B5.058 Prework 1 Electrolyte Abrnormalities Flashcards
(22 cards)
sources of electrolyte disbalances
glomerulus
tubules
mechanisms of regulation (RAA, ADH, ANP)
alterations in filtration with electrolytes and water accumulation
glomerular defects
-renal insufficiency from any origin
alteration in reabsorption and secretion of electrolytes and water
tubular defects
- acquired- injury or inflammatory processes
- genetic- mutation of renal transport systems in both dominant and recessive manner
precursors of renal insufficiency/glomerular damage
DM hypertensive nephropathy glomerulonephritis renal artery stenosis polycystic kidney disease
symptoms of glomerular damage
electrolyte retention
- hypernatremia
- hyperkalemia
- calcium/phosphate imbalance
- acidosis
reasons for acquired tubular injury
ischemic (interrupted blood flow)
toxic (drugs, dyes, gentamicin, heavy metals)
inflammatory
result of acute/chronic renal tubular injury
inability to concentrate urine
salt wasting
metabolic acidosis
variants of Bartters
- neonatal (NKCC)
- neonatal (ROMK1)
- classic (mutated Cl- channel)
pathophysiology of Bartter’s
malfunctions of NKCC, ROMK1, and Cl channels > solute diuresis and wasting of Na+, K+, and Cl-
malfunction of countercurrent mechanisms > polyuria and polydipsia, inability to concentrate urine
malfunction of juxtaglomerular apparatus > hyperreninemia, high aldosterone, alkalosis
why do you get alkalosis in Bartters
high aldosterone stimulates H+ secretion in the collecting ducts/distal tubules
clinical presentation of Bartters
tendency to volume depletion excitability alterations electrolyte disbalance renin up regulation pH problems
electrolyte disbalances in Bartters
hyponatremia hypokalemia hypochloremia ECF volume contraction hypercalciuria
what causes hypercalciuria in Bartters
reduced reabsorption of Cl-, Ca2+ and Mg2+ absorption is reduced
Bartters prognosis
non curable
variable outcome depending on mutation
significant morbidity and mortality
Bartters complications
cardiac arrhythmia and sudden death due to electrolyte disbalance
failure to thrive and developmental delay
diagnosis of Bartters
blood analysis of lytes, renin, and aldosterone
urine tests for lytes and PGE2
why is PGE2 elevated in Bartters
intermediate for products of juxtaglomerular apparatus which is hyperactive
treatment of BArtters
potassium supplements and liberal salt intake aldosterone antagonists (spironolactone) ACE inhibitors to counteract effects of angiotensin II and aldosterone NSAIDs (indomethacin) to decrease PGE2 calcium a nd magnesium supplements
extrarenal causes of hypokalemia
GI
skin
redistribution (insulin, B2 activity alkalosis)
neuromuscular symptoms
renal causes of hypokalemia with metabolic acidosis
renal tubular acidosis (type 1 or 2)
diabetic ketoacidosis
carbonic anhydrase inhibitor therapy
renal causes of hypokalemia with metabolic alkalosis
diuretics
mineralcorticoid excess
Gitelman and Bartters
renal cause of hypokalemia without acid base disorder
osmotic diuresis
