NURS 123 Electrolytes

jasmine's version from 2016-03-23 01:33

Section 1

Question Answer
Na+ (sodium) Most important ion in regulating H2O (osmotic) balance; Pairs with Cl- and HCO3- to neutraulize charge; Responsible for nerve conduction and neuromuscular function
Na+ extracellular fluid range136-145 mEq/L
Manifestations of Hypernatremia (>145 mEq/L)1) H2O movement ICF --> ECF; 2) Intracellular dehydration; 3) Convulsions; and 4) Thirst, fever, muscle twitching, hyperreflexia
Eletrolyte Notation of Hypernatremia Increase Na+ and/or Decrease H2O
Treatment of HypernatremiaImplies deficient of total body H2O; Fluid replacement
Manifestations of Hyponatremia (<136 mEq/L)Lethargy, confusion, depressed reflexes, seizures, coma, hypotension, decrease urine output, tachycardia, muscle cramps, weakness and fatigue with nausea, vomiting, abdominal cramps, and diarrhea can be causes and symptoms
2 types of diagnosis of hyponatremiaDepletional and dilutional
Possible co-existing underlying manifestations associated with hyponatremiaKidney failure, oliguric renal failure, severe CHF, and hyperglycemia
Symptom Inappropriate Anti-Diuretic Hormone (SIADH) Release too much ADH, retain H2O, and dilutes Na+. Appears to be hyponatremia yet retaining H2O due to ADH
Oliguric renal failureDecreased kidney function, decreased urine output, and retaining H2O. Appears to be hyponatremia yet retaining H2O
Congestive heart failure (CHF)Not pumping blood to kidneys, so kidneys cannot get rid of extra H2O. Appears to be hyponatremia yet retaining H2O
Hyperglycemia More sugar in blood; Rationale: Sugar, salt, and protein pull H2O in blood. Too much H2O in blood due to sugar and appears to be hyponatremia
Dilutional Hyponatremia =Hypervolemic (fluid overload: medical condition where there is too much fluid in the blood); Underlying condition may be kidney failure, oliguric renal failure, severe CHF, and hyperglycemia
Depletional Hyponatremia =Hypovolemic (fluid underload: medical condition where there is too little fluid volume in the blood)
Treatment of HyponatremiaRestrictive fluid intake, diuretics (i.e., loop diuretic, which absorbs H2O and Na+ in loop of Henle)
Electrolyte Notation of HyponatremiaDecrease Na+ and Increase H2O

Section 2

Question Answer
Cl- (chlorine) Resting membrane potential; When enters nerves, blocks nerves (i.e., opiates will allow Cl- in nerves, shutting the nerves off and decreasing pain sensation); Moves passively with Na+ and varies inversely in concentration to HCO3-; Provides electron neutrality with exchange of O2 and CO2 in RBC; and helps regulate and neutralize acids (i.e., stomach secretes as HCL)
Cl- extracellular fluid range97-105 mEq/L
Manifestations of Hyperchloremia (>105 mEq/L)Usually result of hyperatremia; decrease HCO3 concentration or Ammonium chloride diuretics; Usually secondary to pathophysiologic processes
Treatment of HyperchloremiaUnderlying cause?; If dehydrated, establish hydration; If kidney disease, possible referral to nephrologist; If endocrine or hormone dysfunction, possible referral to endocrinologist
Manifestations of Hypochloremia (<97 mEq/L)Usually result of hyponatremia; Occurs in Cystic Fibrosis; Increase HCO3 concentration (metabolic alkalosis) that can develop as result of vomiting and loss of HCl
Risks of HypochloremiaAnxiety and heart failure
Complications of HypochloremiaRespiratory arrest, seizures, coma; Muscle weakness, Dry skin, Tetany (condition marked by intermittent muscular spasms, caused by malfunction of the parathyroid glands and a consequent deficiency of calcium), shallow and depressed breathing, muscle cramps, cardiac arrhythmias
Treatment of HypochloremiaUnderlying condition?; Normal saline; electrolyte replacement therapy (potassium chloride, sodium chloride); NSAIDS; Carbonic anhydrase blockers (Acetazolamide)

Section 3

Question Answer
K+ (potassium)The mineral the body needs to work normal; Repolarization: return to resting potential; Maintains cell neutrality; Regulates fluid ion balance inside cell; Causes insulin release; Responsible for cardiac/smooth muscle conduction; Na+ and K+ pump = Repolarization
K+ is stimulated by what?Adolsterone
K+ stimulates this and angiotensin triggers this Adolesterone
K+ extracellular fluid range3.5-4.5 mEq/L
K+ intracellular fluid range~156 mEq/L
Manifestations of Hyperkalemia (>4.5 mEq/L)Slow heartbeat, weak pulse (bradycardia), cardiac standstill (death), nausea, fatigue, muscle weakness, tingling sensations
Causes of HyperkalemiaRenal disease, massive cellular trauma, insulin deficiency, addison's disease (NO ADOLESTERONE), potassium sparing diuretics (drugs that do not promote the secretion of potassium into the urine), decreased blood pH (acid), exercise also causes K+ to move out of cells
Treatments of HyperkalemiaACE (angiotensin converting enzyme) inhibitors; NSAIDS; angiotensin II receptor blockers
Manifestations of Hypokalemia (<3.5 mEq/L)Neuromuscular disorders: hyperpolarization, weakness, flacid paralysis, respiratory arrest, constipation; Dysrhythamias, appearance of U wave; Postural hypotension, and Cardiac arrest
Treatment of HypokalemiaIncrease K+ intake, slowly, preferable by foods
Causes of HypokalemiaTrauma and stress; Increased Aldosterone causes loss of K+
Diabetic warning of HypokalemiaInsulin gets K+ into cell; Ketoacidosis (high levels of blood acids called ketones-develops when body does not produce enough insulin) --> H+ replaces K+ --> K+ lost in urine

Section 4

Question Answer
Ca+ (calcium)Most abundant mineral in body; Bones (99 percent), teeth, hormone secretion; Responsible for cell receptor function; Blood clotting; Parathyroid; GI absorption and renal retention
Ca+ extracellular plasma concentration4.5-5.5 mEq/L or 9-10.5 mg/dL
Ca+ and Parathyroid hormone (PTH)PTH causes blood Ca+ increase; Too much PTH=hypercalcemia, too little PTH=hypocalcemia; Can become life threatening
Manifestations of Hypercalcemia (>5.5 mEq/L or >10.5 mg/dL)Extracellular ion: The block of Ca+ into cells is increased (competitive); Muscle weakness, cardiac arrest, kidney stones, constipation
Causes of HypercalcemiaHyperparathyroidism, hypothyroid states, renal disease, excessive intake of vitamin D, milk-alki syndrome, Malignant tumors (tumor promotes bone breakdown and tumor growth causes Ca+ release),
Treatment of HypercalcemiaCalcimietics, bisphosphonates, IV fluids and diuretics (i.e., dronate [bisphosphonates slow deterioration of bones], dipine [Ca+ blockers], prednisone [anti-inflammatory])
Chvostek signs A clinical sign of existing nerve hyper-excitability (tetany) seen in hypocalcemia. It refers to an abnormal reaction to the stimulation of the facial nerve-twitching of the facial muscles in response to tapping over the area of the facial nerve
Trousseau signs A sign for tetany in which the occurrence of carpopedal spasm accompanied by paresthesia elicited when the upper arm is compressed, as in use of a tourniquet or a blood pressure cuff
Carpopedal SpasmA spasmodic contraction of the muscles of the hands and feet, wrists and ankles in disorders such as alkalosis and tetany
Manifestations of Hypocalcemia (<4.5 mEq/L or <9 mg/dL)Extracellular ion: The block of Ca+ into cells is decreased (non-competitive); Muscle cramps, hyperactive neuromuscular reflexes and tetany (condition marked by intermittent muscular spasms, caused by malfunction of the parathyroid glands and a consequent deficiency of calcium), convulsions in severe classes, memory loss, depression, hallucinations, and chvostek and trousseau's signs
Causes of HypocalcemiaRenal failure, lack of vitamin D, suppression of parathyroid function, hyper-secretion of calcitonin, malabsorption states, abnormal intestinal acidity and acid/base balance, wide spread infection or peritoneal inflammation
Treatment of HypocalcemiaDiet, Ca+ supplementation, Vitamin D, possible parathyroid surgery, calcitriol

Section 5

Question Answer
PO4^3- (Phosphate)Mostly located in bone; Contains phosphorus necessary to build and repair bones and teeth, help nerves function, and make muscles contract; Necessary for high-energy bonds located in creatinine phosphate and ATP and acts as anion buffer; Ca+ and PO4^3- are rigidly controlled (Hypocalcaemia=hyperphosphatemia and hypercalcaemia=hypophosphatemia); Ca+ x PO4^3- = K+ (constant)
PO4^3- intracellular plasma concentration 2.5-4.5 mEq/L
Manifestations of Hyperphosphatemia (>4.5 mEq/L)See hypocalcaemia; Positive chvostek or trousseau sign, fatigue, shortness of breath, anorexia, nausea, vomiting, sleep disturbances, hyper-reflexia, carpopedal spasm, seizure
Causes of HyperphosphatemiaRelated to low Ca+ levels; kidney fail to clear phosphate, cell destruction, long term laxative use
Treatment of Hyperphosphatemia Saline diuresis, limit phosphate intake, enhance renal excretion, loop diuretic (furosemide, bumetanide)
Manifestations of Hypophosphatemia (<2.5 mEq/L)See hypercalcaemia; Osteomalacia (soft bones), muscle weakness, bleeding disorders (platelet impairment), anemia, leukocyte alterations
Causes of HypophosphatemiaMalabsorption, vitamin D deficiency, antacid use (Mg and Al in antacid bind phosphate), alcoholism, respiratory alkalosis, hyperparathyroidism (causes phosphate excretion)
Treatment of Hypophosphatemia IV replacement therapy (ventilated patients), oral replacement therapy (non-ventilated therapy), possible addition of vitamin D

Section 6

Question Answer
Mg+ (Magnesium)Second-most abundant intracellular cation; 40-60 percent stored in muscle and bone; Responsible for enzymatic reactions for activation (ATPase); Serves as a molecular stabilizer of RNA, DNA, and ribosomes; Mg+ and Ca+ interact at cell level, helping Ca+ activity (i.e., smooth muscles contract with Mg+ present with Ca+); Binds to Ca+ or K+ receptors
Mg+ intracellular plasma concentration 1.8-2.4 mEq/L
Manifestations of Hypermagnesemia (>2.4 mEq/L)See hypercalcemia and hyperkalemia; Muscle weakness, skeletal/smooth muscle depression, hypotension, respiratory depression, lethargy, drowsiness, bradycardia, hypoactive reflexes
Causes of Hypermagnesemia Usually by renal failure or overconsumption of Mg+ containing antacids
Treatment of Hypermagnesemia IV calcium gluconate due to actions of Mg+ in neuromuscular and cardiac function are antagonized by Ca+; IV diuretics in presence of normal renal function; dialysis when kidney function is impaired; and patient symptomatic from hypermagnesemia
Manifestations of Hypomagnesemia See hypocalcemia and hypokalemia; neuromuscular irritability, tetany (intermittent muscular spasms caused by parathyroid glands and decreased Ca+), Convulsions, Hyperactive reflexes, diabetics should worry due to decreases insulin sensitivity and secretion; Moreover, deficiency is inherently related to the pathogenesis and development not only of diabetic microangiopathy yet also of lifestyle-related diseases, such as hypertension and hyperlipidemia
Mg+ blocks K+ channels-low Mg+ means more K+ leaving cell and excreted through urine
Treatment of Hypomagnesemia Oral replacement or IV replacement; IV Magnesium sulfate in response to cardiac arrhythmias, pre-eclampsia, and suggested as having potential use in asthma; PO magnesium oxide (less bioavailable) and citrate (more bioavailable)

Section 7

Question Answer
Intracellular Electrolytes K+ (Potassium), Mg+ (Magnesium), PO4^3- (Phosphate)
Extracellular Electrolytes Na+ (Sodium), Cl- (Chlorine), HCO3- (Bi-carbonate), and small quantity of Ca+ (Calcium)
Magnesium Sulfate Anti-epileptic; electrolyte replenisher, Laxative
Therapeutic Use of Magnesium Sulfate Immediate control of life threatening convulsions in the treatment of severe toxemias (pre-eclampsia, eclampsia) of pregnancy and in the treatment of acute nephritis in children
Adverse/Side Effects of Magnesium Sulfate Dizziness, excessive bowel activity, fainting magnesium intoxication, perianal irritation, weakness, and neuromuscular blockade
Magnesium Hydroxide (Milk of Magnesium) Antacid; Laxative; Electrolyte
Pharmacological action of Magnesium Hydroxide Assists all enzymes involved in phosphate transfer reactions that use ATP
Adverse/Effects of Magnesium Sulfate Dizziness, hypermagnesemia, nausea, vomiting, diarrhea, perianal irritation
Nursing Interventions for Magnesium Sulfate Avoid giving oral drugs within two hours of magnesium containing antacid; Medication reaction with anti-parasitic meds; Assess cardiac status, as magnesium may aggravate symptoms of heart block; Risk for magnesium toxicity in patients with renal insufficiency
Hydrochlorothiazide Diuretic; antihypertensive and anti-edema
Therapeutic Use of Hydrochlorothiazide To manage hypertension
Pharmacological Action of Hydrochlorothiazide Promotes movement of Sodium and water into nephron’s convoluted tubule. Initially, it may decrease extracellular fluid volume, plasma volume, and cardiac output, which helps explain blood pressure reduction. It also may reduce blood pressure by direct arterial dilation
Furosemide Loop diuretic; Antihypertensive
Pharmacologic Action of Furosemide Inhibits sodium and water reabsorption in the loop of Henle and increases urine formation. Also increases excretion of calcium, magnesium, bicarbonate, ammonium, and phosphate. Reduces blood pressure and increases cardiac output
Therapeutic Use of Furosemide To reduce edema caused by cirrhosis, heart failure, and renal disease, including nephrotic syndrome
Adverse/Side Effects of Furosemide Anemia, anorexia, dizziness, hyperglycemia, hypokalemia, leukopenia, muscle cramps, nausea, vomiting, orthostatic hypotension, paresthesia, photosensitivity, pruritis, thrombocytopenia, urticaria, xanthopsia
Sodium Plystyrene Sulfonate Anti-hyperkalemic; Potassium removing resin
Pharmacological Action of Sodium Polystyrene Sulfonate Releases sodium ions in exchange for other cations in intestines. Resin enters large intestine and releases sodium ions in exchange for hydrogen ions. As the resin moves through the intestines, hydrogen ions are exchanged for potassium ions, which are in greater concentration. Bound resin leaves the body in feces, carrying potassium and other ions with it, thereby reducing serum potassium level
Therapeutic Use of Sodium Polystyrene Sulfonate To treat hyperkalemia
Medication interactions with Sodium Polystyrene Sulfonate Antacids, laxatives: increased risk of metabolic alkalosis; Potassium sparing diuretics and potassium supplements; Increased risk of fluid retention
Nursing interventions for Sodium Polystyrene Sulfonate Give resin through plastic stomach tube, or mixed with diet appropriate for renal failure; Give enema after cleansing enema, help client retain for at least 30 minutes; If severe constipation, discontinue drug and do not use sorbitol magnesium containing laxatives