12.11.26 cPBL
Potassium handling
Beta agonists => K+ uptake into cells
Beta blockers => K+ release
Insulin => Effect on Na/K ATPase
Bicarbonate => Exchange of cellular H+ for Na+ => Stimulation of the sodium-potassium ATPase
Risonium binds K+ in the gut
One of the only things that actually gets rid of it
Think about INPUT
e.g. Fruit juices
Aldosterone
Required for K+ secretion
Also for H+ secretion (compete)
Hyponatraemia can raise K+ and H+
As there's less available for exchange in DCT
Addison's
Described tuberculous loss of adrenals
=> Lose everything (cortisol and aldosterone)
Contrast with ACTH deficit which specifically drops cortisol
ACTH rises to desperately try to increase cortisol
Cross-reacts with melanocyte stimulating hormone receptors
=> Dark skin
SIADH
Diagnosis of EXCLUSION
Don't just fluid-restrict sick patients!
Exclude:
Thyroid and cortisol dysfunction
Required for water excretion
Kidney injury
Adrenal dysfunction
Medications
Thiazide diuretics
SSRIs
Sulphonylureas
etc..
If you think it's SIADH, try fluid restricting and CHECK IT'S WORKING!
Check urinary sodium
Will be >60 mM
As the body is desperately trying to offload volume
Volume status
Not the same as hydration status
Assess with lying + standing BP
Urine
Max osmolality = 1000 mOsM
Min osmolality = 100 mOsM
[Na] varies but can be undetectable
Compositions of common fluids
Hartmann's
Na -131 mM
Cl - 111 mM
Lactate - 29 mM
K - 5 mM
Ca - 2 mM
Normal saline (300 mOsm/L) (cf hyperchloraemic acidosis)
Na - 154 mM
Cl - 154 mM
Lactated Ringers (273 mOsm/L)
Na - 130 mM
Cl - 109 mM
Lactate - 28 mM
K - 4 mM
Ca - 1.5 mM
5% dextrose
50 g/L dextrose
Gelofusine
Na - 154 mM
Cl - 125 mM
Gelatin 40 g/L
Hyperkalaemia
Excessive intake
Excessive release
Rhabdomyolysis, burns, tumor lysis syndrome
Massive blood transfusion or hemolysis
Shifts/transport out of cells (acidosis, low insulin, beta-blockers, digoxin, succinylcholine)
Ineffective elimination
Renal insufficiency
Medication
ACE inhibitors and ARBs
Potassium-sparing diuretics
NSAIDs
Calcineurin inhibitors
Trimethoprim
Pentamidine
Mineralocorticoid deficiency or resistance
Addison's disease
Aldosterone deficiency
Congenital adrenal hyperplasia
Type IV renal tubular acidosis (resistance of renal tubules to aldosterone)
Gordon's syndrome
Hypokalaemia
Inadequate intake
Gastrointestinal/integument loss
Diarrhoea, perspiration
Vomiting
Urinary loss
Medications
Thiazide diuretics
Loop diuretics
Amphotericin B
Cisplatin
DKA
Obligate loss of potassium from kidney tubules as a cationic partner to the negatively charged ketone, β-hydroxybutyrate
Hypomagnesemia
Mg is required for adequate processing of potassium
Alkalosis 1
Causes a shift of potassium from the plasma and interstitial fluids into cells
Alkalosis 2
Acute rise of plasma HCO3- concentration will exceed the capacity of the renal proximal tubule to reabsorb this anion
Potassium will be excreted as an obligate cation partner to the bicarbonate
Disease states that lead to abnormally high aldosterone levels
Renal artery stenosis
Primary hyperaldosteronism
Hereditary defects of renal salt transporters
Bartter syndrome, Gitelman syndrome
Distribution away from ECF
Insulin, epinephrine, beta agonists, xanthines
Notes
Na/K ATPase
Dies faster in the fridge => Don't refrigerate cold samples!
Genetic trait of fast-dying
Cortisol is normally around 300
But should be >1000 when stressed (e.g. ITU)
Don't forget the context!
Volume status trumps serum osmolality in homeostasis
Normal Na intake = 100 mmol per day
Only about 50% of total calcium is ionised
Glucocorticoids are required to excrete water