Potassium Disorders Flashcards
Clinical manifestations
Normal range 3.5-5.1 mol/L
- ICF/ECF K affects electrical potential and hence the membrane excitability of neuromuscular organs, muscles and heart
HyperK
- depolarise membrane and inactivate Na –> decrease excitability
- risk of arrhythmia
HypoK
- remove Na channel inactivation –> more depolarisation and increase excitability
- muscle weakness, paralysis
Potassium homeostasis
Intake
Transcellular shift (Na/K pump - insulin/ catecholamines/ thyroxine, pH - H in/K out)
Extra-renal excretion e.g. sweat, faeces
Renal excretion
- passive secretion by tubular cell at CCD
- enhanced by flow rate, aldosterone (increase K channels and Na/K pumps – net increase Na reabsorption at expense of K and H)
Approach to HyperK
- Rule out pseudohyperK (very common)
- Assess patient
- DDx of hyperK (often multifactorial)
Cause of PseudohyperK
- Exogenous contamination during blood taking
- EDTA (purple) and fluoride (grey)
- both containing K salts; fluoride has K-oxalate or K-EDTA
–> EDTA and oxalate irreversibly bind Ca and Mg and inhibit ALP activity
==> high K, low Ca/Mg, low ALP - Drip arms
- dextrose drip with K supplement = all analytes diluted except K
- NS with K = Na normal
—> check patient status and presence of drip, check other bloods drawn at the same time for any dilution e.g. Low Hct - Ex vivo release from cells (high K, PO4, AST, ALT, ALP, LDH)
- haemolysis/ traumatic venipuncture/ prolonged tourniquet
- overnight sample (cell lysis, loss of Na/K pump)
- chilled sample (cold inhibition of Na/K pump)
- thrombocytosis, leukocytosis (fragile cells)
Remember order of draw!
Blood culture –> Blue (Na citrate) –> Red (Serum) –> Green (Li Heparin) –> Purple (K3EDTA) –> Grey (NaF/ KOx)
Causes of true HyperK: intake
Increased intake
- contributing factor but rarely sole cause
e. g. K-containing IV fluids, massive GI bleed, transfusions, foods (citrus fruits, bananas, broccoli etc)
Causes of true HyperK: transcellular shift
K shift out as buffer:
- acidosis with minerals i.e. HCl (Not lactic/keto/resp acidosis! – able to enter cell and balance H+ charge)
- hypertonicity
Cell lysis:
- tumour lysis syndrome after chemotherapy –> hyperK, hyperUr, hyperPO4, hypoCa
- rhabodomyolysis –> hyperK, hyperUr, hyperPO4, hypoCa, increase CK, myoglobinuria
- burns, trauma
Na/K ATPase activity decreases
- decrease SNS e.g. beta blockers, alpha agonists
- decrease insulin e.g. DKA, familial hyperK periodic paralysis
- drugs e.g. digoxin
K channel more open (less common)
- drugs: succinylcholine
Causes of true HyperK: decreased excretion
GFR <10-15 ml/min
- ARF, CRF
GFR >10-15 ml/min
- hyperK uncommon in CKD until GFR <15
- low effective circulating volume (K secretion depends on flow) e.g. HF, liver failure
- if r/o above, consider mineralocorticoid deficiency (TTKG)
Drugs: Decrease flow/ Na delivery - NSAID (less vasodilation of afferent) - beta blockers (less vasoconstriction of efferent) - amiloride (block ENaC)
Decrease RAAS
- aldosterone antag e.g. spironolactone
- ACEi/ ARB
- direct renin inhibitors
Trans-tubular potassium gradient (TTKG)
Estimates tubular conc. of K at CCT
- surrogate marker of mineralocorticoid activity
- normalised by urine:plasma Osm
- only valid if Uosm >300 and UNa >25
U[K]/Uosm // S[K]/Sosm
Normal = 6-8
TTKG >10 = not suggestive of mineralocorticoid insufficiency
TTKG <6 = insufficienct activity
Causes of true hyperK: further differentiation of TTKG <6
Low renin - low aldosterone = renin insufficiency
- hyporeninemic hypoaldosteronism
High renin - low aldosterone = aldosterone insufficiency
- adrenal insufficiency
- congenital adrenal hyperplasia
High renin - high aldosterone = aldosterone resistance
- tubular disorders e.g. SLE, amyloidosis, obstructive uropathy
Acute management of hyperK (>6 mmol/L or ECG changes)
Stop all K supplements, NSAIDS, ACEi, K sparing diuretics (aldo antag, ENaC blocker), Digoxin, Succinylcholine
Stabilise membrane:
- *10% Ca gluconate (increase excitability threshold)
Intracellular shift:
- *Dextrose-insulin drip
- IV bicarbonate
- beta agonist
Excretion:
- *resonium C (binds to K in GI system)
- furosemide (if renal failure)
Find and treat underlying cause
Approach to HypoK
- Rule out pseudohypoK (rare)
- marked leukocytosis kept at room temp for long time (alive and uptake K) - Assess patient
- DDx of HypoK (intake, shift, excretion; acid-base status and BP)
Causes of hypoK: intake
Decreased intake fairly common
- anorexia
- alcoholism
- dementia
Cause of hypoK: transcellular shift
Increase Na/K ATPase activity
- increase SNS e.g. stress, beta-2 agonist, theophylline, thyrotoxic hypoK periodic paralysis
- increase insulin e.g. iatrogenic, hypoK periodic paralysis
K shift as buffer
-metabolic alkalosis
Periodic paralysis
Muscle channelopathy, usually AD inheritance
Transient episodes of paralysis due to transcellular shift of K
HyperK periodic paralysis
- infancy/ early childhood
- cold, rest after exercise, ingestion of small amounts of potassium
HypoK periodic paralysis
- men, late childhood/ teenage
- ppt by release of catecholamines/ insulin e.g. rest after exercise, high carb meal
- increase Na/K ATPase activity –> intracellular K shift with defective K efflux –> hyperpolarise membrane
- avg K during attack is 2.4 mmol/L
Thyrotoxic hypoK periodic paralysis
- men
- 2% asians with hyperthyroidism
- like hypoK paralysis but a/w hyperthyroidism (increases adrenergic responses)
Tx: K supplement, propanolol, definitive anti-thyroid treatment
Causes of hypoK: excretion - non-renal
Non-renal loss
- U[K] <20 (not very reliable, easier to diagnose clinically)
- GI e.g. diarrhoea, laxative, villous adenoma (excrete HCO3) –> HCO3 loss and metabolic acidosis
- GI e.g. villous adenoma (excrete Cl) –> metabolic alkalosis
- sweat
Causes of hypoK: excretion - renal, normal BP
U[K] >20 + NORMAL BP
- metabolic alkalosis and U[Cl] <10 = losing HCl via non-renal
- -> Vomiting/ NG tube aspiration
- Cl loss –> increase plasma HCO3 –> stays in tubular lumen and retain Na/H20 –> increase flow and Na delivery at CCD –> increase K secretion
- Maintained by volume depletion –> activate RAAS –> exaggerate hypoK and alkalosis (paradoxical acuduria)
Treat with NS (“saline responsive’)
- metabolic alkalosis and U[Cl] >10 = losing HCl via kidneys
- -> diuretics (loop, thiazide) or channelopathyies (Bartter, Gitelman)
- Cl and K wasting –> alkalosis as HCO3 retained for electroneutrality
- volume depletion –> alkalosis by RAAS
Causes of hypoK: excretion - renal, hypertension
U[K] >20 + HYPERTENSION
- metabolic alkalosis and U[Cl] >10
==> Mineralocorticoid excess!
Hyperaldosteronism
- Low renin, high aldo = primary (Conn’s); ddx adenoma, hyperplasia
- high renin, high aldo = secondary e.g. RAS, Renin-secreting tumour
Cushing’s syndrome
- low/normal renin and aldo
- excessive cortisol activates mineralocorticoid receptor
Hyperaldosteronism mimics
- low renin, low aldo
DDx: Liddle syndrome (+ve ENaC), apparent mineralocorticoid excess (11-beta- HSD2 deficiency), licorice (inhib 11-beta-HSD2)
Causes of hypoK: excretion - renal, others
U[K] >20
Metabolic acidosis
- RTA type I and II
- Carbonic anhydrase inhibitors
Normal acid-base (rare)
- HypoMg – increases renal excretion of K and decreases secretion and action of PTH
- cisplatin (cause hypoMg)
Pearl
HypoK with metabolic alkalosis should always consider aldosterone excess!
U[K] and U[Cl] rarely checked in reality as clinical causes are usually obvious
Treatment of HypoK
Treat underlying cause Correct dehydration (saline response)
Replace K
- oral syrup KCl is safest
- IV KCl if K<2.5mM (must give slowly at low concentration)
- never bolus KCl!!
Diuretics causing dyskalemia
HyperK = K sparing diuretics
- aldosterone antag
- ENaC blockers
HypoK = thiazide, loop
- thiazide: hyperCa
- loop: hypoCa
