Low BP/BV, or increase in osmolarity
Increases water reabsorption, increases BP and lowers osmolarity.
Concentrates urine
Upregulate aquaporins
Aldosterone, when is it excreted, where it acts, effects
Stimulated by increased K+ or A2, mineralocorticoid acting on DCT/CD
Increases Na+ reabsorption (holds onto water), increases potassium excretion, up regulates Na+/K+ ATPase activity
RAAS
Renin produced in response to, low renal BF/GFR, macula densa sense low Na+, sympathetic tone
A2: VC, thirst, increase ADH/aldosterone; increase sodium reabsorption (PCT). Raises GFR (efferent arteriole contriction) lowers by mesangial cell contraction??
Hypernatraemia
causes of
> 145mmol/L
Too much salt/volume depletion(water only):
Impaired thirst/consciousness, so common in hospital
No access to fluids
Large water loss
Solute diuresis, such as in DKA. Hypoglycaemia induced diuresis, where water is lost but normal sodium.
Diabetes insipidus, cause of hypernatraemia
results in?
Reduced amount or efficacy of ADH
Results in polyuria and water loss (dilute urine)
Patient can not drink enough to keep up with losses.
Results in hypernatraemia, elevated plasma osmolarity
Types of DI
Central: most from brain injury/trauma, abnormal production. Can give analogues (intranasal/IM)
Nephrogenic: partial/complete ADH resistance, defective aquaporin channels, drug toxicity such as amiloride
Two common causes of hyponatraemia
Excessive Na+ loss or water retention
Pseudohyponataemia
How to check
causes
When Na+ is falsely low, as serum osmolarity will be normal. Normal osmolarity
Causes:
-Hyperglycaemia: an osmotic water shift into blood stream, artifically lowering [Na+], or with mannitol infusion
-Hyperlipidaemia/hyperproteinaemia
Step one when checking hyponatraemic pateint
Check urine osmolality
- If less than 100mOsmol/kg, very dilute urine (low salt)
- Due to polydipsia,water intoxication. DDx with psychotropic drugs, schizophrenia, beer potomania
Step two in checking hyponatraemic patient
VOLUME STATUS
Hypovolemic patinnt with hyponatraemia
learnt the examples
Dehydrated, water loss and sodium loss
Check urine Na+, if low
-Sodium loss, relatively less water loss such as in: diarrhoea, vomiting, bowel obstruction, skin losses (sweating, burns); urinary losses (diuretics, Addisons, ketonuria, osmotic diuresis)
Hypervolemic pateint with hyponatraemia
Fluid overloaded, too much water!
Sodium is retained, but more water is than sodium!
Cirrhosis, nephrotic syndrome, HF/RF
Euvolemic patient with hyponatraemia
Endocrinopathies: hypothyroid, low cortisol
SIADH
Diuretics
fluid replacement
SIADH
urine tests show
- Inappropriate secretion of ADH in absence of normal stimuli such as low BP or increased osmolarity
- Body accumulates too much water, which is stored in cells, thus euvolemic
- Urine osmolarity is not low, neither is sodium
- Plasma osmolality is low
Causes: head trauma, surgery, tumours (lung), chronic lung disease, SSRI’s
Treat with fluid restriction
Hyponatraemia symptoms
Slow onset (brain adaptation): confusion, not quite self Rapid onset: cerebral oedema, confusion and seizures, coma
Brain adaptation to cerebral oedema due to water gain occurs over time, so treatment must be in consideration. Correction speed= onset speed
Hyponatraemia treatments
Slow onset: gradual, fluid restriction only (no more than 8mmol/L a day)
Rapid onset: vigorous treatment, fluid restriction, normal saline or 3% saline in ICU
Consequence of rapid treatment in hyponatraemia
If patient has cerebral oedema, and done too rapidly, not over time for brain adaptation, can cause central pontine myelosis
Compression of myelin sheaths, quadraparesis, pseudobulbar palsy (can’t control facial movements), locked in syndrome (body/facial paralysis, but conscious+ eye movements)