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Fluids, Electrolytes, Nutrition, and Acid-Base Disturbances Geoff Vana Loyola University Medical Center General Surgery PGY-1.

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Presentation on theme: "Fluids, Electrolytes, Nutrition, and Acid-Base Disturbances Geoff Vana Loyola University Medical Center General Surgery PGY-1."— Presentation transcript:

1 Fluids, Electrolytes, Nutrition, and Acid-Base Disturbances Geoff Vana Loyola University Medical Center General Surgery PGY-1

2 Total Body Water 50-60% of total body weight50-60% of total body weight 50% in males, 60% in females50% in males, 60% in females Reflection of body fat – lean tissues = high water contentReflection of body fat – lean tissues = high water content Adjust down for obesity (10-20%)Adjust down for obesity (10-20%) Highest in newborns ~80%Highest in newborns ~80% Compartments:Compartments: 2/3 (40%) – Intracellular (skeletal muscle)2/3 (40%) – Intracellular (skeletal muscle) 1/3 (20%) – Extracellular1/3 (20%) – Extracellular 2/3 (15%) – Interstitial2/3 (15%) – Interstitial 1/3 (5%) - Plasma1/3 (5%) - Plasma

3 Composition of Fluid ECFECF Sodium – principle cationSodium – principle cation Chloride and Bicarbonate – principle anionsChloride and Bicarbonate – principle anions ICFICF Potassium and Magnesium – cationsPotassium and Magnesium – cations Phosphate and Proteins – anionsPhosphate and Proteins – anions Water diffuses freely according to sodium contentWater diffuses freely according to sodium content Expands intravascular volumeExpands intravascular volume Expands interstitial volume 3x plasmaExpands interstitial volume 3x plasma

4 Fluid Secretion/Losses SecretionSecretion Stomach: 1-2LStomach: 1-2L Small Intestine: 2-3LSmall Intestine: 2-3L Pancreas: ccPancreas: cc Bile: ccBile: cc H 2 O lossesH 2 O losses Urine: ccUrine: cc Stool: 250ccStool: 250cc Insensible: 600ccInsensible: 600cc Increased by fever, hypermetabolism, hyperventilationIncreased by fever, hypermetabolism, hyperventilation To clear metabolites: cc urine per dayTo clear metabolites: cc urine per day

5 Volume Control Extracellular volume deficit – most commonExtracellular volume deficit – most common Loss of GI fluids (suction, emesis, diarrhea, fistula)Loss of GI fluids (suction, emesis, diarrhea, fistula) Acute – CV and CNS signsAcute – CV and CNS signs Chronic – decreased skin turgor, sunken eyes, CV and CNS signsChronic – decreased skin turgor, sunken eyes, CV and CNS signs Urine osmolality is higher than serumUrine osmolality is higher than serum Urine sodium is low (<20mEq/L)Urine sodium is low (<20mEq/L)

6 Volume Control Osmoreceptors and BaroreceptorsOsmoreceptors and Baroreceptors Osmoreceptors in paraventricular and supraventricular nuclei in hypothalamus – control thirst and ADH secretion from posterior pituitaryOsmoreceptors in paraventricular and supraventricular nuclei in hypothalamus – control thirst and ADH secretion from posterior pituitary Increased free water or decreased osmolality = decreased ADH and water reabsorptionIncreased free water or decreased osmolality = decreased ADH and water reabsorption Fine tuning day-to-dayFine tuning day-to-day Baroreceptors in cardiac atrium, aortic arch and carotid sinusesBaroreceptors in cardiac atrium, aortic arch and carotid sinuses Neural and hormonal feedbackNeural and hormonal feedback

7 Volume Control Renin-AngiotensinRenin-Angiotensin Renin: released from juxtaglomerular cells of afferent arterioles in kidney (  BP,  NaCl)Renin: released from juxtaglomerular cells of afferent arterioles in kidney (  BP,  NaCl) Cleaves angiotensinogen ( α -2 globulin produced by liver) to angiotensin 1Cleaves angiotensinogen ( α -2 globulin produced by liver) to angiotensin 1 Angiotensin: cleaved by ACE which is produced by vascular endothelial cellsAngiotensin: cleaved by ACE which is produced by vascular endothelial cells Increases vascular tone, stimulates catecholamine release from adrenal medulla and sympathetic nerve terminalsIncreases vascular tone, stimulates catecholamine release from adrenal medulla and sympathetic nerve terminals Decreases RBF and GFR – increases sodium reabsorption by indirect and direct effect (aldosterone release from adrenal cortex)Decreases RBF and GFR – increases sodium reabsorption by indirect and direct effect (aldosterone release from adrenal cortex) AldosteroneAldosterone Produced in zona glomerulosa of adrenal cortexProduced in zona glomerulosa of adrenal cortex Increased absorption of sodium in CD & DCT– stabilizing Na channel in open state, increases number of channels in apical membraneIncreased absorption of sodium in CD & DCT– stabilizing Na channel in open state, increases number of channels in apical membrane Increases Na/K activityIncreases Na/K activity Increases sodium reabsorption and potassium excretionIncreases sodium reabsorption and potassium excretion

8 Volume Control Natriuretic PeptideNatriuretic Peptide Brain and RenalBrain and Renal Released by atrial myocytes from wall distensionReleased by atrial myocytes from wall distension Inhibitory effect on renal sodium absorptionInhibitory effect on renal sodium absorption Urodilatin – ANP-like substance, synthesized by cortical collecting tubuleUrodilatin – ANP-like substance, synthesized by cortical collecting tubule Released by kidney tubules in response to atrial distension and sodium loadingReleased by kidney tubules in response to atrial distension and sodium loading Twice as potent as ANP, increases cGMP = Na, Cl, water diuresisTwice as potent as ANP, increases cGMP = Na, Cl, water diuresis

9 Volume Replacement Lactated Ringer’s solutionLactated Ringer’s solution Blood loss, edema fluid, small bowel lossesBlood loss, edema fluid, small bowel losses Ideal when electrolytes are normalIdeal when electrolytes are normal Na 130mEq/L – hyponatremia can occur with extended useNa 130mEq/L – hyponatremia can occur with extended use Lactate converted to bicarbonate – no contribution to acidosisLactate converted to bicarbonate – no contribution to acidosis Normal SalineNormal Saline Useful for hyponatremia and hypochloremia (154mEq/L)Useful for hyponatremia and hypochloremia (154mEq/L) Can lead to increased electrolyte concentrationsCan lead to increased electrolyte concentrations Hyperchloremic metabolic acidosisHyperchloremic metabolic acidosis pH between 4-5pH between 4-5 Hypotonic solutions (1/2 or ¼ NS)Hypotonic solutions (1/2 or ¼ NS) Hypoosmotic and hypotonicHypoosmotic and hypotonic Can result in RBC lysisCan result in RBC lysis D5 added to prevent (200 kcal/L)D5 added to prevent (200 kcal/L)

10 Volume Replacement Hypertonic Saline SolutionsHypertonic Saline Solutions 3% NaCl, 5% NaCl, 7.5% NaCl3% NaCl, 5% NaCl, 7.5% NaCl Resuscitation for head trauma, hemorrhagic shock, burnResuscitation for head trauma, hemorrhagic shock, burn Increases intravascular volume quickerIncreases intravascular volume quicker Increases cerebral perfusion and reduces cerebral edemaIncreases cerebral perfusion and reduces cerebral edema Decreases volume requirementDecreases volume requirement rule4-2-1 rule Monitor UOPMonitor UOP

11 Colloids Albumin (5%, 25%)Albumin (5%, 25%) Increases plasma oncotic pressure – reversing diffusion of water into interstitial spaceIncreases plasma oncotic pressure – reversing diffusion of water into interstitial space ARDS, Burns, Infections, SepsisARDS, Burns, Infections, Sepsis Can extravasate into tissues – worsening edemaCan extravasate into tissues – worsening edema HetastarchHetastarch Synthetic plasma expanderSynthetic plasma expander Coagulopathy and bleeding from reduced factor VIII and von Willebrand factor, prolonged PTT and impaired platelet functionCoagulopathy and bleeding from reduced factor VIII and von Willebrand factor, prolonged PTT and impaired platelet function Hextend (6% in LR)Hextend (6% in LR) Plasma expander with no effect on coagulationPlasma expander with no effect on coagulation Reduce fluid requirement, eliminate need for mannitol, improves neurologic outcomeReduce fluid requirement, eliminate need for mannitol, improves neurologic outcome No inhibition of plateletsNo inhibition of platelets

12 Sodium HyponatremiaHyponatremia Sodium depletion or dilutionSodium depletion or dilution Dilution:Dilution: SIADH, anti-psychotics, tricyclics, ACE-IsSIADH, anti-psychotics, tricyclics, ACE-Is Depletion:Depletion: Low-sodium diet, GI losses (emesis, NG, diarrhea), renal d/t diureticsLow-sodium diet, GI losses (emesis, NG, diarrhea), renal d/t diuretics PseudohyponatremiaPseudohyponatremia Elevated glucose level causes influx of H 2 OElevated glucose level causes influx of H 2 O Na + (gluc-100) x.016Na + (gluc-100) x.016 Headache, confusion, N/V, seizures, fatigue, increased ICP, HTN, bradycardia, oliguriaHeadache, confusion, N/V, seizures, fatigue, increased ICP, HTN, bradycardia, oliguria

13 Sodium HypernatremiaHypernatremia Loss off free water or gain of sodiumLoss off free water or gain of sodium Iatrogenic administration of sodium-rich fluidsIatrogenic administration of sodium-rich fluids Mineralocorticoid excess (hyperaldosteronism, Cushing’s syndrome, CAH)Mineralocorticoid excess (hyperaldosteronism, Cushing’s syndrome, CAH) Hypotonic skin losses from fever or tracheostomies during hyperventilationHypotonic skin losses from fever or tracheostomies during hyperventilation Urine Na > 20mEq/LUrine Na > 20mEq/L Ataxia, tonic spasms, delirium, weakness, tachycardia, hypotension, syncope, red swollen tongue, decreased saliva/tears, feverAtaxia, tonic spasms, delirium, weakness, tachycardia, hypotension, syncope, red swollen tongue, decreased saliva/tears, fever Free Water Deficit = TBW x [(Na/140) – 1]Free Water Deficit = TBW x [(Na/140) – 1]

14 Potassium Hypokalemia – more common than hyperkalemiaHypokalemia – more common than hyperkalemia Caused by poor intake, excess renal excretion, diarrhea, fistulas, emesis, high NG output, intracellular shifts from metabolic alkalosis or insulinCaused by poor intake, excess renal excretion, diarrhea, fistulas, emesis, high NG output, intracellular shifts from metabolic alkalosis or insulin Decreases 0.3 mEq/L for every 0.1 increase in pHDecreases 0.3 mEq/L for every 0.1 increase in pH Amphotericin, aminoglycosides, foscarnet, cisplatin, ifosfamide – induce magnesium wastingAmphotericin, aminoglycosides, foscarnet, cisplatin, ifosfamide – induce magnesium wasting Correct magnesiumCorrect magnesium Disorders of muscle contractility in GI smooth muscle, cardiac muscle, skeletal muscleDisorders of muscle contractility in GI smooth muscle, cardiac muscle, skeletal muscle Ileus, constipation, weakness, fatigue, dec DTR, paralysis, cardiac arrestIleus, constipation, weakness, fatigue, dec DTR, paralysis, cardiac arrest

15 Potassium HyperkalemiaHyperkalemia Excessive intake, increased cellular release, impaired excretion from kidneysExcessive intake, increased cellular release, impaired excretion from kidneys PO/IV supplementation, post-transfusion RBC lysis, acidosis, rapid rise in extracellular osmolalityPO/IV supplementation, post-transfusion RBC lysis, acidosis, rapid rise in extracellular osmolality K-sparing diuretics, ACE-Is, NSAIDsK-sparing diuretics, ACE-Is, NSAIDs Spironolactone and ACE-Is inhibit aldosterone (renal excretion)Spironolactone and ACE-Is inhibit aldosterone (renal excretion) N/V, intestinal colic, diarrhea, weakness, ascending paralysis, peaked T-waves, wide QRS, sine wave formation, V-fibN/V, intestinal colic, diarrhea, weakness, ascending paralysis, peaked T-waves, wide QRS, sine wave formation, V-fib

16 Magnesium 1/3 bound to albumin – plasma level poor indicator with hypoalbuminemia1/3 bound to albumin – plasma level poor indicator with hypoalbuminemia HypermagnesemiaHypermagnesemia Severe renal insufficiency, magnesium-containing antacids/laxatives, TPN, massive trauma, severe acidosisSevere renal insufficiency, magnesium-containing antacids/laxatives, TPN, massive trauma, severe acidosis N/V, neuromuscular dysfunction, weakness, lethargy, hyporeflexia, impaired cardiac conduction, elevated T wavesN/V, neuromuscular dysfunction, weakness, lethargy, hyporeflexia, impaired cardiac conduction, elevated T waves HypomagnesemiaHypomagnesemia Regulated by calcium/magnesium receptors in tubular cellsRegulated by calcium/magnesium receptors in tubular cells Starvation, EtOH, prolonged IVF therapy, TPN, diuretic use, amphotericin B, Primary aldosteronism, diarrhea, malabsorption, acute pancreatitisStarvation, EtOH, prolonged IVF therapy, TPN, diuretic use, amphotericin B, Primary aldosteronism, diarrhea, malabsorption, acute pancreatitis CNS hyperactivity, hyperactive DTRs, muscle tremors, ST depression, torsades de pointesCNS hyperactivity, hyperactive DTRs, muscle tremors, ST depression, torsades de pointes Can produce hypocalcemia and persistent hypokalemiaCan produce hypocalcemia and persistent hypokalemia Replace magnesiumReplace magnesium

17 Phosphorus HyperphosphatemiaHyperphosphatemia Decreased urinary excretion, increased intake, impaired renal function, hypoparathyroidism, hyperthyroidism, rhabdomyolysis, tumor lysis syndrome, sepsis, hemolysisDecreased urinary excretion, increased intake, impaired renal function, hypoparathyroidism, hyperthyroidism, rhabdomyolysis, tumor lysis syndrome, sepsis, hemolysis Metastatic deposition of soft tissue calcium-phosphorus complexesMetastatic deposition of soft tissue calcium-phosphorus complexes HypophosphatemiaHypophosphatemia Decreased intake, intracellular shift (alkalosis, insulin, refeeding), decreased GI uptake from phosphate bindersDecreased intake, intracellular shift (alkalosis, insulin, refeeding), decreased GI uptake from phosphate binders

18 Calcium HypercalcemiaHypercalcemia Primary hyperparathyroidism, malignancy (bone metastasis, PTHr)Primary hyperparathyroidism, malignancy (bone metastasis, PTHr) Neurologic impairment, muscle weakness/pain, renal dysfunction, n/v, abdominal pain, worsening of Digitalis toxicity, short QT interval, flat T waves, AV blockNeurologic impairment, muscle weakness/pain, renal dysfunction, n/v, abdominal pain, worsening of Digitalis toxicity, short QT interval, flat T waves, AV block HypocalcemiaHypocalcemia Pancreatitis, soft tissue infection, renal failure, small bowel fistulas, hypoparathyroidism, TSS, abnormal magnesium, tumor lysis syndrome, post-parathyroidectomy, breast/prostate cancer, alkalosisPancreatitis, soft tissue infection, renal failure, small bowel fistulas, hypoparathyroidism, TSS, abnormal magnesium, tumor lysis syndrome, post-parathyroidectomy, breast/prostate cancer, alkalosis Parastheias of face, muscle cramps, carpopedal spasm, stridor, tetany, seizures, hyperreflexia, heart block, prolonged QTParastheias of face, muscle cramps, carpopedal spasm, stridor, tetany, seizures, hyperreflexia, heart block, prolonged QT

19 Vitamin Deficiency DeficiencyEffect ChromiumHyperglycemia, encephalopathy, neuropathy SeleniumCardiomyopathy, weakness, hair loss CopperPancytopenia ZincHair loss, poor healing, rash Trace elementsPoor wound healing PhosphateWeakness (fail to wean vent), encephalopathy, decreased phagocytosis Thiamine (B1)Wernicke’s, cardiomyopathy, peripheral neuropathy Pyridoxine (B6)Sideroblastic anemia, glossitis, peripheral neuropathy Cobalamin (B12)Megaloblastic anemia, peripheral neuropathy, beefy tongue FolateMegaloblastic anemia NiacinPellagra (diarrhea, dermatitis, dementia) Essential Fatty AcidsDermatitis, hair loss, thrombocytopenia Vitamin ANight Blindness Vitamin KCoagulopathy Vitamin DRickets, Osteomalacia Vitamin ENeuropathy

20 Acid-Base Disorder Disorder of balance between HCO 3 - and H +Disorder of balance between HCO 3 - and H + Blood pH: 7.35 – 7.45Blood pH: 7.35 – 7.45 Arterial PCO2: 35 – 45mmHgArterial PCO2: 35 – 45mmHg Plasma HCO3-: 22 – 26mEq/LPlasma HCO3-: 22 – 26mEq/L Lungs compensate for metabolic abnormalitiesLungs compensate for metabolic abnormalities QuickQuick Kidneys compensate for respiratory abnormalitiesKidneys compensate for respiratory abnormalities Delayed, up to 6 hoursDelayed, up to 6 hours Acute – before compensationAcute – before compensation Chronic – after compensationChronic – after compensation

21 Respiratory Acidosis pH 45pH 45 Decreased ventilationDecreased ventilation BiPAP, intubation to increase minute ventilationBiPAP, intubation to increase minute ventilation Chronic form: pCO2 remains constant and HCO3 increases as compensation occursChronic form: pCO2 remains constant and HCO3 increases as compensation occurs Narcotics, Atelectasis, Mucus plug, pleural effusion, pain, limited diaphragmatic excursionNarcotics, Atelectasis, Mucus plug, pleural effusion, pain, limited diaphragmatic excursion

22 Respiratory Alkalosis pH > 7.45, pCO2 7.45, pCO2 < 35 Most cases acute from hyperventilationMost cases acute from hyperventilation Pain, anxiety, neurologic disorders, CNS injury, hypoxemiaPain, anxiety, neurologic disorders, CNS injury, hypoxemia Salicylates, fever, Gram Neg bacteria, thyrotoxicosisSalicylates, fever, Gram Neg bacteria, thyrotoxicosis Acute hypocapnia: uptake K and phosphate into cells, increased Ca binding to albuminAcute hypocapnia: uptake K and phosphate into cells, increased Ca binding to albumin Symptomatic hypokalemia, hypophosphatemia, hypocalcemiaSymptomatic hypokalemia, hypophosphatemia, hypocalcemia

23 Metabolic Acidosis pH < 7.35, HCO3 < 22pH < 7.35, HCO3 < 22 Increased acid intake, increased generation of acids, increased loss of bicarbonateIncreased acid intake, increased generation of acids, increased loss of bicarbonate Response: increase buffers (bone/muscle), increase respiration, increased renal reabsorption and generation of bicarbonate and excretion of hydrogenResponse: increase buffers (bone/muscle), increase respiration, increased renal reabsorption and generation of bicarbonate and excretion of hydrogen Calculate Anion Gap = (Na) – (Cl + HCO3)Calculate Anion Gap = (Na) – (Cl + HCO3) Corrected AG = AG – [2.5(4.5-albumin)]Corrected AG = AG – [2.5(4.5-albumin)] AG > 12: Methanol, Uremia, DKA, Paraldehyde, INH, Lactic acidosis, Ethanol, SalicylatesAG > 12: Methanol, Uremia, DKA, Paraldehyde, INH, Lactic acidosis, Ethanol, Salicylates AG < 12: RTA, Carbonic anhydrase inhibitor, GI lossesAG < 12: RTA, Carbonic anhydrase inhibitor, GI losses

24 Metabolic Alkalosis pH > 7.45, HCO3 > 26pH > 7.45, HCO3 > 26 Loss of fixed acids, gain of bicarbonate (worsened by potassium depletion), pyloric stenosis and duodenal ulcer disease (hypochloremic, hypokalemic)Loss of fixed acids, gain of bicarbonate (worsened by potassium depletion), pyloric stenosis and duodenal ulcer disease (hypochloremic, hypokalemic) Increased urine bicarbonate, reabsorption of hydrogen and potassium excretionIncreased urine bicarbonate, reabsorption of hydrogen and potassium excretion Aldosterone causes Na reabsorption and increased K excretion – H+/K+ interchange results in paradoxical aciduriaAldosterone causes Na reabsorption and increased K excretion – H+/K+ interchange results in paradoxical aciduria

25 Nutrition Pre-operative EvaluationPre-operative Evaluation Albumin: 20 daysAlbumin: 20 days Transferrin: 10 daysTransferrin: 10 days Pre-albumin: 2 daysPre-albumin: 2 days Poor nutrition:Poor nutrition: Weight loss >10% in 6 monthsWeight loss >10% in 6 months Albumin < 3.0Albumin < 3.0 Weight = <85% IBWWeight = <85% IBW

26 Nutrition Caloric Need – kcal/kg/dayCaloric Need – kcal/kg/day Fat: 9kcal/gFat: 9kcal/g Carbohydrate: 4kcal/gCarbohydrate: 4kcal/g Dextrose: 3.4kcal/gDextrose: 3.4kcal/g Protein: 4kcal/gProtein: 4kcal/g RequirementsRequirements Normal: 1-1.5g/kg/d protein, 20% AA, 30% calories from fat, carbohydratesNormal: 1-1.5g/kg/d protein, 20% AA, 30% calories from fat, carbohydrates Trauma/Surgery/Sepsis: increase 20-40%Trauma/Surgery/Sepsis: increase 20-40% Pregnancy: increase by 300 kcal/dayPregnancy: increase by 300 kcal/day Lactation: increase 500 kcal/dayLactation: increase 500 kcal/day Burns:Burns: Calories:25 kcal/kg/day + (30kcal/d X %burn)Calories:25 kcal/kg/day + (30kcal/d X %burn) Protein: 1-1.5g/kg/day + (3g X %burn)Protein: 1-1.5g/kg/day + (3g X %burn)

27 Starvation Brain: glucoseBrain: glucose Colonocytes: Short-chain fatty acidsColonocytes: Short-chain fatty acids Enterocytes: glutamineEnterocytes: glutamine Glycogen stores converted to glucoseGlycogen stores converted to glucose hours of starvation24-36 hours of starvation Low insulin, high glucagonLow insulin, high glucagon Lipolysis into glycerol and FFA – gluconeogenesisLipolysis into glycerol and FFA – gluconeogenesis 2-3 days2-3 days Amino acids from protein (glutamine and alanine) converted to glucoseAmino acids from protein (glutamine and alanine) converted to glucose Muscle breakdownMuscle breakdown Ketones from fatty acidsKetones from fatty acids Brain utilizationBrain utilization Resumption of glucose intake can reverseResumption of glucose intake can reverse

28 TPN 3-1 mixture of protein (AA), carbohydrate (dextrose), and fat (lipid emulsion)3-1 mixture of protein (AA), carbohydrate (dextrose), and fat (lipid emulsion) Fat can be separate piggy-backFat can be separate piggy-back Standard Solution: 50-60% dextrose, 24-34% fat, 16% proteinStandard Solution: 50-60% dextrose, 24-34% fat, 16% protein Additives:Additives: Electrolytes adjusted daily for pt needsElectrolytes adjusted daily for pt needs Na: 60-80mEq/day K: 30-60mEq/day Cl: mEq/day Ca: mEq/day Mg: mEq/day PO4: 12-24mmol/day Anions and Cations must balance Use chloride and acetate Low bicarbonate, increase acetate Trace elements and multivitamins added as prepared mixture Vitamin K not included

29 RQ Ratio of CO2 produced to O2 consumedRatio of CO2 produced to O2 consumed RQ = CO 2 produced / O 2 consumedRQ = CO 2 produced / O 2 consumed Energy expenditureEnergy expenditure Fat = 0.7Fat = 0.7 Protein = 0.8Protein = 0.8 Carbohydrate = 1Carbohydrate = 1 RQ >1 = lipogenesis (overfeeding)RQ >1 = lipogenesis (overfeeding) Decrease carbohydrates and caloric intakeDecrease carbohydrates and caloric intake High cholesterol can inhibit ventilator weaningHigh cholesterol can inhibit ventilator weaning RQ <.7 = ketosis and fat oxidation (starvation)RQ <.7 = ketosis and fat oxidation (starvation) Increase carbohydrates and caloriesIncrease carbohydrates and calories

30 Post-Operative Catabolic: POD 0-3Catabolic: POD 0-3 Negative nitrogen balanceNegative nitrogen balance Diuresis: POD 2-5Diuresis: POD 2-5 Anabolic: POD 3-6Anabolic: POD 3-6 Positive nitrogen balancePositive nitrogen balance

31 Question 1 A 72-year-old man from a nursing home is admitted to the hospital with severe volume depletion. Her serum sodium is 180 mEq/L and she weighs 45 kg. Her estimated relative free water deficit is: A. 4L B. 5L C. 7.2L D. 6L E. 3L

32 Answer 1 D. 6L Whenever hypernatremia develops, a relative free water deficit exists and must be replaced. The water deficit can be approximated using the formula: water deficit = 0.5 x wt(kg) × [(Na/140)-1]

33 Question 2 Which of the following statements regarding hypokalemia is correct? A. Metabolic acidosis may contribute to renal potassium wasting B. The degree of hypokalemia correlates very well with total body potassium deficit C. High levels of aldosterone stimulate potassium reabsorption in the distal tubule D. Diuretics rarely cause hypokalemia E. Hypokalemia in patients who are vomiting is primarily due to renal potassium losses

34 Answer 2 E. Hypokalemia in patients who are vomiting is primarily due to renal potassium losses Hypokalemia can have profound physiologic consequences. Of greatest clinical concern are cardiac arrhythmias and exacerbation of digitalis toxicity. Muscle weakness, cramps, myalgias, paralysis, and when severe, rhabdomyolysis can result. Hypokalemia also enhances renal acid excretion, which can generate and maintain metabolic alkalosis. Potassium may be lost through the gastrointestinal (GI) tract, primarily in patients with diarrhea, and through the kidneys. The most important cause of renal potassium loss is diuretics. Metabolic alkalosis also contributes to renal potassium wasting. Whenever large quantities of NaHCO 3 transit the distal parts of the nephron, potassium secretion is stimulated. High levels of aldosterone, whether due to volume depletion or autonomous secretion, also stimulate potassium secretion. When hypokalemia develops in patients with vomiting or nasogastric suction, it is primarily caused by renal potassium losses, and not the small amount of potassium lost in the vomitus. The high aldosterone levels and metabolic alkalosis associated with the gastric losses combine to stimulate renal potassium excretion.

35 Question 3 All of the following are associated with hypomagnesemia except: A. Previous treatment with cisplatin B. Alcoholics C. Poor oral intake D. Diuretics E. Oral potassium supplements

36 Answer 3 E. Oral potassium supplements Hypomagnesemia is a less common and frequently overlooked electrolyte abnormality. It should be suspected in patients on an insufficient diet, especially alcoholics, or in patients chronically using diuretics. Both alcohol and most diuretics increase renal magnesium excretion. Hypomagnesemia is clinically important not just because it has direct effects, but also because it can produce hypocalcemia and contribute to the persistence of hypokalemia. Magnesium deficiency will cause renal potassium wasting. When hypokalemia and hypomagnesemia coexist, magnesium should be aggressively replaced to restore potassium balance. The same is true for hypocalcemia. The level of plasma magnesium is a poor indicator of the degree of total body magnesium stores. Magnesium should be replaced until the plasma level returns to the upper normal range. Magnesium can be replaced either intravenously or, in less acute circumstances, through oral supplements. Gastrointestinal absorption of this cation, which occurs with greatest facility in the duodenum, is variable. In addition, all magnesium salts have a laxative effect when taken by mouth.

37 Question 4 The primary substrate for starvation-induced gluconeogenesis is A.Liver glycogen B.Organ protein C.Skeletal muscle protein D.Free fatty acids E.Keto acids

38 Answer 4 C. Skeletal muscle protein Following a few days of starvation, the body begins a period of catabolism in which muscle is broken down in order to use the protein found therein. The protein is subsequently converted to glucose by gluconeogenesis.

39 Question 5 Enterocytes energy requirements are provided by: A. Arginine B. Alanine C. Glutamine D. Glycine

40 Question 6 Decreasing glucose and increasing fat in total parenteral nutrition will: A. Increase respiratory quotient B. Increase CO2 production C. Decrease minute ventilation D. Delay weaning from mechanical ventilation


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