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Hypokalemia due to Transcellular Potassium Shift

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1. Hypokalemia due to Transcellular Potassium Shift

Hypokalemia due to Transcellular Potassium Shift Hypokalemia due to Transcellular Potassium Shift Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer (...) Administration 4 Hypokalemia due to Transcellular Potassium Shift Hypokalemia due to Transcellular Potassium Shift Aka: Hypokalemia due to Transcellular Potassium Shift , Transcellular Potassium Shift From Related Chapters II. Causes: Medications Beta-agonist ( s) s Xanthines Amphotericin B excess Acute load ( ) Barium or cesium III. Causes: Medical Conditions Anabolic states IV. References Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term

2018 FP Notebook

2. Hypokalemia due to Transcellular Potassium Shift

Hypokalemia due to Transcellular Potassium Shift Hypokalemia due to Transcellular Potassium Shift Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer (...) Administration 4 Hypokalemia due to Transcellular Potassium Shift Hypokalemia due to Transcellular Potassium Shift Aka: Hypokalemia due to Transcellular Potassium Shift , Transcellular Potassium Shift From Related Chapters II. Causes: Medications Beta-agonist ( s) s Xanthines Amphotericin B excess Acute load ( ) Barium or cesium III. Causes: Medical Conditions Anabolic states IV. References Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term

2015 FP Notebook

3. Hypokalemia (Follow-up)

could either overestimate or underestimate the true potassium deficit. For example, do not overcorrect potassium in patients with periodic hypokalemic paralysis. This condition is caused by transcellular maldistribution, not by a true deficit. Patients who have mild or moderate hypokalemia (potassium level of 2.5-3.5 mEq/L) are usually asymptomatic; if these patients have only minor symptoms, they may need only oral potassium replacement therapy. If cardiac arrhythmias or significant symptoms (...) to prevent an insulin-induced shift of potassium into the cells. If the patient is acidotic, correct the potassium first to prevent an alkali-induced shift of potassium into the cells. Evaluation for potential toxicities Monitor for toxicity of hypokalemia, which generally is cardiac in nature. Monitor the patient if evidence of cardiac arrhythmias is observed, and institute very aggressive replacement parenterally under monitored conditions. Previous Next: Addressing the Cause of Hypokalemia Determine

2014 eMedicine.com

4. Hypokalemia (Treatment)

could either overestimate or underestimate the true potassium deficit. For example, do not overcorrect potassium in patients with periodic hypokalemic paralysis. This condition is caused by transcellular maldistribution, not by a true deficit. Patients who have mild or moderate hypokalemia (potassium level of 2.5-3.5 mEq/L) are usually asymptomatic; if these patients have only minor symptoms, they may need only oral potassium replacement therapy. If cardiac arrhythmias or significant symptoms (...) to prevent an insulin-induced shift of potassium into the cells. If the patient is acidotic, correct the potassium first to prevent an alkali-induced shift of potassium into the cells. Evaluation for potential toxicities Monitor for toxicity of hypokalemia, which generally is cardiac in nature. Monitor the patient if evidence of cardiac arrhythmias is observed, and institute very aggressive replacement parenterally under monitored conditions. Previous Next: Addressing the Cause of Hypokalemia Determine

2014 eMedicine.com

5. Hypokalemia

or gastric suction (which removes volume and hydrochloric acid) causes renal potassium losses due to and stimulation of aldosterone due to volume depletion; aldosterone and metabolic alkalosis both cause the kidneys to excrete potassium. Intracellular shift The transcellular shift of potassium into cells may also cause hypokalemia. This shift can occur in any of the following: Glycogenesis during TPN or enteral hyperalimentation (stimulating insulin release) After administration of insulin Stimulation (...) of the sympathetic nervous system, particularly with beta 2-agonists (eg, albuterol , terbutaline ), which may increase cellular potassium uptake Thyrotoxicosis (occasionally) due to excessive beta-sympathetic stimulation (hypokalemic thyrotoxic periodic paralysis) Familial periodic paralysis is a rare autosomal dominant disorder characterized by transient episodes of profound hypokalemia thought to be due to sudden abnormal shifts of potassium into cells. Episodes frequently involve varying degrees of paralysis

2013 Merck Manual (19th Edition)

6. Assessment of respiratory alkalosis

, Chow CM. Hyperventilation as a strategy for improved repeated sprint performance. J Strength Cond Res. 2014 Apr;28(4):1119-26. http://www.ncbi.nlm.nih.gov/pubmed/23838981?tool=bestpractice.com Respiratory alkalosis also alters electrolyte homeostasis, separate from its renal compensatory mechanisms. Initially, hyperkalaemia occurs owing to hyperventilation-induced augmentation of alpha-adrenergic activity. Afterwards, hypokalaemia ensues owing to transcellular shift, decreased renal reabsorption (...) 16;280(3):117-23. http://www.ncbi.nlm.nih.gov/pubmed/5782512?tool=bestpractice.com Santra G, Paul R, Das S, et al. Hyperventilation of pregnancy presenting with flaccid quadriparesis due to hypokalaemia secondary to respiratory alkalosis. J Assoc Physicians India. 2014;62:536-538 http://www.japi.org/june_2014/16_cr_hyperventilation_of_pregnancy.pdf Berend K, de Vries AP, Gans RO. Physiological approach to assessment of acid-base disturbances. N Engl J Med. 2014 Oct 9;371(15):1434-45. http

2018 BMJ Best Practice

7. Odefsey (emtricitabine / rilpivirine / tenofovir alafenamide) - HIV-1

elvitegravir (Vitekta ® ) FAS Full Analysis Set FTC, F emtricitabine (Emtriva ® ) FTC-DP emtricitabine diphosphate HDL high-density lipoprotein INSTI integrase strand-transfer inhibitor LDL low-density lipoprotein Assessment report EMA/335723/2016 Page 5/120 LOCF last observation carried forward LSM least-squares mean M = F missing = failure mtDNA mitochondrial DNA N or n number of subjects in a population (N) or subset (n) NCEP National Cholesterol Education Program NNRTI nonnucleoside reverse (...) European Pharmacopoeia EU European Union FT-IR Fourier Transform Infrared Spectroscopy GC Gas Chromatography HDPE High Density Polyethylene HPLC High performance liquid chromatography ICH International Conference on Harmonisation of Technical Requirements for Registration of Pharmaceuticals for Human Use IPC In-process control IR Infrared KF Karl Fischer titration LDPE Low Density Polyethylene LT Less than Assessment report EMA/335723/2016 Page 7/120 MA Marketing Authorisation MS Mass Spectrometry NLT

2016 European Medicines Agency - EPARs

8. Treatment of Acute Hyperkalaemia in Adults

is not my main concern. It is acute rises in potassium that are associated with cardiac mortality, and the guidelines from the Renal Association (certainly the flow diagrams anyhow) do not seem to make this distinction. We come across many serum potassiums in the range from 6.1-7.0 mmol/l in patients with CKD and on potassium sparing agents such as ACEI or ARBs which we generally don't tend to treat as acute emergencies unless there are significant ECG changes, which is very rare. Also as you are well (...) published in english pertaining to the treatment of hyperkalaemia in adults. The keywords used for literature search were – hyperkalaemia, potassium, treatment, arrhythmias, insulin, salbutamol, calcium, dialysis and cardiac arrest. The hyperkalaemia module comprises of a series of guideline statements accompanied by supporting evidence and audit measures. The recommendations in each guideline statement have been graded using the GRADE system (www.gradeworkinggroup.org) in evaluating the strength

2014 Renal Association

9. Hyperkalemia Causes

: Hyperkalemia Causes , Pseudohyperkalemia , Hyperkalemia due to Decreased Renal Excretion , Hyperkalemia due to Redistribution , Hyperkalemia due to Excessive Potassium Load , Potassium Intoxication From Related Chapters II. Causes: Decreased renal excretion Hypoaldosteronism Hyporeninemic hypoaldosteronism Intrinsic renal disease (provoked by dehydration) (esp. ) Prostaglandin synthetase inhibitors Primary Hypoaldosteronism Medication-induced hypoaldosteronism See medications below (volume low, decreased (...) shift or redistribution (ICF to ECF) (more likely with mineral acids NH4, HCl) Hyperkalemic periodic paralysis deficiency or resistance ( ) Rapid ECF rise Hypertonic or mannitol infused Coronary bypass Cell lysis Any significant cause of cell turnover releases significant 98% of body is intracellular Tissue necrosis, , crush injury, tumor lysis Massive Surgery transfusion Hypertonicity (e.g. , mannitol) Medications (if concurrent tissue damage) s Digitalis ( ) Arginine tostatin IV. Causes: Potassium

2018 FP Notebook

10. Hyperkalemia

: Electrocardiogram EKG changes occur when >6.0 meq/L Initial s peaked or Tented (increased amplitude) in V2, V3, II, III Next ST depression First degree ( increases) shortening Next (ominous harbinger) widening Loss of Final Biphasic wave (sine wave) QRS and T fusion Imminent , or Changes exacerbated by with frequent, recurrent Hyperkalemia Change from normal EKG to may be rapid in these patients VI. Evaluation: Non-Renal Causes (transcellular shift, Potassium load, Pseudohyperkalemia) Serious signs (...) of Hyperkalemia present (EKG, symptoms) Urgent Consider Consider confirmatory testing (re-draw sample) Consider exogenous source or transcellular shift See Eliminate causative factors VII. Evaluation: Decreased renal excetion <25 mEq/L suggests decreased distal renal flow See or >25 mEq/L with normal serum aldosterone Primary tubular defects (e.g. RTA-4) Obstructive uropathy Tubular unresponsiveness to aldosterone (e.g. SLE, , ) Medications (e.g. sparing s, , Trimethoprim) >25 mEq/L with low serum aldosterone

2018 FP Notebook

11. Hypomagnesemia (Overview)

role in normal magnesium hemostasis. Next: Pathophysiology Related metabolic abnormalities is a common event in patients with hypomagnesemia, occurring in 40-60% of cases. [ ] This is partly due to underlying disorders that cause magnesium and potassium losses, including diuretic therapy and diarrhea. The mechanism for hypomagnesemia-induced hypokalemia relates to the intrinsic biophysical properties of renal outer medullary K (ROMK) channels mediating K + secretion in the TAL and the distal (...) with tumor type. [ ] The mechanism of basolateral transport into the interstitium is unknown. Magnesium has to be extruded against an unfavorable electrochemical gradient. Most physiologic studies favor a sodium-dependent exchange mechanism driven by low intracellular sodium concentrations; these concentrations are generated by Na + /K + - ATPase, also known as the sodium-potassium pump. A mutation in the gene FXYD2 , encoding gamma subunit of Na + /K + -ATPase, is responsible for isolated dominant

2014 eMedicine.com

12. Hyperkalemia (Overview)

intake of potassium Decreased excretion of potassium A shift of potassium from the intracellular to the extracellular space In many cases a combination of these factors is involved. For example, a person with a GFR of less than 45 mL/min who consistently eats large amounts of high-potassium foods and is taking a medication that blocks the rennin-angiotensin-aldosterone system is at very high risk for hyperkalemia due to limitations in renal excretion of potassium in the face of high intake. A person (...) with diabetes mellitus who has hyporeninemic hypoaldosteronism associated with diabetic nephropathy is at high risk for hyperkalemia due to a diminished ability to shift potassium into the intracellular space (insulin deficiency) and impaired renal excretion (aldosterone deficiency). A third circumstance is acute kidney injury from rhabdomyolysis or tumor lysis syndrome, in which hyperkalemia results from impaired renal excretion in addition to the release of large amounts of potassium from intracellular

2014 eMedicine.com

13. Metabolic Acidosis (Diagnosis)

. Approximately 90% of the filtered HCO 3 - is reabsorbed in the proximal tubule, and the remainder is reabsorbed in the thick ascending limb and the medullary collecting duct. The 3Na + -2K + /ATPase (sodium-potassium/adenosine triphosphatase) provides the energy for this process, which maintains a low intracellular Na + concentration and a relative negative intracellular potential. The low Na + concentration indirectly provides energy for the apical Na + /H + exchanger, NHE3 (gene symbol SLC9A3 ), which (...) transports H + into the tubular lumen. H + in the tubular lumen combines with filtered HCO 3 - in the following reaction: HCO 3 - + H + ↔H 2 CO 3 ↔H 2 O + CO 2 Carbonic anhydrase (CA IV isoform) present in the brush border of the first 2 segments of the proximal tubule accelerates the dissociation of H 2 CO 3 into H 2 O + CO 2 , which shifts the reaction shown above to the right and keeps the luminal concentration of H + low. CO 2 diffuses into the proximal tubular cell perhaps via the aquaporin-1 water

2014 eMedicine.com

14. Hypomagnesemia (Diagnosis)

role in normal magnesium hemostasis. Next: Pathophysiology Related metabolic abnormalities is a common event in patients with hypomagnesemia, occurring in 40-60% of cases. [ ] This is partly due to underlying disorders that cause magnesium and potassium losses, including diuretic therapy and diarrhea. The mechanism for hypomagnesemia-induced hypokalemia relates to the intrinsic biophysical properties of renal outer medullary K (ROMK) channels mediating K + secretion in the TAL and the distal (...) with tumor type. [ ] The mechanism of basolateral transport into the interstitium is unknown. Magnesium has to be extruded against an unfavorable electrochemical gradient. Most physiologic studies favor a sodium-dependent exchange mechanism driven by low intracellular sodium concentrations; these concentrations are generated by Na + /K + - ATPase, also known as the sodium-potassium pump. A mutation in the gene FXYD2 , encoding gamma subunit of Na + /K + -ATPase, is responsible for isolated dominant

2014 eMedicine.com

15. Hyperkalemia (Diagnosis)

intake of potassium Decreased excretion of potassium A shift of potassium from the intracellular to the extracellular space In many cases a combination of these factors is involved. For example, a person with a GFR of less than 45 mL/min who consistently eats large amounts of high-potassium foods and is taking a medication that blocks the rennin-angiotensin-aldosterone system is at very high risk for hyperkalemia due to limitations in renal excretion of potassium in the face of high intake. A person (...) with diabetes mellitus who has hyporeninemic hypoaldosteronism associated with diabetic nephropathy is at high risk for hyperkalemia due to a diminished ability to shift potassium into the intracellular space (insulin deficiency) and impaired renal excretion (aldosterone deficiency). A third circumstance is acute kidney injury from rhabdomyolysis or tumor lysis syndrome, in which hyperkalemia results from impaired renal excretion in addition to the release of large amounts of potassium from intracellular

2014 eMedicine.com

16. Hypomagnesemia (Overview)

role in normal magnesium hemostasis. Next: Pathophysiology Related metabolic abnormalities is a common event in patients with hypomagnesemia, occurring in 40-60% of cases. [ ] This is partly due to underlying disorders that cause magnesium and potassium losses, including diuretic therapy and diarrhea. The mechanism for hypomagnesemia-induced hypokalemia relates to the intrinsic biophysical properties of renal outer medullary K (ROMK) channels mediating K + secretion in the TAL and the distal (...) with tumor type. [ ] The mechanism of basolateral transport into the interstitium is unknown. Magnesium has to be extruded against an unfavorable electrochemical gradient. Most physiologic studies favor a sodium-dependent exchange mechanism driven by low intracellular sodium concentrations; these concentrations are generated by Na + /K + - ATPase, also known as the sodium-potassium pump. A mutation in the gene FXYD2 , encoding gamma subunit of Na + /K + -ATPase, is responsible for isolated dominant

2014 eMedicine Pediatrics

17. Hyperkalemia (Overview)

to maintain electrical neutrality. Acidosis is the most common cause of hyperkalemia due to transcellular potassium shift, but any process that leads to cellular injury or death (eg, , , crush injury, massive hemolysis) can cause hyperkalemia, as intracellular potassium is released by disruption of the cell membrane. Other causes of hyperkalemia due to transcellular shift of potassium include propofol ("propofol infusion syndrome"), [ ] toxins (digitalis intoxication or fluoride intoxication (...) is oliguric renal failure. Other causes include primary adrenal disease (eg, Addison disease, salt-wasting forms of congenital adrenal hyperplasia), hyporeninemic hypoaldosteronism, renal tubular disease (pseudohypoaldosteronism I [ ] or II), or medications (eg, ACE inhibitors, angiotensin II blockers, spironolactone or other potassium-sparing diuretics). Transcellular potassium shifts: In a transcellular potassium shift, a hydrogen ion enters a cell and leads to decreased K + uptake by the cell in order

2014 eMedicine Pediatrics

18. Perioperative Management of the Female Patient

secondary to the loss of these ions in the vomitus and resultant hypochloremic metabolic alkalosis, which is associated with renal sodium and potassium loss. Women with severe diarrhea also lose sodium and potassium and present with hyperchloremic acidosis. Electrolyte abnormalities, especially potassium, must be corrected before surgery. Hypokalemia potentiates neuromuscular blocking agents (eg, ), creates cardiac arrhythmias, and leads to acid-base imbalance. In the early 1990s, medical journals (...) explain that treatment of complications or unexpected findings may require consultation with other surgical specialists. Discussing what the surgeon will do to prevent complications, such as use of prophylactic antibiotics to lower the risk of infection or low molecular weight heparin to prevent pulmonary embolism, may be helpful. Previous Next: Preoperative Indications for Laboratory Tests In the current climate of the desire of high-quality, low-cost health care, the use of many "routine

2014 eMedicine.com

19. Hypomagnesemia (Diagnosis)

role in normal magnesium hemostasis. Next: Pathophysiology Related metabolic abnormalities is a common event in patients with hypomagnesemia, occurring in 40-60% of cases. [ ] This is partly due to underlying disorders that cause magnesium and potassium losses, including diuretic therapy and diarrhea. The mechanism for hypomagnesemia-induced hypokalemia relates to the intrinsic biophysical properties of renal outer medullary K (ROMK) channels mediating K + secretion in the TAL and the distal (...) with tumor type. [ ] The mechanism of basolateral transport into the interstitium is unknown. Magnesium has to be extruded against an unfavorable electrochemical gradient. Most physiologic studies favor a sodium-dependent exchange mechanism driven by low intracellular sodium concentrations; these concentrations are generated by Na + /K + - ATPase, also known as the sodium-potassium pump. A mutation in the gene FXYD2 , encoding gamma subunit of Na + /K + -ATPase, is responsible for isolated dominant

2014 eMedicine Emergency Medicine

20. Metabolic Acidosis (Overview)

. Approximately 90% of the filtered HCO 3 - is reabsorbed in the proximal tubule, and the remainder is reabsorbed in the thick ascending limb and the medullary collecting duct. The 3Na + -2K + /ATPase (sodium-potassium/adenosine triphosphatase) provides the energy for this process, which maintains a low intracellular Na + concentration and a relative negative intracellular potential. The low Na + concentration indirectly provides energy for the apical Na + /H + exchanger, NHE3 (gene symbol SLC9A3 ), which (...) transports H + into the tubular lumen. H + in the tubular lumen combines with filtered HCO 3 - in the following reaction: HCO 3 - + H + ↔H 2 CO 3 ↔H 2 O + CO 2 Carbonic anhydrase (CA IV isoform) present in the brush border of the first 2 segments of the proximal tubule accelerates the dissociation of H 2 CO 3 into H 2 O + CO 2 , which shifts the reaction shown above to the right and keeps the luminal concentration of H + low. CO 2 diffuses into the proximal tubular cell perhaps via the aquaporin-1 water

2014 eMedicine.com

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