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46 Cards in this Set
- Front
- Back
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Fluid and Electrolyte Balance
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Body Water
Body Fluids: vital to life; maintain body temp, cell shape; involved in transport of nutrients, gases and wastes Fluid balance: maintained by skin, lungs, kidneys. Daily: fluid gained = fluid lost Sensible (measurable) and insensible losses |
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Fluid and Electrolyte Balance
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Fluid Compartments
Intracellular Extracellular Intercellular or interstitial Plasma, lymph |
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Fluid and Electrolyte Balance
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Fluid movements
Fluids are found in solutions Isotonic Hypotonic Hypertonic |
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Fluid and Electrolyte Balance
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Movement Within the Vascular System
Hydrostatic pressure / oncotic pressure Albumin Edema “third-space”fluid |
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Fluid and Electrolyte Balance
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Osmolality
Measureofosmoticallyactiveparticles/Kgof solvent or mOsm/Kg Preferredtermforconcentrationoffluidsin clinical setting Serumandextracellularfluidosmolalitycanbe calculated to be ~ 290 mOsm/L (text ~ 300) Osmolality<285mOsm/Lindicateswaterexcess(dilute) Osmolality>295mOsm/Lindicateswaterdeficit (concentrated) (text > 300 = deficit) |
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Electrolytes
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Na
Principle cation of extracellular fluids (135-145mEq/L) K Principle cation of intracellular fluids; small amounts found extracellularly (3.5-5mEq/L) Cl Principle anion of extracellular fluids (100-110mEq/L) All quickly respond to changes in hormone, drug, acid base levels, and kidney function. Electrolyte levels affected very little by dietary intake |
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Acid - Base Balance
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pH
Normal Low (acidosis) < 7.35 High (alkalosis) > 7.45 |
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Acid - Base Balance
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Regulating Acids and Bases
Buffers: Weak acids or bases; minimize pH effect of strong acids or bases Bicarbonate: Main extracellular buffer Phosphate: Main intracellular buffer Protein: Main intracellular buffer |
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Acid - Base Balance
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Regulating Acids and Bases
Respiratory system: Controls depth of breathing to alter amount of CO2 expired decreased ventilation causes CO2retention and possible acidosis Kidneys: Regulate H+ secretion and HCO3 resorption |
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Acid – Base Disorders
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Metabolic Acidosis
Acid accumulates DKA Lactic acidosis Uremia Bicarbonate loss Kidneys GI |
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Acid – Base Disorders
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Metabolic Alkalosis
Acid loss Vomiting NG suctioning Bicarbonate accumulates Increased resorption of Na, water and bicarb with blood volume depletion Increased resporption of bicarb with severe hypokalemia K leaves cell, H+ enters and increased bicarb resorption results |
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Acid – Base Disorders
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Respiratory Acidosis
CO2 retention in blood Asthma COPD ARDS Severe obesity, sleep apnea Starvation, cachexia Respiratory Alkalosis CO2 decreased in blood Stroke Anxiety CHF |
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Acid – Base Disorders
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Therefore -
Metabolic Acidosis / Alkalosis or Respiratory Acidosis / Alkalosis causes Compensation Kidneys altered bicarb resorption Ventilation altered depth of breathing Buffer system |
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Lab Data
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Advantage of controlled environment
As good as the lab used for analysis Lab data includes Biochem assays and other tests of blood, tissue, fluid, wastes |
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Lab Data
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Nutritional status
changes slowly, causing changes inmedical status later rapidly declines with illness or injury assessment includes evaluation of lab indicators (markers, parameters) of nutritional status |
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Specimen
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Whole blood; Serum; Plasma Blood cells; Erythrocytes; Leukocytes Tissue samples Urine Feces Less common, questionable validity: breath tests, saliva, hair, nails, sweat |
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Assays
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Static
Measures actual level of a nutrientin a specimen Functional Measureslevelofamolecule’sactivityinthe body that depends on the nutrient of interest Example: Ferritin Level in the blood depends on the amount of Fe in body stores Functional measure which indicates Fe stores Problem: other nutrients/ factors can affect ferritin |
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Hydration Status
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Hydration status is determined in conjunction with physical assessment.
Lab indicators of hydration status are: Na BUN Osmolality Urine specific gravity |
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Lab Data in Stress-Related PEM
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Help determine the body’s protein and energy stores and status
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Lab Data in Protein-Energy Status
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Illness, injury, trauma, (stress) causes inflammation, PEM
Stress causes cytokine release Alters synthesis of plasma protein by the liver Increases catabolism of muscle protein for energy needed for the stress response |
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Lab Data in Protein-Energy Status
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Negative acute phase respondents
Albumin, transferrin, transthyretin, retinol binding protein Decrease during acute phase of illness Positive acute phase respondents C-reactive protein, fibrinogen Increase during acute phase of illness Degree of changes in these proteins reflect the severity of injury |
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Lab Data in Protein-Energy Status
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During stress, decreased albumin occurs mainly due to a shift from intravascular space to extravascular space
During starvation, albumin remains in the intravascular space Somatic = muscle protein Visceral = plasma, organ protein |
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C-Reactive Protein
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Positive acute phase reactant
CRP increases up to1000x due to the stress response. As CRP decreases stress response is waning and aggressive nutrition support can begin As CRP decreases, TTHY increases can use either for evaluation of recovery in the stress response |
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Urinary Creatinine
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Used to determine body composition in relation to somatic muscle protein
Creatinine is aby-product of creatine metabolism; creatine mainly found in muscle tissue Measure of urinary creatinine indirectly reflectsLBM Ratio of urinary creatinine excretion (from24hr urine collection) to expected creatinine excretion (based on sex and ht of the pt) may be used to assess degree of muscle depletion |
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Urinary Creatinine and CHI Limitations
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24 hr urine collection
Standards based on healthy young adults creatinine excretion decreases with age May be affected by dietary intake, exercise, metabolic stress Mainly used in research settings |
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Total Lymphocyte Count (TLC)
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Total Lymphocyte Count (TLC) Lymphocyte – WBC involved in production of antibodies Indicates immune function and protein nutrition status Easily calculated from the CBC with differential Monitored every 7-10 days
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TLC
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TLCNeed differential:Total WBC (leukocytes) 5,000 -10,000/mm3 lymphocytes (40-60% of total WBC) Monocytes (4-8%)Neutrophils (55-70%)Eosinophils (1-4%) Basophils (0.5%-1%)TLC = (WBC x % lymphocytes) / 100Example. Calculate:TLC = (4000mm3 x 25) /100 TLC = 1000WNL: >2700Moderate depletion: 900-1800 Severe depletion: <900
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Nitrogen Balance
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Biochemical measure
Reflects somatic and visceral protein stores Assessesshort-term changes in total body protein Estimate of protein repletion or depletion During hypermetabolic stress, protein is utilized for energy Can measure degree of metabolic stress All protein contains N |
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Nitrogen Balance
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NBalance:differencebetweenNintakeandN excretion N balance = N intake – N output
+Nbalance=anabolism - N balance = catabolism 0 N balance=“normal, healthy” Reflects balance between N intake and renal N removal which can indicate level of protein usage, synthesis vs. degradation What patients would typically be in Negative N balance? Positive N balance? |
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How is Nitrogen Balance Determined?
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Determine N intake
Tally the amount of protein ingested and divide by 6.25 (6.25 g protein yields 1 g of N)N (g) = pro (g) / 6.25 Determine N output Use urinary urea nitrogen (UUN) |
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Nitrogen Balance (UUN)
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UUN
An estimate of N excreted in the urine asa waste product of protein catabolism Not valid if renal insufficiency When using UUN as a measure of Nexcreted + 4 g for insensible losses |
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Nitrogen Balance
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N balance= N intake – N output= pro (g)/24 hr – (UUN + 4) 6.25
Find the difference between the two results. Determine, based on the patient’s condition, if the result indicates negative or positive N balance. |
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Hepatic Transport Protein Indicators
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Functional indicators of visceral protein stores Negative acute phase respondents
Albumin Transferrin Transthyretin Retinol binding protein Positive acute phase respondents C-reactive protein |
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Albumin
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~60% of all serum protein Transports nutrients, drugs and hormones Can indicate prolonged protein depletion Liver function test as it is synthesized in the liver Helps maintain fluid balance When albumin < 3 g/dl may see symptoms of edema |
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Albumin Limitations
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1⁄2 life=18-21days
Concentration increases slowly in recovery Increased in dehydration and hormone therapy Large extra-vascular pool replenishes supply in blood when it decreases (if extravascular pool decreasing blood test will not show it) Early starvation album in may be normal in routine blood test Poor indicator of PEM Negative acute phase respondent Inflammation will show decreased albumin |
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Transferrin
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Fe transport between intestine and sites of Fe stores
Beta globulin protein More sensitive indicator of PEM Responds promptly to changes in protein intake 1⁄2life of 8 days |
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Transferrin Limitations
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Level dependent on Fe stores
if stores increase then transferrin synthesis decreases and vice versa Level can reflect Fe status and not PEM Negative acute phase protein |
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Transthyretin (TTHY) or Prealbumin (PAB)
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Also known as thyroxin binding pre-albumin
Binds retinol binding protein and thyroxin Indicator of protein status 1⁄2 life of 2 days |
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Transthyretin or Prealbumin Limitations
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Negative acute phase respondent
useful when inflammation wanes Zn def affects hepatic synthesis of TTHY Look at Zn when evaluate TTHY |
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Retinol Binding Protein
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Circulates in complex with TTHY
Transports retinol (metabolite of vit A) Synthesized in the liver and released with retinol After release of retinol at peripheral tissue, TTHY RBP complex declines Indicator of protein status 1⁄2 life of 12 hours |
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Retinol Binding Protein Limitations
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Negative acute phase respondent but not affected by inflammation as much as alb, PAB and transferrin are
Retinol status effects RBP level; not useful if vit A status is compromised Renal failure: increased RBP (not filtered at the glomerulus) |
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Anemia
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Decreased RBC or decreased Hgb
Hgb below 85th percentile of the reference population Symptom not a disease Must differentiate between a nutritional deficiency and another cause |
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Anemia
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Classification
MCV: < 80 fl = microcytic; often but not always associated with Fe def 80-99 fl = normocytic > 100 fl = macrocytic; associated with B12and folate def (fl femtoliters) |
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Lab Tests for Fe Deficiency Anemia
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Hemoglobin
Hgb Respiratory protein of RBC Hematocrit Hct % of RBC in a volume of whole blood Serum Fe Poor indicator of Festatus (diurnalvariation) Transferrin Fetransportprotein TIBC Numberofavailablebindingsitesontransferrin As transferrin saturation (Tsat) increases, TIBC decreases Ferritin Storage pro for Fein liver, spleen, marrow Serum ferritin is in direct proportion to storage ferritin Ferritin increases due to inflammation Anemia of chronic disease seen with inflammation Lack of movement of Fe from stores Decreases Fe availability for growth enhancement of pathogens? Important to differentiate anemia of chronic disease from deficiency anemias |
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Lab Tests for Macrocytic Anemia
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Static tests
Direct measure levels of B12 and folate Homocysteine Functional measure B12 and folate needed to convert homocysteine to methionine B6 needed to convert homocysteine to cysteine When these vitamins not available, homcys teine levels increase in the blood
Methylmalonic Acid (MMA) Urine levels increase when B12 unavailable as a coenzyme in metabolic pathway MM CoA to succinyl CoA More sensitive than static assay of B12 Schilling’s Test Determines if B12 deficiency is due to lack of intrinsic factor 1. Stores saturated (inject B12) 2. Radio-labeled B12 given orally 3. Test urine levels of B12 All radio-labeled B12 should show up in urine If no B12 in urine then there is lack of intrinsic factor for B12 absorption at the gut Rarely used today |
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Other Tests
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Malabsorption (discuss in GI)
Tests for CVD risk (discuss in CVD) Tests for Diabetes (discuss in DM) Oxidative Stress (discuss in CVD) |
