electrolyte disorders Flashcards
↑↑ ADH → reabsorb H20 in collecting tubules→ concentrate urine:
low serum osmolality, low serum Na
syndrome of inappropriate ADH (SIADH)
causes of SIADH
1) ectopic ADH from small cell lung cancer (paraneoplastic syndrome)
2) pulm disease: COPD, pneumonia
3) head trauma, stroke, CNS infection
4) drugs: cyclophosphamide (immunosuppresant)
5) idiopathic
common cause of low serum Na (hyponatremia)
SIADH
complication of correcting low serum Na+ too quickly
central pontine myelinolysis: lysis of myelin in pons
causes LOCKED IN SYNDROME (conscious, can’t move, can’t communicate)
↓ ADH → ↓ H20 absorption in collecting tubules →↑ urine volume = dilute urine:
high serum osmolarity
low urine specific gravity
diabetes insipidus
abnormal ADH production by hypothalamus
if no ADH = complete central DI
insufficient ADH = partial central DI
central diabetes insipidus
kidneys unresponsive to ADH
nephrogenic diabetes insipidus
causes of nephrogenic diabetes insipidus (kidneys don’t respond to ADH)
1) lithium: interferes with aquaporin channel insertion due to ADH
2) demeclocycline: interferes with ADH function in kidney (use: SIADH)
3) hypercalcemia
4) ADH receptor gene mutation (hereditary)
evaluation of excessive thirst, polyuria
1) DM: urine glucose, serum glucose (if normal):
2) DI: urine + serum osmolarity (if low urine osmolarity, high serum osmolarity):
3) confirm dx of DI: water deprivation test: restrict drinking water → recheck urine osmolality
(normal response: secrete ADH and ↑ urine osmolality, abnormal response: no ADH and urine osmolarity stays low)
4) differentiate type DI: desmopressin (ADH analog) challenge: if improve = ↑ urine osmolarity = central DI, if no change = nephrogenic DI
central DI treatment
intranasal desmopressin (ADH analog)
nephrogenic DI treatment
1) hydrochlorothiazide - DOC: thiazide makes dehydrated → PT will reabsorb more H20 → concentrated urine by time in distal tubule
2) indomethacin(can use in combo with thiazide): inhibit PG synthesis, ↓ RBF →↓ UO
3) amiloride for lithium-induced (can stay on lithium): block Na channel lithium uses to enter PC
presentation of hyponatremia
alters resting membrane potential of neurons → CNS problems confusion AMS (esp elderly) seizures stupor coma
presentation of hypercalcemia
“stones, bones, ab groans, psychiatric overtones (confusion, delerium)”
may not have calciuria
presentation of hypocalcemia
tetany: Trousseau sign (Tighten cuff - carpopedal spasm) Chvostek sign (tap cheek - facial nerve spasm)
presentation of hypomagnesemia
tetany
EKG changes: wide QRS, torsades de pointes (type of vtach with variable amp)
presentation of hypermagnesemia
depress reflexes (IV mag during preterm labor to suppress muscle contractions and prevent labor, do serial neuro exams for DTR, stop for while if too much)
presentation of hypokalemia
EKG changes: prolong QT interval → vtach, torsades de pointes (like low Mg)
*flattened T WAVES, if very low K+: U wave (after T wave)
presentation of hyperkalemia
EKG changes: vtach (K can’t to too high or too low)
*tall + peaked (sharp) T WAVES
causes of K+ shift out of cells → hyperkalemia
low insulin (diabetic pt, esp in DKA)
ß blockers
acidosis (remove H+ in blood, exchange for K+)
digoxin
cell lysis: leukemia (K+ in cell leaks out)
other causes of high K+: K+ sparing diuretics, ACEi
causes of K+ shift into cells → hypokalemia
insulin ß agonist alkalosis cell creation/proliferation (cancer) other causes of low K+: loop diuretics, thiazides
EMERGENCY treatment for hyperkalemia: shift K+ into cells
B agonist: albuterol
IV bicarb
dextrose (prevent hypoglycemia) then IV insulin
electrolyte disturbances with tetany
hypocalcemia
hypomagnesemia
electrolyte disturbances with arrhythmias
hypomagnesmia
hypokalemia
hyperkalemia
causes of hypernatremia
6 D's: diuretics dehydration diabetes insipidus diarrhea disease of kidney docs (iatrogenic)
