Electrolyte disturbance: Difference between revisions
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|[[ | |[[Hyperkalemia]]<ref name="pmid17395950">{{cite journal |vauthors=Smellie WS |title=Spurious hyperkalaemia |journal=BMJ |volume=334 |issue=7595 |pages=693–5 |date=March 2007 |pmid=17395950 |pmc=1839224 |doi=10.1136/bmj.39119.607986.47 |url=}}</ref><ref name="pmid5092154">{{cite journal |vauthors=Gonick HC, Kleeman CR, Rubini ME, Maxwell MH |title=Functional impairment in chronic renal disease. 3. Studies of potassium excretion |journal=Am. J. Med. Sci. |volume=261 |issue=5 |pages=281–90 |date=May 1971 |pmid=5092154 |doi= |url=}}</ref><ref name="pmid2376088">{{cite journal |vauthors=Arthur S, Greenberg A |title=Hyperkalemia associated with intravenous labetalol therapy for acute hypertension in renal transplant recipients |journal=Clin. Nephrol. |volume=33 |issue=6 |pages=269–71 |date=June 1990 |pmid=2376088 |doi= |url=}}</ref> | ||
| colspan="2" |[[ACE inhibitors]], [[acidosis]], [[Addison's disease|addisonian crisis]], [[beta blockers]], [[blood transfusion]], [[cirrhosis]], [[diabetic nephropathy]], high potassium diet, [[malnutrition]], [[renal tubular acidosis]] type IV, [[Renal insufficiency|renal failure]] | | colspan="2" |[[ACE inhibitors]], [[acidosis]], [[Addison's disease|addisonian crisis]], [[beta blockers]], [[blood transfusion]], [[cirrhosis]], [[diabetic nephropathy]], high potassium diet, [[malnutrition]], [[renal tubular acidosis]] type IV, [[Renal insufficiency|renal failure]] | ||
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| rowspan="2" |Ca<sup>2+</sup> | | rowspan="2" |Ca<sup>2+</sup> | ||
| rowspan="2" |8.9-10.1 | | rowspan="2" |8.9-10.1 | ||
|[[ | |[[Hypocalcemia]]<ref name="pmid19923405">{{cite journal |vauthors=Riccardi D, Brown EM |title=Physiology and pathophysiology of the calcium-sensing receptor in the kidney |journal=Am. J. Physiol. Renal Physiol. |volume=298 |issue=3 |pages=F485–99 |date=March 2010 |pmid=19923405 |pmc=2838589 |doi=10.1152/ajprenal.00608.2009 |url=}}</ref><ref name="pmid7024719">{{cite journal |vauthors=Neufeld M, Maclaren NK, Blizzard RM |title=Two types of autoimmune Addison's disease associated with different polyglandular autoimmune (PGA) syndromes |journal=Medicine (Baltimore) |volume=60 |issue=5 |pages=355–62 |date=September 1981 |pmid=7024719 |doi= |url=}}</ref><ref name="pmid6709029">{{cite journal |vauthors=Cholst IN, Steinberg SF, Tropper PJ, Fox HE, Segre GV, Bilezikian JP |title=The influence of hypermagnesemia on serum calcium and parathyroid hormone levels in human subjects |journal=N. Engl. J. Med. |volume=310 |issue=19 |pages=1221–5 |date=May 1984 |pmid=6709029 |doi=10.1056/NEJM198405103101904 |url=}}</ref> | ||
| colspan="2" |[[Hypoparathyroidism]], [[pseudohypoparathyroidism]], [[hypomagnesemia]], [[Vitamin D deficiency|hypovitaminosis D]], | | colspan="2" |[[Hypoparathyroidism]], [[pseudohypoparathyroidism]], [[hypomagnesemia]], [[Vitamin D deficiency|hypovitaminosis D]], | ||
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|[[hypercalcemia] | |[[Hypercalcemia]]<ref name="pmid2239937">{{cite journal |vauthors=Meric F, Yap P, Bia MJ |title=Etiology of hypercalcemia in hemodialysis patients on calcium carbonate therapy |journal=Am. J. Kidney Dis. |volume=16 |issue=5 |pages=459–64 |date=November 1990 |pmid=2239937 |doi= |url=}}</ref><ref name="pmid9612524">{{cite journal |vauthors=Glendenning P, Gutteridge DH, Retallack RW, Stuckey BG, Kermode DG, Kent GN |title=High prevalence of normal total calcium and intact PTH in 60 patients with proven primary hyperparathyroidism: a challenge to current diagnostic criteria |journal=Aust N Z J Med |volume=28 |issue=2 |pages=173–8 |date=April 1998 |pmid=9612524 |doi= |url=}}</ref><ref name="pmid8865795">{{cite journal |vauthors=Alikhan Z, Singh A |title=Hyperthyroidism manifested as hypercalcemia |journal=South. Med. J. |volume=89 |issue=10 |pages=997–8 |date=October 1996 |pmid=8865795 |doi= |url=}}</ref><ref name="pmid2679445">{{cite journal |vauthors=Distler W |title=[The climacteric--physiology or pathology?] |language=German |journal=Arch. Gynecol. Obstet. |volume=245 |issue=1-4 |pages=947–52 |date=1989 |pmid=2679445 |doi= |url=}}</ref> | ||
| colspan="2" |[[Hyperparathyroidism]], [[familial hypocalciuric hypercalcemia]], [[Cancer|malignancy]], [[Milk-alkali syndrome]], | | colspan="2" |[[Hyperparathyroidism]], [[familial hypocalciuric hypercalcemia]], [[Cancer|malignancy]], [[Milk-alkali syndrome]], | ||
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| rowspan="2" |PO<sub>4</sub><sup>3-</sup> | | rowspan="2" |PO<sub>4</sub><sup>3-</sup> | ||
| rowspan="2" |2.5-4.5 | | rowspan="2" |2.5-4.5 | ||
|[[ | |[[Hypophosphatemia]]<ref name="pmid15888903">{{cite journal |vauthors=Marinella MA |title=Refeeding syndrome and hypophosphatemia |journal=J Intensive Care Med |volume=20 |issue=3 |pages=155–9 |date=2005 |pmid=15888903 |doi=10.1177/0885066605275326 |url=}}</ref><ref name="pmid14105225">{{cite journal |vauthors=MOSTELLAR ME, TUTTLE EP |title=EFFECTS OF ALKALOSIS ON PLASMA CONCENTRATION AND URINARY EXCRETION OF INORGANIC PHOSPHATE IN MAN |journal=J. Clin. Invest. |volume=43 |issue= |pages=138–49 |date=January 1964 |pmid=14105225 |pmc=289504 |doi=10.1172/JCI104888 |url=}}</ref><ref name="pmid8743494">{{cite journal |vauthors=Murer H, Lötscher M, Kaissling B, Levi M, Kempson SA, Biber J |title=Renal brush border membrane Na/Pi-cotransport: molecular aspects in PTH-dependent and dietary regulation |journal=Kidney Int. |volume=49 |issue=6 |pages=1769–73 |date=June 1996 |pmid=8743494 |doi= |url=}}</ref> | ||
| colspan="2" |[[Refeeding syndrome]], [[respiratory alkalosis]], [[Alcoholism|alcohol abuse]], [[malabsorption]] | | colspan="2" |[[Refeeding syndrome]], [[respiratory alkalosis]], [[Alcoholism|alcohol abuse]], [[malabsorption]] | ||
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Revision as of 16:09, 30 May 2018
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Electrolyte Disturbance Main Page | |
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Patient Information |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
Synonyms and keywords: abnormal electrolytes, abnormal lytes, lytes
Overview
Electrolytes are electrically charged solutes necessary to maintain body homeostasis. The main electrolytes include Sodium (Na), Potassium (K), Chloride (Cl), Calcium (Ca), Phosphorus (P), and Magnesium (Mg). These electrolytes are involved in multiple physiologic and neurohormonal reactions necessary to maintain neuromuscular, neuronal, myocardial, and acid-base balance. Their balance are mainly regulated by renal and endocrine systems, any changes in their balance may be life threatening. Electrolytes are in balance to achieve neutral electrical charges. Electrolytes could be classified based on their electrical charge to anions and cations. Anions include bicarbonate, chloride, and phosphorus. Cations are calcium, magnesium, potassium, and sodium. Sodium and chloride are the major extracellular ions that has the greatest impact on serum osmolality (solute concentration in 1 liter of water). Calcium and bicarbonate are the other major extracellular electrolytes. Main intracellular electrolytes are potassium, phosphorus, and magnesium.
Causes
- Drug side effect: Hydrochlorothiazide, Pergolide
Table of common electrolyte disturbances
Electrolyte Abnormalities and ECG Changes
The most notable feature of hyperkalemia is the "tent shaped" or "peaked" T wave. Delayed ventricular depolarization leads to a widened QRS complex and the P wave becomes wider and flatter. When hyperkalemia becomes severe, the ECG resembles a sine wave as the P wave disappears from view. In contrast, hypokalemia is associated with flattenting of the T wave and the appearance of a U wave. When untreated, hypokalemia may lead to severe arrhythmias.
The fast ventricular depolarization and repolarization associated with hypercalcemia lead to a characteristic shortening of the QT interval. Hypocalcemia has the opposite effect, lengthening the QT interval.
Differentiating electrolyte disturbances from other diseases
Electrolyte disturbance must be differentiated from other causes of headache, altered mental status and seizures such as brain tumors and delirium trmemns.
References
- ↑ Smellie WS (March 2007). "Spurious hyperkalaemia". BMJ. 334 (7595): 693–5. doi:10.1136/bmj.39119.607986.47. PMC 1839224. PMID 17395950.
- ↑ Gonick HC, Kleeman CR, Rubini ME, Maxwell MH (May 1971). "Functional impairment in chronic renal disease. 3. Studies of potassium excretion". Am. J. Med. Sci. 261 (5): 281–90. PMID 5092154.
- ↑ Arthur S, Greenberg A (June 1990). "Hyperkalemia associated with intravenous labetalol therapy for acute hypertension in renal transplant recipients". Clin. Nephrol. 33 (6): 269–71. PMID 2376088.
- ↑ Riccardi D, Brown EM (March 2010). "Physiology and pathophysiology of the calcium-sensing receptor in the kidney". Am. J. Physiol. Renal Physiol. 298 (3): F485–99. doi:10.1152/ajprenal.00608.2009. PMC 2838589. PMID 19923405.
- ↑ Neufeld M, Maclaren NK, Blizzard RM (September 1981). "Two types of autoimmune Addison's disease associated with different polyglandular autoimmune (PGA) syndromes". Medicine (Baltimore). 60 (5): 355–62. PMID 7024719.
- ↑ Cholst IN, Steinberg SF, Tropper PJ, Fox HE, Segre GV, Bilezikian JP (May 1984). "The influence of hypermagnesemia on serum calcium and parathyroid hormone levels in human subjects". N. Engl. J. Med. 310 (19): 1221–5. doi:10.1056/NEJM198405103101904. PMID 6709029.
- ↑ Meric F, Yap P, Bia MJ (November 1990). "Etiology of hypercalcemia in hemodialysis patients on calcium carbonate therapy". Am. J. Kidney Dis. 16 (5): 459–64. PMID 2239937.
- ↑ Glendenning P, Gutteridge DH, Retallack RW, Stuckey BG, Kermode DG, Kent GN (April 1998). "High prevalence of normal total calcium and intact PTH in 60 patients with proven primary hyperparathyroidism: a challenge to current diagnostic criteria". Aust N Z J Med. 28 (2): 173–8. PMID 9612524.
- ↑ Alikhan Z, Singh A (October 1996). "Hyperthyroidism manifested as hypercalcemia". South. Med. J. 89 (10): 997–8. PMID 8865795.
- ↑ Distler W (1989). "[The climacteric--physiology or pathology?]". Arch. Gynecol. Obstet. (in German). 245 (1–4): 947–52. PMID 2679445.
- ↑ Marinella MA (2005). "Refeeding syndrome and hypophosphatemia". J Intensive Care Med. 20 (3): 155–9. doi:10.1177/0885066605275326. PMID 15888903.
- ↑ MOSTELLAR ME, TUTTLE EP (January 1964). "EFFECTS OF ALKALOSIS ON PLASMA CONCENTRATION AND URINARY EXCRETION OF INORGANIC PHOSPHATE IN MAN". J. Clin. Invest. 43: 138–49. doi:10.1172/JCI104888. PMC 289504. PMID 14105225.
- ↑ Murer H, Lötscher M, Kaissling B, Levi M, Kempson SA, Biber J (June 1996). "Renal brush border membrane Na/Pi-cotransport: molecular aspects in PTH-dependent and dietary regulation". Kidney Int. 49 (6): 1769–73. PMID 8743494.
- ↑ Tsokos GC, Balow JE, Spiegel RJ, Magrath IT (May 1981). "Renal and metabolic complications of undifferentiated and lymphoblastic lymphomas". Medicine (Baltimore). 60 (3): 218–29. PMID 6894477.
- ↑ Grossman RA, Hamilton RW, Morse BM, Penn AS, Goldberg M (October 1974). "Nontraumatic rhabdomyolysis and acute renal failure". N. Engl. J. Med. 291 (16): 807–11. doi:10.1056/NEJM197410172911601. PMID 4423658.
- ↑ Shah GM, Kirschenbaum MA (1991). "Renal magnesium wasting associated with therapeutic agents". Miner Electrolyte Metab. 17 (1): 58–64. PMID 1722865.
- ↑ Elisaf M, Merkouropoulos M, Tsianos EV, Siamopoulos KC (December 1995). "Pathogenetic mechanisms of hypomagnesemia in alcoholic patients". J Trace Elem Med Biol. 9 (4): 210–4. doi:10.1016/S0946-672X(11)80026-X. PMID 8808192.
- ↑ Tosiello L (June 1996). "Hypomagnesemia and diabetes mellitus. A review of clinical implications". Arch. Intern. Med. 156 (11): 1143–8. PMID 8639008.
- ↑ RANDALL RE, COHEN MD, SPRAY CC, ROSSMEISL EC (July 1964). "HYPERMAGNESEMIA IN RENAL FAILURE. ETIOLOGY AND TOXIC MANIFESTATIONS". Ann. Intern. Med. 61: 73–88. PMID 14178364.
- ↑ Clark BA, Brown RS (1992). "Unsuspected morbid hypermagnesemia in elderly patients". Am. J. Nephrol. 12 (5): 336–43. doi:10.1159/000168469. PMID 1489003.