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21 Cards in this Set
- Front
- Back
Sodium (Na+)
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Normal range: 136-145 mEq/L *or 135*
Most abundant cation in the extracellular fluid Role in body physiology Maintains appropriate transmembrane electric potential for neuromuscular function Major contributor of serum osmolality Regulates water movement between the extracellular and intracellular compartments |
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Presentation of Hypovolemic
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>2kg in <1 week
Acute weight loss (1 kg = 1 Liter) Tachycardia, (+) Orthostasis(SBP↓) Dry mouth, dry skin, Skin turgor (↓’ed) BUN/SCr > 20 |
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Presentation of Hypervolemic
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Acute weight gain
(+)Edema: Extremities (all causes) Pulmonary edema (heart failure) Ascites (liver failure) Anasarca (nephrotic syndrome) BUN/SCr < 20 |
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Hypotonic
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Na+ < 135 mEq/ L
Loss of water and sodium : H2O loss >> Na loss If you loose more water than sodium (sweating, vomiting) hyoptonic fluids, serium sodium will increase leaving you hypovolemic hypernatremia |
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Hypertonic
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Na+ > 145 mEq/L
Loss of water and sodium Na loss >> H2O loss |
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Hypovolemic Hypernatremia
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LOSS of hypotonic fluids AND Patient unable to access Water (Na+ >145)
Presentation of Hypovolemia: Acute weight loss Dry mouth, (+) Orthostasis, BUN:SCr > 20 Common causes: GI: Vomiting, diarrhea Skin: ↑ Sweating/ fevers ALL in patients who cannot access water |
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Hypervolemic HYPERnatremia
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Pathology - Administration of excessive hypertonic fluids
i.e., Hypertonic saline (3% NaCl= 513 mEq of Na+ / Liter) NS is 0.9% and 153 mEq Causes: Excessive hypertonic saline solutions: i.e.,NaHCO-3 solution Hypertonic saline enemas EC Sodium Gain >> EC Water Gain |
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Euvolemic Hypernatremia
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Loss of total body water with minimal loss of total body sodium
NOT enough water loss for dehydration Seen in conditions promoting Na+-free water loss: Diabetes insipidus – they cannot retain free water due to the lack of response/production of ADH Osmotic diuretics * Loss of Small amount of Water Only (Sodium free water) |
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Presentation of Acute Hypernatremia
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If serum Na+2 < 160 mEq/L
Patient may be asymptomatic Neuromuscular irritability: Thirst, Lethargy Restlessness, hyperreflexia Irritability, muscle twitching Seizure, Coma Due to Cerebral dehydration |
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Hypovolemic Hyponatremia
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Presentation of Hypovolemia:
Acute weight loss Dry mouth, Orthostasis, BUN:SCr > 20 Common causes: Overconsumption of hypotonic fluids (i.e., tap water) following severe vomiting, diarrhea, excessive sweating Overdiuresis (medications) Commonly Overcorrection of Hypotonic fluid Losses OR Overdiuresis (Na+ Loss >> Water loss) |
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Hypervolemic Hyponatremia
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Presentation of HYPERvolemia:
Acute weight gain (all causes): ± Ascites (liver failure), ± Pulmonary edema (heart failure) ± Peripheral edema (heart failure) ± Anasarca (nephrotic syndrome) Common causes (fluid retentive states): Cirrhosis CHF Nephrotic syndrome ↑↑EC Water >> ↑↑ EC Sodium (due to impaired Na+2/ H20 excretion) |
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Euvolemic Hyponatremia
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Slightly increased total body water relative to total body sodium due to impaired secretion
Not enough water retention to cause edema Impaired excretion due to SIADH: Syndrome of Inappropriate antidiuretic hormone* Diseases causes= CNS & pulmonary disease Drug-induce causes= Chlorpropamide, carbamazepine *Inappropriate (excessive) ADH (antidiuretic hormone)= aka vasopressin Slightly ↑ EC Water with normal EC Sodium NOT enough fluid retention for hypervolemia |
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Presentation of Acute HYPONATREMIA
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125 mEq/L:
nausea, vomiting *115-120 mEq/L: headache, tremors incoordination, lethargy,delirium, obtundation *110-115 mEq/L: Seizures, coma **Symptoms due to Cerebral edema |
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Potassium (K+)
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Normal range 3.5 – 5.0 mEq/L
Primary cation in intracellular space (98%) Regulates muscle and nerve excitability especially myocardial conduction Factors effecting regulation: Renin-angiotensin system (Aldosterone) Metabolic Acid-Base disorders Large GI absorption followed by renal filtration Both with prominent renal reabsorption Renal (major regulatory system): Freely filtered, nearly completely reabsorbed Dependent on aldosterone for regulation Arterial pH (temporary redistribution): Metabolic Acidosis (Renal): ↑ Extracellular potassium (< Blood pH = > [H+] = > Serum K+) Metabolic Alkalosis (GI): ↓ Extracellular potassium (> Blood pH = < [H+] = < Serum K+) |
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Magnesium (Mg++)
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Normal range= 1.5 – 2.2 mEq/L
Bone (50-60%), Intracellular (30-40%)(2nd big) Extracellular only 1- 2% Role in neuromuscular and enzymatic function: Cofactor in ADP to ATP conversion Helps regulate neuromuscular conduction Myocardial or skeletal muscle Gastrointestinal 30% absorption (diet) 60% of elimination (fecal) Renal: Mg+ that is absorbed (30% of intake) Freely filtered with 97% reabsorption (Loop of Henle) Serum Mg and K = highly dependent on normal oral intake and renal elimination for maintenance of normal serum concentrations ONLY Serum K+ significantly affected by metabolic acid-base disorders |
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HYPERkalemia & HYPERmagnesemia
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Renal Causes:
Renal failure ↑ [K+] and ↑[Mg+] Acute & Chronic failure ESRD – End Stage Renal Disease Non-renal Causes: Metabolic acidosis (↑ [K+] only) Medications (↑ [K+] only ) ACE inhibitors/ ARBs Excessive Intake Excess K+ or Mg+ suppliments Hyperkalemia Presentation (Serum K+> 5.0 mEq/L): EKG Abnormalities Widened QRS complex ST Segment depression Peaked T waves Cardiovascular Hypotension Bradycardia Cardiac Arrest (asystole) Neuromuscular Cramps, Weakness *Peaked T waves – represents the cardiac cells continually repolarizing due to high K levels. NaCO2 can be given to promote alkylosis and drive K intracellular Hypermagnesemia Presentation(serum Mg+2 >2.2 mEq/L): Magnesium < 5.0 mEq/L: Rarely symptomatic Magnesium = 6- 10 mEq/L: Drowsiness, ↓DTR, Bradycardia Magnesium = 10 - 15 mEq/L: PR & QRS Prolongation, Paralysis Magnesium > 15 mEq/L: Respiratory arrest, Asystole |
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HYPOkalemia & HYPOmagnesemia
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Renal Causes:
Drug- induced (Drug-induced acute tubular necrosis or overdiuresis) Amphotericin Cisplatin Diuretics (ALL) Non-renal Causes: Metabolic alkalosis (↓ [K+] only) GI sources (both) Diarrhea Vomiting Decrease Intake (Both) Anorexia, Alcoholism Hypokalemia Presentation (Serum K+ < 3.5 mEq/L): EKG Abnormalities: PR Prolongation ST segment depression Flattened T –waves Prominent U-waves (U wave is another attempt to repolarize the cell) Cardiovascular: Hypotension ↑Risk of Digoxin toxicity Neuromuscular: Cramps, Weakness Hypomagnesemia Presentation (Serum Mg+2 < 1.5 mEq/L): Neuromuscular: Tremors, tetany Weakness ↑Deep tendon reflexes CNS: Irritability, combativeness Psychosis Convulsions, coma *If the patient is having a seizure then Mg levels must be checked and possible given |
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Calcium (Ca+2)
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Normal range 8.5 – 10.8 mg/dL
99.5% of body calcium is integrated within bones (0.5% extracellular) Major physiologic roles: Neuromuscular/ Myocardial functions Blood coagulation Bone Metabolism Extracellular Ca+2 is 40% protein bound (54% unbound) Unbound “ionized” fraction is physiologically active Unbound fraction is affected by available serum albumin Must correct total calcium level when albumin levels are low: Corrected Ca = [(4-albumin) x 0.8] + CaMeasured Vitamin D3 & PTH = ↑Calcium resorption (bone), absorption (GI), & reabsorption (renal) *Chronic renal failure = ↓’ed Vitamin D3 activation and ↓’ed response to PTH |
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Phosphate (PO4)
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Normal range 2.6 – 4.5 mg/dL
85% of body’s phosphate is integrated within bones with 15% found intracellular Major physiologic roles: Forms high energy bonds for ATP Essential component of nucleic acids |
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HYPOcalcemia & HYPERphosphatemia
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Renal Causes:
Chronic renal failure Kidneys are responsible for eliminating phosphate’s ESRD Non-renal Causes: Hypoparathyroidism ↓’ed Intake (Vit D & Ca+) Excess Intake (PO4 supplimt) Hypocalcemia Presentation:(serum Ca+2 < 8.5 mg/dL) Neuromuscular: Tetany, Seizures ↑Deep tendon reflexes Paresthesias CNS: Confusion, hallucinations Mental instability Cardiovascular: Hypotension, Bradycardia Cardiac arrhythmias Heart failure (depressive) *These symptoms are similar to hypomagnesium Hyperphosphatemia Presentation: (serum PO4 > 4.5 mg/dL) Mostly asymptomatic (symptoms of concurrent hypocalcemia) Extracellular PO4 complexes with extracellular Ca+2 to form a crystal IF their product (Ca x PO) > 55 i.e. Phosphate = 8 mg/dL & Calcium = 9 mg/dL (Product= 72) Ca+2-PO4 crystals deposit: Bone (arthritis-like) Skin (Rash, ischemic ulcers) Eyes (“Redeye”/ conjunctivitis) Vascular (may lead to cardiac arrhythmias) |
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HYPERcalcemia & HYPOphosphatemia
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Hypercalcemia (Serum Ca+ > 10.8 mg/L):
Malignancy (i.e, bone) Hyperparathyroidism Highly symptomatic for cancer Calcium < 13 mg/dL: Asymptomatic Calcium 13- 15 mg/dL: Renal effects= Polyuria, nocturia, polydipsia GI complaints Nausea, vomiting, constipation Calcium > 15 mg/dL: Lethargy, obtundation Acute renal failure Coma, death Hypophosphatemia (Serum PO4 < 2.6 mg/L): Phosphate binders – antacids (Mg) Refeeding syndrome – patient has not eaten in weeks and then suddenly eats lowers phosphates Hyperparathyroidism Neuromuscular: Weakness, parathesias Rhabdomyolysis Cardiac/ Respiratory failure CNS: Confusion, hallucinations Delirium, Seizures (often masked by hyper-Ca+) Hematologic: Hemolysis WBC & Platelet dysfunction *Without phosphates, there is little ATP |