(Ebook) Clinical nutrition 2nd Edition by Marinos Elia ISBN 1118457757 9781118457757

(Ebook) Clinical nutrition 2nd Edition by Marinos Elia ISBN 1118457757 9781118457757

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ISBN 10: 1118457757 
ISBN 13: 9781118457757
Author: Marinos Elia

In this second edition of final text in the acclaimed Nutrition Society Textbook Series, Clinical Nutrition has been revised and updated to meet the needs of the contemporary student.

(Ebook) Clinical nutrition 2nd Table of contents:

1 Principles of Clinical Nutrition: Contrasting the Practice of Nutrition in Health and Disease
Key messages
1.1 Introduction
1.2 The spectrum of nutritional problems
Table 1.1 Physical and psychosocial effects of under-nutrition.
Figure 1.1 Effect of omitting potassium (K) and phosphate (P) from a parenteral nutrition regimen on the nitrogen (N) balance of depleted patients receiving hypercaloric feeding. Data from Rudman et al. (1975).
1.3 Nutritional requirements
Effect of disease and nutritional status
Fluid and electrolytes
Figure 1.2 Frequency distribution of nutrient requirements in health and disease.
Table 1.2 Electrolyte contents of some body secretions (mmol/l).
Table 1.3 Some problems caused by oedema.
Protein
Figure 1.3 Effect of increasing protein (N) intake on N balance in depleted, healthy, and catabolic patients close to energy balance.
Energy
Figure 1.4 Effect of acute disease severity (expressed as multiples of normal BMR) on total energy expenditure (shaded area). The difference between total energy expenditure and BMR is due to physical activity (and some thermogenesis, which typically accounts for ~10% of energy intake). The increase in BMR is counteracted by a decrease in physical activity. (a) Infection, persistent fever (1 °C); (b) infection, persistent fever (2 °C); (c) burns 10% (first month), single fracture (first week), postoperative (first 4 days); (d) burns 10–25% (first month), multiple long-bone fractures (first week); (e) severe sepsis/multiple trauma (patient on respirator); (f) burns 25–95% (first month).
Metabolic blocks and nutritional requirements
Inborn errors of metabolism
Acquired metabolic blocks
Figure 1.5 Metabolism of vitamin D in the liver and kidney. In renal failure, the formation of 1,25-dihydroxy vitamin D (1,25 (OH)2 D) in the kidney may be inadequate, in which case 1,25-dihydroxy vitamin D or 1-hydroxy vitamin D (25 (OH) D) can be prescribed.
Table 1.4 Some examples of nutritional pharmacology.
Effect of the route of feeding on nutrient requirements
Parenteral nutrition
Figure 1.6 Recommended doses of vitamins and trace elements for intravenous (IV) nutrition expressed as a percentage of the recommended nutrient intake (UK values). Those marked with an asterisk indicate nutrients for which there was inadequate information to establish a reference nutrient intake (RNI). For these nutrients, the midpoint of the estimated average oral intake is used for comparative purposes.
Gastric and jejunal feeding
Cutaneous (skin)
Subcutaneous
Rectal
Peritoneal
Effect of the phase of disease on nutritional requirements
Figure 1.7 Time frame for the management of a child with severe malnutrition (the 10-step approach recommended by the WHO (2000)).
Feeding schedules
Structure and function
1.4 Management pathways
Figure 1.8 Similarities in nutritional and general clinical management pathways and the interaction between the two. Based on Elia (2003).
1.5 Concluding remarks
References and further reading
2 Nutritional Screening and Assessment
Key messages
2.1 Introduction
2.2 Nutritional screening
Figure 2.1 A framework for screening-tool selection. Reprinted from Elia & Stratton (2012), © BioMed Central.
Figure 2.2 Subjective Global Assessment (SGA) Detsky AS et al. J Parenter Enteral Nutr (Vol. 11, No. 1) pp. 8–13, copyright © 1987 by SAGE Publications. Reprinted by permission of SAGE Publications.
Figure 2.3 Short-form Mini Nutritional Assessment (NMA) (Guigoz, 2006; Kaiser et al., 2009; Rubenstein et al., 2001; Vellas et al., 2006). ® Société des Produits Nestlé, S.A., Vevey, Switzerland; Trademark Owners © Nestlé, 1994, Revision 2009. N67200 12/99 10 M. For more information: www.mna-elderly.com.
Figure 2.4 ‘Malnutrition Universal Screening Tool’ (‘MUST’). The ‘Malnutrition Universal Screening Tool’ (‘MUST’) is adapted and reproduced here with the kind permission of BAPEN (British Association for Parenteral and Enteral Nutrition). For further information on ‘MUST’ see www.bapen.org.uk.
2.3 Nutritional assessment
Clinical history
Protein–energy malnutrition
Specific nutrient deficiencies
Dietary history
Table 2.1 Number of days necessary to obtain estimates of dietary intake within 10% of average intake in healthy people using weighed food intakes. Data from Bingham (1987).
Clinical examination
Protein–energy malnutrition
Specific nutrient deficiencies
Table 2.2 Clinical signs and nutritional causes.
Table 2.3 Some vitamin deficiencies and their manifestations.
Table 2.4 Trace-element deficiencies and their manifestations.
Box 2.1 Calculating the cross-sectional area of muscular and nonmuscular limb tissues
2.4 Concluding remarks
References and further reading
3 Water and Electrolytes
Key messages
3.1 Introduction
3.2 Fluid compartments of the body
Figure 3.1 The body water compartments. Figures are approximate percentages of body weight in the average individual.
Table 3.1 Electrolyte concentrations in body water compartments. ECF, extracellular fluid; ICF, intracellular fluid.
Figure 3.2 Diagrammatic model showing the effect of hydrostatic and oncotic pressure gradients on fluid movements across the capillary wall. P, hydrostatic pressure; Π, oncotic pressure; cap, capillary; int, interstitial.
Figure 3.3 Capillary permeability and albumin flux in (a) health and (b) critical illness. ISS, interstitial space; IVS, intravascular space.
3.3 Flux of fluid through the kidney and gastrointestinal tract
Figure 3.4 Flux of fluid across the gastrointestinal tract.
3.4 Body electrolyte content and concentration
Fluid shifts between ECF and ICF compartments
Figure 3.5 Diagrammatic model showing the effect of the osmotic pressure gradient on water movement across the cell membrane.
3.5 Regulation of body water compartments
Control of body fluid osmolality
Figure 3.6 Responses to changes in extracellular osmolality.
Control of effective circulatory volume
Table 3.2 Efferent signals as a response to changes in blood volume/pressure, and their actions on renal sodium excretion. ADH, antidiuretic hormone.
Thirst regulation and water balance
Thirst stimulated by plasma osmolarity and sodium concentration
Thirst stimulated by hypovolaemia
3.6 The metabolic response to starvation and injury
Starvation
Injury
3.7 Body water compartments and electrolytes in starvation and injury
Extracellular fluid
Intracellular fluid
Interstitial fluid
3.8 Effects of salt and water overload
Table 3.3 Properties of commonly prescribed crystalloids. From Queen’s Medical Centre, Nottingham, UK.
Gastrointestinal function
Renal function
Low serum albumin concentrations
Figure 3.7 Schematic representation of the two major hypotheses explaining distributional hypoalbuminaemia in acute illness.
3.9 Fluid therapy: practical aspects
Assessment
Box 3.1 Clinical features and consequences of salt and water depletion
Treatment
Resuscitation
Maintenance fluid
Fluid therapy for ongoing losses
Table 3.4 Approximate electrolyte content of gastrointestinal secretions.
3.10 Goal-directed fluid therapy
3.11 Implications of water and sodium metabolism in nutrition therapy for specific clinical conditions
Diarrhoeal illness
Congestive heart failure and cirrhosis
Stroke, dysphagia, and the elderly
3.12 Concluding remarks
References and further reading
4 Over-nutrition
Key messages
4.1 Introduction
Definitions and classification
Table 4.1 WHO classification of overweight and obesity in adults according to body mass index (BMI). © WHO (2000).
The scale of the problem
Figure 4.1 Increase in the prevalence of obesity in the UK since 1980 and the estimated figures for 2015–2050.
Economic impact and global burden
Table 4.2 Reported economic costs of obesity. Adapted from Caterson et al. (2004) © Informa Healthcare.
Table 4.3 Diseases used in studies of costs of obesity, and the relative risks (RR) utilised. From Caterson et al. (2004) © Informa Healthcare.
4.2 Aetiology
Figure 4.2 Schematic representation of the multifactorial factors influencing the development of obesity (GI: gastrointestinal).
The energy-balance equation
Energy intake
Table 4.4 Main influences affecting the human appetite system.
Table 4.5 Hormones, neurotransmitters, and peptides implicated in food intake control.
Energy expenditure
Figure 4.3 Major components of daily energy expenditure in humans (example for a 70 kg man).
Genetic factors
Figure 4.4 Obesity as a complex oligogenic disease.
Genetic epidemiology
Molecular epidemiology
Single gene-mutation mouse models
Table 4.6 Single-gene mutations of mouse models of obesity and their corresponding chromosomal regions in the human genome.
Functional candidate genes
Positional candidate genes
Table 4.7 Disorders with Mendelian inheritance in humans which have obesity as a clinical feature. NA, not available.
Table 4.8 Genomic regions with obesity quantitative trait loci (QTLs) found in at least two of the studies in Box 4.1.
Box 4.1 First relevant studies to perform genome-wide scans of obesity
Endocrine disorders
Endocrinopathies
Endocrine changes as a consequence of obesity
Table 4.9 Disturbances in the main hormonal axes in obesity. ACTH, adrenocorticotropic hormone; GH, growth hormone; GHBP, growth hormone-binding protein; IGFBP, insulin-like growth factor-binding protein; LH, luteinizing hormone; SHBG, sex hormone-binding globulin; PCOS, polycystic ovary syndrome.
Figure 4.5 Main endocrine changes associated with increased adiposity.
Environmental factors
Figure 4.6 Multifaceted influences and institutions in the UK impinging on the family and the individual with a potential impact on reversing the current obesogenic environment.
Psychosocial influences
Miscellaneous causes
Table 4.10 Drugs commonly associated with weight gain.
4.3 Clinical presentation
Table 4.11 Methods for the assessment of overweight and obesity.
Body composition
Table 4.12 Characteristics of body-fat estimation methods applied to obesity. DXA, dual-energy X-ray absorptiometry; BOD-POD, air-displacement plethysmography.
Fat distribution
Comorbidities
Figure 4.7 Main comorbidities associated with obesity.
Table 4.13 Association of systemic comorbidities with overweight and obesity. FRC, functional residual capacity; FVC, forced vital capacity; TLC, total lung capacity.
4.4 Clinical assessment
Figure 4.8 Algorithms developed to identify and manage overweight and obesity: (a) global screening for treatment selection; (b) initial steps for weight-loss therapy; (c) regular follow-up on treatment progress; (d) special considerations for instauration of pharmacotherapy.
4.5 Treatment approaches
General principles
Lifestyle changes
Dietary management
Physical activity
Pharmacotherapy
Bariatric surgery
Other options
Intragastric balloon
Gastric pacing
4.6 Prevention
Childhood obesity
Initiatives in key settings
Figure 4.9 Multidimensional approach to target the obesity epidemic.
4.7 Concluding remarks
Acknowledgements
References and further reading
Web sites of interest
5 Under-nutrition
Key messages
5.1 Introduction
Table 5.1 Some of the functional consequences of under-nutrition.
5.2 Pathophysiology of under-nutrition
Body composition
Energy metabolism
Figure 5.1 Components of total 24-hour energy expenditure.
Figure 5.2 Changes in body weight with negative energy balance in seven pairs of twins. Twin A on the ordinate, twin B on the abscissa. Reprinted from Bouchard et al. (1994), with permission of Nature Publishing Group.
Figure 5.3 Interaction between factors leading to lowered energy expenditure as a result of negative energy balance. BMR, basal metabolic rate.
Protein metabolism
Figure 5.4 Rate of change in nitrogen (N) excretion after changing from a high to a low protein intake. Data from Quevedo et al. (1994) © The Biochemical Society.
Figure 5.5 Relationship between N balance and energy intake. From Elwyn DH. Nutritional requirements of adult surgical patients. Crit Care Med 1980; 8: 9–20. Copyright © Wolters Kluwer Health.
Hormonal mediators
Immune function in under-nutrition
5.3 Pathophysiology of under-nutrition complicated by stress
Figure 5.6 Effect of infection and injury on weight loss. Souba WW & Wilmore DW. In: Modern Nutrition in Health and Disease, 9th ed (Shils M, Olson J, Shike M & Ross A, eds). Lippincott Williams & Wilkins, 1999.
Energy metabolism
Figure 5.7 The effect of disease and malnutrition on the basal metabolic rate (BMR). Modified from Elia (1991).
Protein metabolism
Hormonal mediators
5.4 Chronic under-nutrition
5.5 Under-nutrition in the elderly
5.6 Severe acute malnutrition in children
5.7 Assessment of under-nutrition
5.8 Treatment
Assessment of energy and protein requirements
Figure 5.8 Physical-activity levels (PALs). This factor is multiplied into the basal metabolic rate (BMR) to obtain total energy expenditure.
Table 5.2 Nonessential amino acids in maintenance functions of the body. Glu, glutamate; Asp, asparate; Gly, glycine; Cys, cysteine; Arg, arginine; Gln, glutamine. Modified from J Nutr (2000; 130: 1835S-1840S), American Society for Nutrition.
Table 5.3 Clinical manifestations of micronutrient deficiencies.
Requirements for other nutrients
5.9 Potential problems with nutritional supplementation in under-nutrition
Refeeding syndrome
Nutritional supplementation in chronic under-nutrition
5.10 Prevention
5.11 Concluding remarks
References and further reading
6 Metabolic Disorders
Key messages
6.1 Introduction
6.2 Energy intake, health and longevity
Figure 6.1 Putative mechanisms linking caloric intake with longevity.
6.3 The metabolic syndrome
Box 6.1 The metabolic syndrome: WHO criteria
6.4 Pathophysiology of insulin resistance
Figure 6.2 Insulin concentrations required to half-maximally affect various metabolic steps. This illustrates the differential insulin sensitivity of various tissues.
6.5 Insulin resistance
Box 6.2 Factors involved in insulin resistance
6.6 The role of affluence in diabetes, dyslipidaemia, and essential hypertension
Type 2 diabetes mellitus
Box 6.3 Pathogenesis of hyperglycaemia in type 2 diabetes
Insulin resistance and dyslipidaemia
Dietary management of the metabolic syndrome
Box 6.4 Dietary management of the metabolic syndrome
Insulin resistance and hypertension
Figure 6.3 Possible mechanisms linking insulin resistance with the metaboli

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