Apllied Nutrition

8/2/2019 Apllied Nutrition

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METABOLISM

Presentors

Gee.Cherry.Sheena


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OUTLINE OF PRESENTATION

I. Normal Metabolism

II. Metabolismi. During Starvation

ii. Following an Injury

III. Nutrition in the Surgical Patients

III. Fluid and Electrolyte Management


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I. NORMAL METABOLISM

i. Metabolic Regulation

ii. Energy Metabolismiii. Carbohydrate Metabolism

iv. Lipid Metabolism

v. Protein Metabolism

II. METABOLISM DURING STARVATION

OUTLINE OF PRESENTATION


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NORMAL METABOLISM

METABOLISM

- Sum total of chemical reactions required for

cell function, an energy requiring process.

- [ANABOLISM] chemical processes by which livingorganism is produced and maintained

- [CATABOLISM] Transformation by which energy ismade available for the uses of organism


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NORMAL METABOLISM

SURVIVE


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ATP- MOST IMPORTANT storage for chemicalenergy in all cells.

Oxidative Phosphorylation - most importantpathway for the synthesis of ATP

Fermentation / Glycolysis - less efficient type of

ATP synthesis utilized in anaerobic conditions

NORMAL METABOLISM


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REGULATORY MECHANISMS

In order to adjust the synthesis and

degradation of metabolites to physiologicrequirements.

Mainly determined by the activities of theENZYMES involved.

Most METABOLIC PATHWAYS have KEYENZYMES

NORMAL METABOLISM


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REGULATORY MECHANISMS

The activity of KEY ENZYMES is regulated

at three independent levels:

1. Transcriptional Control

2. Interconversion

3. Modulation by Ligands

NORMAL METABOLISM


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GLYCOLYSIS- is a catabolic pathway in the cytoplasm that is

found in almost all organism- irrespective if theylive aerobically or anaerobically.

- In the anaerobic state, glycolysis is the only meansof obtaining ATP.

- This pathway involves 10 individual steps.

- NET OUTCOME: 2 moles of ATP are used

2 moles of ATP are formed/mole of glucose

CARBOHYDRATE

METABOLISM


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CARBOHYDRATE

METABOLISM

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GLYCOLYSIS BALANCE


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PENTOSE PHOSPHATE PATHWAY- or hexose monophosphate pathway

- Oxidative metabolic pathway located in thecytoplasm, wich starts from glucose 6-phosphate.

- It supplies two important precursors for anabolicpathways:

1. NADPH+H+2. Ribose 5-phosphate

CARBOHYDRATE

METABOLISM


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PPP: OXIDATIVE PART

CARBOHYDRATE

METABOLISM


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GLUCONEOGENESIS

- Takes place when reserves of glucose are alreadyexhausted

- Liver is mainly responsible, but tubular cells ofthe kidney also show a high level ofgluconeogenic acivity

- MAIN PRECURSORS: Amino acids & Lactate

CARBOHYDRATE

METABOLISM


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GLYCOGEN METABOLISM- Used as carbohydrate reserve, that can be

released as glucose phosphates and glucosewhen needed.

- Insoluble glycogen has only low osmotic activity.

- The human organism can store up to 450g ofglycogen, 1/3 in the liver and almost all of the

remaining in muscle.- HEPATIC GLYCOGEN: maintain blood glucose

level in the postresorptive phase.

MUSCLE GLYCOGEN: serves as energy reserve,not involved in blood glucose regulation

CARBOHYDRATE

METABOLISM


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REGULATION OF CARBOHYDRATEMETABOLISM:

- involves hormones, metabolites and coenzymes- HORMONES: Insulin, Glucagon, Cortisol,Epinephrine

- METABOLITES: High concentration of ATP andCitrate

- LIVER: central function in carbohydratemetabolism

CARBOHYDRATE

METABOLISM


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FATS (triacylglycerols) are the most importantenergy reserve

- mostly stored in insoluble form in the cells of adiposetissue - the adipocytes.

- Metabolism of fatty acids is particularly intensive in thehepatocytes in the liver.

- DEGRADATION: mitochondrial matrix of hepatocytesSYNTHESIS: mainly in the liver, adipocytes,Kidneys, lungs and mammary glands.

Occurs in the cytoplasm

FAT METABOLISM


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Quantitatively, proteins are the most important

group of endogenous macromolecules.

A persons nitrogen balance is primarilydetermined by protein metabolism.

Several hormones - mainly testosterone and

cortisol - regulate the nitrogen balance.

CHON METABOLISM


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METABOLISM DURINGFASTING

Fuel Metabolism During Unstressed

Fasting States

- standard to which metabolic alterationsfollowing acute injury and critical illness arecompared.

To maintain BASAL METABOLIC needs- NORMAL: 25 kcal/kg/day

- In severe states: 40 kcal/kg/day


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Fuel Metabolism During Unstressed

Fasting States


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In the healthy adult:- Principal sources of fuel during short-term fasting

(< 5 days) are derived from muscle protein and

body fat.- The greater glycogen stores within the muscle are

not readily available for systemic use due to adeficiency in Glucose 6-phosphatase.

- Therefore, HEPATIC GLYCOGEN stores arerapidly and and preferentially depleted ---> fall inserum glucose concentration within hours (16hours).



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Regulation of Gluconeogenesis


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Fuel Utilization in Long-Term

Fasting Man


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Lipid Metabolism

Lipid Absorption

Lipolysis and Fatty Oxidation

Ketogenesis

Carbohydrate Metabolism

Protein Metabolism


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Injuries or infections induce unique

neuroendocrine and immunologic

responses

The magnitude of metabolicexpenditure appears to be directly

proportional to the severity of insult


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Adipose stores within the body

(triglycerides) are the predominant energy

source (50 to 80%) during critical illnessand following injury

Fat mobilization (lipolysis) occurs mainlyin response to catecholamine stimulus of

the hormone-sensitive triglyceride lipase


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Increased lipolysis and reduced systemic

carbohydrate availability during

starvation diverts excess acetyl-CoAtoward hepatic ketogenesis

The rate of ketogenesis appears to be

inversely related to the severity of

injury


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oxidation of 1 g of carbohydrate yields 4

kcal

the primary goal for maintenance

glucose administration in surgical

patients serves to minimize muscle

wasting


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Injury and severe infections acutely induce a

state of peripheral glucose intolerance

Excessive glucose administration results in

elevated carbon dioxide production, which may

be deleterious in patients with suboptimal

pulmonary function

The increase in plasma glucose levels is

proportional to the severity of injury


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young adults ranges from 80 to 120 g/d

every 6 g of protein yields approximately

1 g of nitrogen

The degradation of 1 g of protein yields

approximately 4 kcal

Following injury the initial systemic

proteolysis, mediated primarily by


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Protein catabolism following injury

provides substrates for

gluconeogenesis and for the synthesisof acute phase proteins

The net changes in protein catabolism

and synthesis correspond to the severity

and duration of injury


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Estimating Energy Requirements

Vitamins and Minerals

Overfeeding

Enteral Nutrition

Parenteral NutritionSpecial Formulations

Glutamine and Arginine

Omega-3 Fatty Acids


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The goal of nutritional support in the

surgical patient is to

prevent or reverse the catabolic

effects of disease or injury


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Rationale

Enteral Formula

Low Residue Isotonic

Isotonic formula with fiber

Immune-enhancing

Calorie-dense

High-protein

Elemental

Renal-failure

Pulmonary-faliure

Hepatic-failure


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Rationale

Indications

Contraindications

Total Parenteral

Peripheral


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Fluids and Electrolyte

Management ofSurgical Patients


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Total Body Water = 60% of total body weight


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Daily water requirement: 2000 2500ml Rule of thumb: 30 ml / kg BW / 24 hours

Daily Water and Salt Losses: INSENSIBLE

600 1000 ml / day

mainly from the skin (perspiration) and lungs(respiration)

SENSIBLE 1000 1500 ml / day

mainly from urine (1L) and feces (250 ml)


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Sodium: 1-2 mEq/kg/d

Potassium: 0.5-1 mEq/kg/d

Calcium: 800 - 1200 mg/d

Magnesium: 300 - 400 mg/d

Phosphorus: 800 - 1200 mg/d Rule of thumb

K and Na/ 24 hrs = 1 meq/kg BW

60-70 meq/ day for each


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VOLUME CHANGES Water or isotonic salt solution gained or loss Water deficit or water excess

CONCENTRATION CHANGES Changes in the concentration of osmotically active

particles Mainly involved sodium with accompanying changes in

osmolality

Hypernatremia or hyponatremia COMPOSITIONAL CHANGES

Acid-base disorders and changes in the concentration ofall other ions in the ECF compartment (eg. potassium,calcium and magnessium)

Acidosis or alkalosis depending on etiology andaccompanying electrolyte changes


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Volume Replacement

Crystalloid

Colloidal solutions (starch containing solutions)

Blood


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Volume replacement and restoration Specific electrolyte replacement

Preoperative Fluid Therapy


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Preoperative Fluid TherapyMaintenance

first 0 10 kg --- 100 ml/kg/day

Next 10 20 kg --- 50 ml/ kg/day>20 kg --- 20 ml/kg /day

+ volume deficit isotonic crystalloid+ symptomatic electrolyte abnormalities w/

volume deficit abnormality should be correctedto the extent that the acute symptom is relievedprior to surgical intervention

Intraoperative Fluid Therapy


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Intraoperative Fluid Therapy the induction of anesthesia, compensatory

mechanisms are lost and hypotension will developdeficits are not appropriately corrected prior tosurgery

Postoperative Fluid TherapyBased on the patients current estimated volume

status and projected ongoing fluid loses.

Preexisting deficits and 3rd space losses shouldbe included in the maintenance.

Initial fluids should be isotonic and then can bechanged to 0.45 % saline with added dextroseafter the initial 24-48 hr.

IV potassium


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PULSE 100 - 120 bpm

URINARY OUTPUT

CHILDREN = 1.0 ml/kg/hr ADULT = 0.5 ml/kg/hr

Clearance of lactate

Resolution of base deficit

BLOOD PRESSURE POOR INDICATOR


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Water restriction (1500 ml/ day)

Diuretics

Sodium restrictions

Albumin infusion

Supportive care cadiac pulmonary, renal


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Changes in the concentration of

osmotically active particles in the body

fluid compartments.

Mainly changes in sodium ion

concentration in the ECF.

Hypernatremia or Hyponatremia


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Treatment of the associative water deficit In hypovolemic patients, volume should be restore

with normal saline.Once adequate volume status has been achieved,

the water deficit is replaced using hypotonic fluid. Water deficit (L) = serum Na 140/ 140 x TBW

Estimate TBW as 50% of lean body mass in men and 40%in women

acute hypernatremia The rate of fluid administered should be titrated to achieve

decrease in serum Na of no more than 1 mEq/ h and 12mEq/L for

Chronic Slower 0.7 mEq/L/ hr


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Symptomatic occur when serum Na level is < /= 120 mEq/ L w/ neurologic symptoms

3% normal saline to increase the Na by no more than 1 mEq/ L /h until the serum sodium level reaches 130 mEq/ L / h

Correction of asymptomatic hyponatremia should increasethe sodium level by no more than 0.5 mEq/ L to a maximumof 12 mEq/ L / day

Rapid correction Pontine myelinolysis Seizures

Weakness, paresis Akinetic movements Unresponsiveness Permanent brain damage


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Acid- Base Balance

Specific electrolyte changes

Potassium

Ca

Phosphorus

Magnesium


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Goal is to maintain pH between 7.35 7.45 fornormal metabolism / enzymatic activities


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ABG data Values

pH 7.35 7.45

pCO2 35 45 mmHg

pO2 80 100 mmHg

HCO3 22 26 mmHg

O2 saturation 90% and above

Venous O2 saturation 75%

Total CO2 24 29 mEq/L


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Management principles:

Treat the underlying cause giving rise to the acid-base problem

Examples: Sepsis metabolic acidosis

Ventilatory compromise respiratory acidosis

Administration of acid or base is rarely indicated


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K+ is the major ICF cation; the small

ECF conc.

Is critical for cardiac and neuromuscular

functions

Normal serum potassium = 3.5 5.5

mEq/

Hyperkalemia


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HyperkalemiaGoal

Reduce total body K

Shift K from extracellular to intracellularProtect cells from the effects of increase K

Discontinue all exogenous source of KKayexalate- binds K in exchange of Na

Measures should also include shifting Kintacellularly w/ glucose and bicarbonateCirculatory overload kayexalate & bicarbonateECG changes are present - give CaCl and Ca

gluconate (5-10 ml of 10% solution) to avoid

myocardial effectsShould be used cautiously in patients on digitalisDialysis may be considered


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Hypokalemia

Mild and asymptomaticOral repletion

IV repletion is required give no more than 10-20 mEq/ L/ h is advisable in unmonitored

setting40 mEq/L/h when accompaied by ECG monitoring

Higher if cardiac arrest is imminent from a malignantarrythmia


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Hypermagnesemia

Withhold exogenous source of magnesium

Correct volume deficit and acidosis if present .

Management of symptoms

Calcium chloride (5-10 ml) will antagonize the

cardiovascular effects.Dialysis

H i


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Hypomagnesemia

Oral or IV

Severe deficits (< 1.0 mEq/ L) or symptoms

Administer 1-2 g of magnesium sulfate IV over 15min or over 2 min if secodary to torsades de pointes

Simultaneous calcium gluconate willcounteract the adverse side effects of rapidlyrising magnesium level an correcthypocalcemia


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Calcium is essential for neuromuscular activitiesand as co-factors in various metabolic pathways

Normal serum calcium = 9 11 mg / dL

Hypercalcemia


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symptomatic hypercalcemia which usually occurs whenthe serum exceeds 12 mg/dl

Treatment is requiredThe initial treatment

Repleting volume deficits

Inducing diuresis with normal saline

Hypocalcemia

Symptomatic

10% of IV Ca gluconate until serum levels are 7-9mg/dl.

Chronic

Oral calcium (calcium lactate tabs) supplemental Vit D

Associated deficits in Mg, K and pH also must becorrected


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Magnessium ion needed in most

enzymatic systems and depletion may

lead to neuromuscular and CNShyperactivity


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Hypermagnesemia

Withhold exogenous source of magnesium

Correct volume deficit and acidosis if present .

Management of symptoms

Calcium chloride (5-10 ml) will antagonize the

cardiovascular effects.Dialysis

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Hypomagnesemia

Oral or IV

Severe deficits (< 1.0 mEq/ L) or symptoms

Administer 1-2 g of magnesium sulfate IV over 15min or over 2 min if secodary to torsades de pointes

Simultaneous calcium gluconate willcounteract the adverse side effects of rapidlyrising magnesium level an correcthypocalcemia


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Phosphate abnormalities

Hyperphosphatemia

phosphate binders (suralfate or aluminum

containing acids)Calcium acetate tablets

HypophosphatemiaOral and IV supplementation


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Syndrome of Inappropriate Secretion of

Antidiuretic hormone (SIADH)

Head injury or surgery of the CNSAlso seen with drugs (morphine, nsaids and

oxytocin), pulmonary, endocrine dses,

malignanciesCorrection of underlying dses.

Restriction of free water Furosemide

Diabetes Insipidus


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pDisorder of ADH stimulation and is manifested by

dilute urine in the face of hypernatremia

Central DIResults from a defect of in ADH secretion

Pituitary surgery or injury

Nephrogenic DI

Defect from end- organ responsiveness to ADH.

Hypokalemia, radiocontrast dye, and drugs such asaminoglycosides and amphothericin

Dx can be confirmed by increase in urine

osmolality in response to a period of waterdeprivation

Mild- free water replacement

Severe- vasopressin (5 units subq) can be

added.

Malnourished patients: Refeeding


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Malnourished patients: RefeedingSyndrome

Potentially lethal that can occur with rapid andexcessive feeding of patients with severeunderlying malnutrition With refeeding, a shiftin metabolism from fat to carbohydratestimulates insulin release, resulting n the

uptake of PO4, Mg, K, and Ca.Cardiac arrythmia, confusion, respi failure,

and even deathCaloric repletion should be instituted slowly

Acute Renal Failure


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Acute Renal Failure

Onset of renal failure correction of

underlying volume deficit is mandatoryATN restrict daily fluid intake

Oliguric RF requires close monitoring ofserum K

TX should be early and may include dialysis

Hyponatremia is common

Dialysis required

Hypocalcemia, hypermagnesemia andhyperphosphatemia

Metabolic acidosis

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