tonystep1's version from 2017-08-01 06:41


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GI causes of Hypokalemia a. Vomiting and nasogastric drainage (volume depletion and metabolic alkalosis also result) b. Diarrhea c. Laxatives and enemas d. Intestinal fistulae e. Decreased potassium absorption in intestinal disorders
Renal causes of Hypokalemiaa. Diuretics b. Renal tubular or parenchymal disease c. Primary and secondary hyperaldosteronism d. Excessive glucocorticoids e. Magnesium deficiency f. Bartter's syndrome (hyperplasia of juxtaglomerular apparatus)
Iatrogenic causes of Hypokalemiaa. Insufficient dietary intake b. Insulin administration c. Certain antibiotics d. Epinephrine ({32 agonists)-Hypokalemia occurs in 50% to 60% of trauma patients, perhaps due to increased epinephrine levels.
Exercised induced HypokalemiaProfuse sweating
Causes of Increased total body potassiuma. Renal failure (acute or chronic) b. Addison's disease c. Potassium-sparing diuretics (spironolactone) d. Hyporeninemic hypoaldosteronism e. ACE inhibitorsf. Iatrogenic overdose-Exercise particular caution when administering potassium to patients with renal failure. g. Blood transfusion
Causes of redistribution of potassium translocation of potassium from intracellular to extracellular space a. Acidosis (not organic acidosis) b. Tissue/cell breakdown-rhabdomyolysis (muscle breakdown) , hemolysis, burns c. GI bleeding d. Insulin deficiency-Insulin stimulates the Na+ -K+ -ATPase and causes K+ to shift into cells. Therefore, insulin deficiency and hypertonicity (high glucose) promote K+ shifts from ICF to ECF. e. Rapid administration of f3-blocker
Causes of PseudohyperkalemiaThis refers to an artificially elevated plasma K+ concentration due to K+ movement out of cells immediately before or after venipuncture. // Other contributing factors include leukocytosis, hemolysis, and thrombocytosis


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Hypokalemial. Arrhythmias-prolongs normal cardiac conduction 2. Muscular weakness, fatigue, paralysis, and muscle cramps 3. Decreased deep tendon reflexes 4. Paralytic ileus 5. Polyuria and polydipsia 6. Nausea/vomiting 7. Exacerbates digitalis toxicity
Hyperkalemial. Arrhythmias-The most important effect of hyperkalemia is on the heart. Check an ECG immediately in a hyperkalemic patient. 2. Muscle weakness and (rarely) flaccid paralysis 3. Decreased deep tendon reflexes 4. Respiratory failure 5. Nausea/vomiting, intestinal colic, diarrhea
ECG changes in hyperkalemia K+ >6.0• Peaked T waves (by 10 mm) • A prolonged PR interval • Widening of QRS and merging of QRS with T wave • Ventricular fibrillation and cardiac arrest (with increasing levels of K+)
ECG changes in hypokalemia• T wave flattens out; if severe, T wave inverts • U wave appears
Normal serum range of PotassiumNormal K+ levels: 3.5 to 5.0 mEq!L


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Hypokalemial. Identify and treat the underlying cause. 2. Discontinue any medications that can aggravate hypokalemia. 3. Oral KCl is the preferred (safest) method of replacement and is appropriate in most instances. Always retest the K+ levels after administration. a. Using 10 mEq of KCl increases K+ levels by 0. 1 mEq!L.
Severe Hypokalemia K+ <2.5IV KCl // a. Give slowly to avoid hyperkalemia. b. Monitor K+ concentration and monitor cardiac rhythm when giving IV potassium. c. Infusion pearls • Maximum infusion rate of 10 mEqlhr in peripheral IV line • Maximum infusion rate of 20 mEqlhr in central line • May add l% lidocaine to bag to decrease pain (potassium burns! )
If the hyperkalemia is severe, or if ECG changes are presentfirst give IV calcium//Sodium bicarbonate
Reserved for intractable hyperkalemia and for those with renal failureHemodialysis
HyperkalemiaGlucose and insulin // Kayexalate // Diuretics (furosemide)


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GI causes of Hypomagnesemiaa. Malabsorption, steatorrheic states (most common cause) b. Prolonged fasting c. Fistulas d. Patients receiving TPN without Mg2+ supplementation
Renal causes of Hypomagensemiaa. SIADH b. Diuretics c. Bartter's syndrome d. Drugs: gentamicin, amphotericin B, cisplatin e. Renal transplantation
Misc causes of HypomagensemiaAlcoholism (common cause) Other causes: postparathyroidectomy, DKA, thyrotoxicosis, lactation, burns, pancreatitis
Hypermagnesemia causesl. Renal failure (most common cause) 2. Early-stage burns, massive trauma or surgical stress, severe ECF volume deficit, severe acidosis 3. Excessive intake of magnesium-containing laxatives or antacids combined with renal insufficiency 4. Adrenal insufficiency 5. Rhabdomyolysis 6. Iatrogenic-in the obstetric setting in women with preeclampsia or eclampsia


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Hypermagnesemial. Nausea, weakness 2. Facial paresthesias 3. Progressive loss of deep tendon reflexes 4. ECG changes resemble those seen with hyperkalemia (increased P-R interval, widened QRS complex, and elevated T waves) . 5 . Somnolence leading to coma and muscular paralysis occur late. 6. Death is usually caused by respiratory failure or cardiac arrest.
ECG Changes in Hypermagnesemia ECG changes resemble those seen with hyperkalemia (increased P-R interval, widened QRS complex, and elevated T waves)
ECG Changes in HypomagnesemiaECG changes-prolonged QT interval, T wave flattening, and ultimately, torsade de pointes
HypomagenesemiaMarked neuromuscular and CNS hyperirritability a. Muscle twitching, weakness, tremors b. Hyperreflexia, seizures c. Mental status changes // Coexisting hypocalcemia // Coexisting hypokalemia-in up to 50% of case
Normal levels of magnesiumNormal Mg2+ levels: 1 .8 to 2.5 mg!dL


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mild hypomagnesemiaoral MgH (e.g. , magnesium oxide)
severe hypomagnesemiaparenteral MgH (e.g., magnesium sulfate)
Hypermagnesemial. Withhold exogenously administered magnesium. 2. Prescribe IV calcium gluconate for emergent symptoms (cardioprotection). 3 . Administer saline and furosemide. 4. Order dialysis in renal failure patients.


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Hypophosphatemia due Decreased intestinal absorptionalcohol abuse, vitamin D deficiency, malabsorption of phosphate, excessive use of phosphate-binding antacids, hyperalimentation (TPN ) , and/or starvation
Hypophosphatemia due to Increased renal excretiona. Excess PTH states (vitamin D deficiency, hyperparathyroidism) b. Hyperglycemia (glycosuria) , oncogenic osteomalacia, ATN, renal tubular acidosis, and so on c. Hypokalemia or hypomagnesemia
Hypophosphatemia other causesOther causes: respiratory alkalosis, anabolic steroids, severe hyperthermia DKA, hungry bones syndrome (deposition of bone material after parathyroidectomy)
Hyperphosphatemia Decreased renal excretion of P043-due to renal insufficiency (most common cause), bisphosphonates, hypoparathyroidism, vitamin D intoxication, and/or tumor calcinosis
Hyperphosphatemia due Increased phosphate administration (e.g. , P043- repletion or P043- enemas)
Hyperphosphatemia due to (releases P043- into the ECF)Rhabdomyolysis, cell lysis, or acidosis


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Normal Serum Phosphate levels3.0 to 4.5 mg!dL
if the hypophosphatemia is mildNone
hypophosphatemia neuro symptomsNeurologic: encephalopathy, confusion, seizures, numbness, paresthesias
hypophosphatemia Musculoskeletalmuscular weakness, myalgias, bone pain, rickets/osteomalacia
hypophosphatemia Hematologichemolysis, RBC dysfunction, WBC dysfunction, platelet dysfunction
hypophosphatemia Cardiaccardiomyopathy and myocardial depression secondary to low ATP levels, may lead to cardiac arrest
hypophosphatemia other signs/symptomse. Rhabdomyolysis f. Anorexia g. Difficulty in ventilator weaning
HyperphosphatemiaThis results in metastatic calcification and soft-tissue calcifications // The associated hypocalcemia can lead to neurologic changes (tetany; neuromuscular irritability).
calcium phosphorus product (serum calcium X serum phosphorus) > 70 indicatescalcification is likely to occur.


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If mild (> l mg!dL) Hypophosphatemiaoral supplementation: Neutra-Phos capsules, K-Phos tablets, milk (excellent source of phosphate)
If severe/symptomatic or if patient is NPO (Hypophosphatemia)parenteral supplementation
HyperphosphatemiaPhosphate-binding antacids containing aluminum hydroxide or carbonate (bind phosphate in bowel and prevent its absorption) // Hemodialysis (if patient has renal failure)