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48 Cards in this Set
- Front
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Normal plasma osmolality
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285-295mmol/L; Calculated POSMc = 2[Na] + [glucose]/18 + [BUN]/2.8. Normal osmolar gap is <10mmol/L; osmolar gap >10mmol/L --> THINK lactic acid, ketones, methanol, or ethanol
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Normal plasma osmolality
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285-295mmol/L; Calculated POSMc = 2[Na] + [glucose]/18 + [BUN]/2.8. Normal osmolar gap is <10mmol/L; osmolar gap >10mmol/L --> THINK lactic acid, ketones, methanol, or ethanol
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ICF and ECF
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2/3 of TBW = ECF; 1/3 of TBW = ICF. Of the 1/3 that is ICF, 1/4 is Plasma and 3/4 is Interstitial (capillary wall separating these compartments)
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Function of aldosterone at distal tubule
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Stimulates K+ secretion and Na+ reabsorption
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Losses that Mimic ECF
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(1) Hemorrhage; (2) Loss of GI fluid - vomiting, NG suction, diarrhea, fistular drainage; (3) Postop fluid sequestration (third spacing): intestinal obstruction; (4) Intra-abdominal and retroperitoneal inflammation (e.g., pancreatitis, peritonitis); (5) SIRS, burns, sepsis
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Signs of volume deficit
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(1) Weight loss and decreased skin turgor; (2) Tachycardia, orthostasis/hypotension, collapsed neck veins; (3) Oliguria/azotemia; (4) Ileus
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Signs of volume overload
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(1) Weight gain and peripheral edema; (2) Increased CO, CVP; distended neck veins; heart murmur; (3) Bowel edema; (4) Pulmonary edema
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Third spacing
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Shift of ECF from plasma to elsewhere, such as interstitial or transcellular spaces
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IVF requirements for average 70kg adult patient?
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About 2.5 L/ day (1,000 + 500 + (20 × 50) = 2,500) or 100 mL/hr (2,500/24 =104) unless other factors warrant a higher rate.
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Normal UO
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0.5 cc/kg/hr for adults, 1 cc/kg/hr for kids.
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Blood urea nitrogen (BUN)/creatinine (Cr) > 20 and FeNa < 1%
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Indicates hypovolemia!
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Chronic hyponatremia
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Chronic hyponatremia may be asymptomatic until < 120 mEq/L. For every 100-mg/dL increment in plasma glucose above normal, the plasma sodium should decrease by 1.6 mEq/L.
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Normal plasma osmolality
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285-295mmol/L; Calculated POSMc = 2[Na] + [glucose]/18 + [BUN]/2.8. Normal osmolar gap is <10mmol/L; osmolar gap >10mmol/L --> THINK lactic acid, ketones, methanol, or ethanol
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ICF and ECF
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2/3 of TBW = ECF; 1/3 of TBW = ICF. Of the 1/3 that is ICF, 1/4 is Plasma and 3/4 is Interstitial (capillary wall separating these compartments)
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Function of aldosterone at distal tubule
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Stimulates K+ secretion and Na+ reabsorption
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Losses that Mimic ECF
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(1) Hemorrhage; (2) Loss of GI fluid - vomiting, NG suction, diarrhea, fistular drainage; (3) Postop fluid sequestration (third spacing): intestinal obstruction; (4) Intra-abdominal and retroperitoneal inflammation (e.g., pancreatitis, peritonitis); (5) SIRS, burns, sepsis
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Signs of volume deficit
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(1) Weight loss and decreased skin turgor; (2) Tachycardia, orthostasis/hypotension, collapsed neck veins; (3) Oliguria/azotemia; (4) Ileus
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Signs of volume overload
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(1) Weight gain and peripheral edema; (2) Increased CO, CVP; distended neck veins; heart murmur; (3) Bowel edema; (4) Pulmonary edema
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Third spacing
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Shift of ECF from plasma to elsewhere, such as interstitial or transcellular spaces
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IVF requirements for average 70kg adult patient?
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About 2.5 L/ day (1,000 + 500 + (20 × 50) = 2,500) or 100 mL/hr (2,500/24 =104) unless other factors warrant a higher rate.
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Normal UO
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0.5 cc/kg/hr for adults, 1 cc/kg/hr for kids.
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Blood urea nitrogen (BUN)/creatinine (Cr) > 20 and FeNa < 1%
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Indicates hypovolemia!
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Chronic hyponatremia
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Chronic hyponatremia may be asymptomatic until < 120 mEq/L. For every 100-mg/dL increment in plasma glucose above normal, the plasma sodium should decrease by 1.6 mEq/L.
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Hyponatremia with high plasma osmolality (pseudohyponatremia)
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Causes include (1) HYPERGLYCEMIA (either physiologyic or 2/2 rapid infusion of glucose or mannitol) will cause increased osmotic pressure that shifts fluid from ICF to ECF. The total body sodium in this case is normal but has become diluted due to the fluid shift; (2) Expected Na = 1.6*every 100mg/dL over 100 --> remember 'sweet 16'
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Hyponatremia with hypotonicity (true hyponatremia)
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Reflects excess ingestion of water that overwhelms the kidneys (either normal or diseased) or due to increased ADH. Hyponatremia is not due to increased excretion of sodium
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SIADH
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Increased vasopressin release from posterior pituitary or ectopic source causes decreased renal free water excretion.
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Hypovolemic hyponatremia
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Give e0.9%NaCl. Na repletion with saline isotonic to the patient avoids rapid changes in ICF volume. A major complication of rapid correction fo chronic hyponatremia is CENTRAL PONTINE MYELINOLYSIS
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How does Ca+ help with hyperkalemia?
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It stabilizes the membrane potential of cardiac muscle, which would abnormally fire in the presence of high potassium. It does not actually have any effect on the amount of K+ present.
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Treatment of hyperkalemia
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(1) 10% calcium gluconate 1 g IV; (2) Albuterol, insulin with glucose, or sodium bicarbonate promote cellular reuptake of K; (3) Kayexalate - cation exchange resin. As opposed to above measures, which immediately protect against dangers of high K+, this actually removes K+ from body; (5) Dialysis
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S&S of hyperkalemia
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Cardiac effects are most significant. Confirm hyperkalemia and obtain an ECG. (1) EARLY: peaked T waves, wide QRS, ST depression; (2) LATE: disappearance of T waves, heart block, sine wave - ominous for impending fatal arrhythmia
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Causes of hyperkalemia
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(1) MCC is renal failure; (2) K+ spillage from severe injury; (3) In metabolic acidosis, cells take up H+ ions in exchange for intracellular K+, acting as a buffer in states of acidosis and leading to hyperkalemia
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Causes of hypokalemia
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(1) MCC is excessive renal secretion; (2) Loss of K+ 2/2 excess mineralocorticoid activity: primary hyperaldosteronism, Cushing's, renal artery stenosis (hyperreninism), congenital adrenal hyperplasia (will cause concomitant hypernatremia); (3) Movement of K into cells 2/2 insulin, catecholamines, alkalemia; (4) Prolonged administration of K-free TPN; (5) Loss of excessive lower GI secretions such as diarrhea, colonic fistulas, VIPoma; (6) Diuretics
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S&S of hypokalemia
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(1) Flattened T waves, ST depression, U waves
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Equation for corrected calcium
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Corrected Calcium = 0.8 (Normal Albumin – Observed Albumin) + Observed Calcium
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Ratio of ionized to nonionized Ca is related to pH…how?
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(1) Acidosis causes an increase in ionized fraction; (2) Alkalosis causes decreased in ionized fraction
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Causes of hypocalcemia
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(1) Acute pancreatitis; (2) Massive soft-tissue infections (nec fasc); (3) Acute/chronic renal failure; (4) Pancreatic/small bowel fistulas; (5) HypoPTH; (6) Hypoproteinemia; (6) Severe Mg depletion (preventing PTH secretion)
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S&S of hypocalcemia
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(1) Numbness and tingling of fingers, toes, and around mouth; (2) Increased reflexes; (3) Chvostek's sign: tapping ovre facial nerve in front of tragus of ear causes ipsilateral twitching; (4) Trousseau's sign: Carpopedal spasm following inflation of sphygmomanometer cuff to above systolic BP for several minutes; (5) Muscle and abdominal cramps
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Causes of hypercalcemia
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(1) Hyperparathyroidism; (2) Cancer [esp. breast, multiple myeloma]; (3) Drugs [thiazides]
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Treatment of hypercalcemia
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(1) Vigourous repletion with salt solution - dilates Ca and increases urinary calcium excretion; (2) May be augmented with furosemide; (3) Definitive treatment of acute hypercalcemic crisis in patients with hyperPTH is surgery
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Harris-Benedict equation and Fick equation (in patients with Swan-Ganz catheters) used to estimate basal energy expenditure (BEE).
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General estimate of BEE: (1) Males: 25kcal/kg/day; (2) Females: 22kcal/kg/day. Multiply this by the desired goal (postsurgery gets 1.3-1.5xBEE); Fever gets 12% increase per degree celsius
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Respiratory quotient
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RQ is defined as the ratio of carbon dioxide released to oxygen consumed per unit metabolism of a substrate (i.e., VCO2/VO2).
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Causes of elevated anion gap metabolic acidosis
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MUDPILES: (1) Methanol/Metabolism [inborn errors]; (2) Uremia; (3) DKA; (4) Paraldehyde; (5) Iron/INH; (6) Lactic acidosis; (7) Ethylene glycol; (8) Salicylates/Stychnine. NARROW DOWN TO FOUR: Ketoacidosis, lactic acidosis, renal failure, intoxication!
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Causes of normal gap metabolic acidosis
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HARD-UP: (1) Hyperparathyroidism; (2) Adrenal insufficiency/Anhydrase [carbonic anhydrase] inhibitors; (3) RTA; (4) Diarrhea; (5) Ureteroenteric fistula; (6) Pancreatic fistulas
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Assess the acid-base disorder step by step
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(1) Acidosis [pH < 7.40] or Aklalosis [pH > 7.40]? (2) Respiratory [pH and PCO2 move in opposite directions] or Metabolic [pH and PCO2 move in same direction]? (3) Simple or mixed?
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Metabolic acidosis: two kinds
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(1) Anion gap acidosis: due to addition of unmeasured acid; (2) Nonanion gap acidosis: due to HCO3 loss; REMEMBER: AG = Na - [Cl + HCO3]. Normal AG = 10
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Metabolic alkalosis: two kinds
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(1) Loss of H+ from kidneys or GI tract --> renal: mineralocorticoid excess, diuretics, K+-losing nephropathy; GI: vomiting, gastric drainage, villous adenoma of colon; (2) Gain of HCO3: milk-alkali syndrome, exogenous NaHCO3, lactated ringers, packed RBC, TPN all contain substrates that metabolize to bicarbonate!
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Respiratory acidosis
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HYPERCAPNIA 2/2 one of two mechanisms: (1) Hypoventilation (brain stem injury, neuromuscular disease, ventilator malfunction); (2) Ventilation-perfusion (V/Q) mismatch (COPD, pneumonia, PE, foreign body, pulmonary edema)
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Respiratory alkalosis
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Hyperventilation 2/2 anemia, anxiety, increased ICP, salicylates, fever, hypoxemia, sepsis, pregnancy, CHF, pneumonia, asthma, liver disease; Alkalosis causes a decreased in serum K+ and ionized Ca, resulting in paresthesias, carpopedal spasm, and tetany
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