Clinical Nutrition Review Guide
Special Notes/Areas of Focus
Nutrition Overview and Basics – Reinhard
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Main differences between previous RDI and new DRI
o New focus is on preventing chronic disease and quantitative nutrient
intakes to reflect this – “optimal” intake of nutrients vs. “deficiency focus”
or merely “adequate”
o DRIs encompass both essential nutrients and other food components –
fiber, carotenoids, phytoestrogens, etc.
DRI categories
o Recommended Daily allowance (RDA) – meets needs of 95% of healthy
people within an age/gender group (EAR + “margin of safety”)
o Estimated Average Requirement (EAR) – meets needs of 50% population
within an age/gender group
o Adequate Intake (AI) – Similar to and RDA but signifies the “absence of
definitive data on which to base an RDA” (lower confidence)
o Tolerable Upper Intake Level (UL) – NOT a recommended level for
intake; the maximum level that is not likely to pose adverse health risks
for most healthy people
Problems with DSHEA
o Allowed health claims on food supplements without proof of effectiveness
of safety
 No specific disease claim can be made but structure/function
claims are allowed
o Shifted the burden of proof for efficacy and safety for dietary supplements
away from the manufacturer to the FDA
o DSHEA blurs the lines between what is a supplement, food additive food,
and drug – No clear definition of what is covered by DSHEA and what is
not
o Drugs are highly regulated while supplements are not
o DSHEA has no oversight and thus has enforcement issues
Main concerns related to food safety
o Nutrient content (nutrient loss/retention)
o Fortification, supplementation
o Pesticide residues, intentional food additives, unintentional contaminants
o Microbial contamination
More info:
o Carcinogens and contaminants have long-term effects
o Microbes and contaminants have short-term effects
o Mad Cow (BSE) – prion or misfolded protein in mammalian brain tissue
deforms into amyloid protein and induces abnormality on other proteins
 Scrapie in sheep, BSE in cows, Creutzfeld-Jakob in humans
 Only 1 in 106 exposed will experience symptoms
 FDA declared BSE is not a threat but is worth monitoring
o Food-borne illness (FBI) causes 5,700 deaths/year, often mistaken for flu
 Eating out increases the risk of FBI
 Cross-contamination in preparation increases risks
 CDC reports over 250 types of FBI
 Bacteria, parasitic protozoa and worms, viruses, natural toxins,
Mad Cow Disease (not pathogen)
 USDA is lead agency for preventing FBI, but FDA plays role
 HACCP gives control points for food, all food service operations
need to have them
o Unintentional additives – Environmental contaminants and pesticide
residues
o Intentional food additives – approved, regulated by FDA, periodically
reviewed
 Delaney clause: risk from 0 risk to negligible is acceptable
Blackboard stuff (mostly redundant)
o RDA used to be the only nutrient standard for most of the essential nutrients. It
did not include compounds that may have been essential, but that we get too
much of (e.g., fat, salt) and others which were not essential but needed to be
considered for health (carbohydrate, sugar, fiber).
o The US RDA was what was used on food labels to show essential nutrients
levels, and it was based on the 1968 RDAs. When the NLEA was passed in
1992-93, the food label was changed to what we currently have (Nutrition Facts).
They continued to use the US RDA for essential nutrients (vitamins, minerals,
protein) and called this RDIs. They added those other nutrients and compounds
that were not included in the past (fat, sugar, salt, fiber) and called this DRVs.
Together, the RDIs and DRVs make up the DVs (Daily Values), which includes
essentials and nonessentials and that's what you see on the label.
o When the RDAs were last updated, it was changed into the DRIs (Dietary
Reference Intakes), and it established new categories that should still be referred
to collectively as DRIs, but here's the breakdown:  RDA: this is a recommended level of intake for a specific nutrient, which
covers 95% of the healthy population and has very good science behind
it
 AI (adequate intake): this is a recommended level of intake for a specific
nutrient, which covers 95% of health population, but the data behind it is
less certain than that for a nutrient with an RDA (calcium is an example
of a nutrient with an AI vs an RDA)
 Tolerable Upper Limit: this is NOT a recommended level for a nutrient,
but a level at which no assurance can be made, that when exceeded, it
won't cause harm. This is a new category to reflect that many people take
supplements at high doses, which may be harmful.
Nutritional Assessment – Width
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Calculate IBW using Hamwi
o Females: 100 lb for 5 feet, add 5 lb for each inch over 5 feet
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o Males: 106 lb for 5 feet, add 6 lb for each inch over 5 feet
o % IBW = (current wt)/IBW X 100
o BMI = wt (kg) / ht (m)2
How to adjust IBW for amputation
o (100 - % amputation)/100 X IBW for original ht
Discuss assessment parameters for visceral protein status (pre-albumin,
albumin, transferring)
o Albumin has half-life 14-20 days. Assessment is good indicator of longterm PRO status, is most widely used, correlates well with patient
outcomes and loss, is not a good indicator of recent changes in PRO status
o Pre-albumin has half-life of 48 hours, is a highly sensitive marker of
recent nutrition status
o Transferring has half-life of 8-10 days, reflects PRO status well but is poor
marker for protein malnutrition in older adults, and is inversely related to
Fe status.
Definition of positive and negative acute phase proteins (APP)
o Positive APP are plasma proteins that increase in concentration in
response to inflammation
o Negative APP are plasma proteins that decrease in concentration in
response to inflammation
Identify types of nutritional anemias
o Iron: hypochromic (light color), microcytic (small)
o B12: normochromic (normal color), macrocytic/megaloblastic (big)
o Folate: normochromic, macrocytic/megaloblastic
Discuss common drug-nutrient interactions (antibiotics, diuretics,
antineoplastics, corticosteroids, warfarin, MAOIs, problems with grapefruit
juice)
o Grapefruit compounds block hepatic enzymes that normally metabolize
drugs, enhancing drug interactions (Cyt450 enzymes), effect lasts for days
o Antibiotics: GI disturbances, diarrhea; dairy products (calcium) interferes
with tetracycline absorption
o Diuretics: Excess mineral excretion (potassium)
o Antineoplastics: taste changes/loss of appetite, GI disturbances, mouth
sores
o Corticosteroids: weight gain/appetite increase, glucose homeostasis
o Warfarin: requires constant vitamin K intake because it blocks Vitamin K
dependent coagulation enzymes
o MAOI: increase sensitivity to tyramine (a monoamine) and possibly
precipitate hypertensive crisis (HBP)
Pregnancy, Infants, Children and Adolescents –
Reinhard
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Importance of maternal weight (pre-pregnancy and during pregnancy)
o LBW for fetus is <5.5 lb, leads to 25% higher mortality and morbidity
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 Higher complications during delivery, higher health care cost
o Major determinants of infant birth weight are length of gestation, mother’s
pre-pregnant weight, and mother’s weight gain during pregnancy
Category
BMI
Wt. gain (lb)
Underweight
<19.8
27.5 - 39.6
Normal
19.8 - 25
25.3 - 35.2
Overweight
25 - 29
15.4 - 25.3
Obese
>29
>12.9
Twins
35-45
o Rate of weight gain is more important in trimesters 2-3
Risk factors for poor pregnancy outcome (high risk groups, weight gain, prepregnancy weight, gynecologic age, etc)
o Preconception Nutritional status (Vit B9)
o Underweight (BMI < 19.8)
o Nutrient intake during pregnancy
o Weight gain during pregnancy
o Age (gynecological)
o Race/ethnicity
o Adequacy prenatal care (timing, frequency)
o Chronic disease
o Poor Gyn. Hx
o Parity: # previous births, spacing
o Socioeconomic status (SES)
o Social supports
o Smoking; alcohol, drugs
Low Birth weight definition (differentiate between SGA and LBW, especially
relative to risk)
o Premature/pre-term, small for gestational age (SGA) – birth weight is
<10th percentile for the gestational age, higher risk with SGA vs.
premature
o Large for gestational age (LGA) – >9 lb, high risk for future gestational
diabetes
o Low birth weight (LBW) – weight < 5.5 lb or 2500 g
o LBW can describe a SGA (born at term, but below the norm for weight)
and a premature infant (who is not born at term, and can weigh more than
2.5).
 The higher risk is with the SGA, since the reason for lower weights
is most likely some type of gestational insult/deficit, versus some
other factor that caused early delivery
Consequences of alcohol intake during pregnancy
o Fetal Alcohol Syndrome (FAS) – congenital defect caused by alcohol
intake of ~3oz/day during pregnancy
 LBW; limb, face/head deformities, impaired physical and
cognitive development
o Leading cause of developmental defects
Breastfeeding benefits
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Emotional bonding
Jaw and tooth alignment
Microbial safety (sterile in breast but not after it leaves breast)
Nutrient content
Hormones (leptin, adiponectin, may protect against obesity later in life)
Antibacterial compounds (high in colostrum, lower rate of respiratory
infection)
o Antioxidant Defense System (ADS) – Preterm infants have immature
ADS, prone to oxidative stress; human milk enhances ADS to fight OH
radical
o Allergy Development – research is conflicting
o Cost (maybe)
Infant feeding recommendations (milk, solid food)
o Breastfeeding or Fe-fortified formula recommended, soy milk only if
allergic
o Special nutrients – Vitamins D, A and protein
o First solids: Iron fortified cereal started 4-6 months (still need breast milk
or formula through first year of life)
o 6 months to 1 year – breastfeed
o 3-4 months – formula feed
o No strict cut-offs, look for signs to introduce solid food: still hungry after
formula, can hold head steady, sit with support, can keep food in mouth
and swallow
o Start with rice cereal and mix with formula, eat from a spoon
o After 6 months – Strained vegetables and fruits, add foods singly and at
least 2 days apart (check for allergy)
 can add juice diluted with water in a cup (not bottle)
o After 8 months – Decrease milk/formula, can add crackers/biscuit,
strained meat, poultry, fish, tofu, cheese, hard boiled egg yolk, rice pasta,
potatoes, and mash potatoes
American Academy of Pediatrics recommendations for blood cholesterol
screening/interventions
o Screening
 Screen (>2 yrs) if they have family Hx of dyslipidemia or
premature CVD
 Screen (>2 yrs) if they don’t have family Hx but have risk factors
overweight, obesity, diabetes, cigarette smoking, hypertension
 If lipids normal, rescreen in 3-5 years
o Recommendations
 All children > 2yrs follow US dietary guidelines
 High risk groups 1-2 yrs should consume low fat milk
o Intervention: Nutrition counseling/diet change, exercise, weight
management, start early
 Goal is LDL<160mg/dL or 110 in high risk group
 Medication at 8 years if meet any 1 of below:
 LDL > 190 mg/dL
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 >160 with family Hx or early CHD
 >2 additional risk factors present
 >130 mg/dL if DM
Common feeding problems in young children
o Obesity, low calcium, eating disorders
Specific nutrient concerns for major age groups (infants; preschool age;
adolescents)
o Infants – breastfeeding, introduction to solid foods
o Preschool age – independence, innate taste preference, division of
responsibility between parent and child
 Iron-deficiency anemia, dental caries, ADHD, chronic diseases,
obesity and eating disorders, inactivity
o Adolescents – eating disorders, obesity, inactivity
National Center for Health Statistics (NCHS) BMI categories
o Overweight risk is 85th to <95th percentile
o Overweight is > 95th percentile
o Underweight is < 5th percentile
Aging and Obesity – Reinhard
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Nutrients of concern in the elderly
o Energy, fluid, protein, B vitamins, Ca, Vitamin D, Sodium, Fiber
Consequence of reduction in BMR
o Weight gain is common
Reasons for dehydration risk among elderly
o Weak thirst signal, other body compositional changes
o Medications (diuretics), dementia, constipation
Impact of chronic disease on nutritional status in the elderly
o Chronic disease causes arthritis, heart disease, strokes, hearing and vision
loss, nutritional deficiencies, oral-dental problems
o Need a therapeutic diet for chronic disease which are a risk because they
may decrease appetite, food intake
Health risks of obesity (specific chronic diseases and conditions)
o Type 2 diabetes
o CVD – MI and stroke, hypercholesterolemia, hypertension
o Gall bladder disease
o Some types of cancers
National Heart Lung and Blood Institute Obesity Guidelines (BMI and waist
circumference cutoff points)
o Overweight is BMI 25-29.9, obesity is BMI > 30, Normal BMI < 25
o BMI should be assessed in all adults; if normal, reassess in 2 yrs
o Also assess waist circumference (>40 inches in men and >35 inches in
women), and risk factors for CVD, DM
o Patients with BMI > 25 with 2 other risk factors should try weight loss
 If no risk factors, maintain weight and prevent further gain
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High risk groups for obesity
o Young African American females
o Young females, all groups
 Lesbians – 2X risks vs heterosexual women
o Lower SES
o Recent immigration status
o Age 5th decade
o College freshman and sophomores
Safe rate of weight loss
o Lose 0.5 to 1 lb per week
Bariatric surgery guidelines
o BMI between 35 - 39.9 with comorbidities
o BMI > 40 without comorbidities
o Full awareness of complications, lifelong dietary changes
NIH weight loss maintenance statistics
o Of those who lose 10% body wt, 66% regain all in 1 year, 95% regain all
in 3-5 years
Describe characteristics of the “Toxic Environment” theory for obesity
o The environment in today’s society is conducive to obesity because of the
availability and types of foods (fast food), larger portion sizes, and the
restrain/binge cycle
o Blackboard: According to Kelly Brownell, who posited the TE theory, our
environment contains readily available/yummy foods that are high in
energy and we are much less physically active than our even recent
generations. For many people this results in too much energy coming in
and not enough being expended, with weight gain the result.
Gastrointestinal Disease – Reinhard
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Nutritional side effects of common meds used for UGI disease
o Drug treatments for GERD can lead to possible malabsorption of Folic
Acid, Fe, Zn, Ca (nutrients that need acid to be absorbed)
Specific nutrient issues (B12, iron, etc.) associated with UGI and LGI
diseases and treatments
o Antacids
 Fe, Zn, Folic Acid aren’t absorbed
 Al OHs bind phosphorous
 Ca-containing can stimulate acid secretion; predisposition to renal
calculi
 Mg salts may produce cathartic effect
 Mineral-mineral interactions (Mg, Cr)
 Chronic use may cause neglect of serious problem, not seek
treatment
o Gastric surgery may adversely affect stomach functions:
 Reservoir for food (reduced capacity)
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 Mechanical breakdown of food
 Enzymatic breakdown (proteins)
 Chemical breakdown (HCl, PRO, minerals)
 Controlled release of food (transit time)
 Intrinsic factor/R-PRO, B12
Beneficial compounds/treatments and reasons for the benefit (medium chain
triglyceride, probiotics/prebiotics, etc.)
o Blind loop treatments
 Antibiotics eradicate bacteria
 Lactose free diet (lactose intolerance)
 Supplement with B12 (microbes consume the vitamin)
 Medium chain triglycerides (MCT)
 6-10 carbon FAs hydrolyzed from longer FAs
 Provide 8.3 kcal/gm; no EFAs provided
 Require no emulsification and minimal digestion
 May require surgical repair if severe
o Gut enhancers – compounds which accelerate intestinal adaptation and
growth
 Short chain fatty acids
 Amino acids: Glutamine, arginine, cysteine
 Growth hormones: Transforming growth factor B-2
 Probiotics and prebiotics
Identify factors other than HP infection that are related to gastritis and PUD
o Gastritis – inflammation of gastric mucosa
 Increased risk for ulcer and cancer
 Symptoms – nausea, vomiting, pain, anorexia, hemorrhage
 Causes – H. pylori, NSAIDS, xs EtOH, trauma, injury, surgery,
fever, burns, radiation therapy, renal failure, MI, TB
o Atrophic gastritis – atrophy of parietal cells; associated with aging
 Results in reduced gastric HCl, Iron deficiency anemia, B12
deficiency (intrinsic factor)
o Peptic Ulcer Disease (PUD) – circumscribed loss of mucosa adjacent to an
acid producing area
 2 types: gastric (stomach), duodenal
 Stress ulcers – surgery, trauma, shock, burns
 NSAID drugs, other Rx meds,
 EtOH
 Smoking, nicotine
 Diet? (fiber, caffeine, vit. A/C, PUFAs, cranberries,
fruits/vegetables)
 Stress?
 Genetics?
 Toothpicks
Differentiate between UGI and LGI diseases (symptoms, nutritional
problems)
o LGI disorders tend to be functional with problems involving:
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Motility (transit time)
Absorption
 SI: nutrients, bile salts
 LI: H2O, electrolytes, gases
 Secretion
 SI: enzymes, HCO3
 LI: mucous
o Common LGI problems – gas, diarrhea, constipation, irritable bowel
syndrome (IBS), Diverticular disease, Inflammatory bowel disease (IBD),
surgeries for LGI
o Symptoms from LGI disease can greatly affect nutritional status indirectly
o Problems in LGI not as likely to have as severe impact on nutritional
status as are those in the small intestine
Blackboard concerns:
List Sx and nutritional problems for GERD, hiatal hernia, gastritis/atrophic gastritis,
gastrectomy, Crohn’s Disease, ulcerative colitis, celiac disease, ileostomy
o GERD – chronic reflux or backflow of stomach contents into esophagus
when LES doesn’t close properly
o Symptoms: heartburn (simulates heart attack), pain, waterbrash
o Diet in Acute Esophagitis (inflamed, irritated):
 Avoid acidic foods (citrus fruits, tomatoes)
 Avoid spicy foods (red, black pepper)
 Follow a bland, soft diet
 Eat small frequent meals
o Diet to Prevent Reflux:
 Eat small frequent meals
 Avoid large meals, especially single high-fat meals
 at low-fat, higher protein meals
 Fried foods (independent of fat content) may delay GER
 Limit alcohol
 Avoid foods which lower LES pressure:
 Chocolate, coffee, mints, garlic*, onions*, cinnamon*
 Avoid drinking liquids with meals; drink between meals
 Weight loss for abdominal obesity
 * Individualize
o Hiatal Hernia: Outpouching of stomach through diaphragm
 Etiology: Congenital: Shortening of esophagus which occurs
during gestation; trauma; extreme physical exertion; pregnancy
 Diet approach: avoid acidic food; avoid spicy food, soft bland diet;
small frequent meals; low fat high protein; avoid alcohol; avoid
liquids with meal; lose weight
o Gastritis: inflammation of the gastric mucosa
 Treatment objectives: Antibiotic therapy, reduce gastric acidity,
eliminate irritating foods
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Therapy: NPO x 1-2 days, progress to liquids (to minimize GI
stimulation); bland diet (no caffeine, no coffee, no EtOH); antacids
 Increased risk for ulcers and cancer
 Symptoms: nausea, vomiting, pain, anorexia, hemorrhage
 Causes: H. pylori, NSAIDs, xs EtOH, Trauma, injury, surgery,
fever, burns, radiation therapy, renal failure, MI, TB
Atrophic Gastritis
 Atrophy of parietal cells; associated with aging
 Results in:
 reduced gastric HCl (achlorhydria)
 Iron deficiency anemia
 B-12 deficiency (intrinsic factor)
Gastrectomy: Postgastrectomy Diet
 Objectives: Control DS Symptoms and Hypoglycemia
 High PRO, mod. Fat, low CHO
 Avoid concentrated sweets
 Smaller, more frequent meals
 45 min. delay after eating for liquid intake
 Lie down after eating
 Avoid hypertonic liquids (pop, soup)
 Possible functional lactose intolerance
 Fe++ deficiency common
 Need B12supplement if total gastrectomy
Crohns: chronic disease involving lesions in the ileum and jejunum,
may affect colon
 Clinical presentation: mucosal and submucosal damage; bleeding
 Incidence: higher among jewish people; especially crohns
 Nutrition concerns: nutrient malabsorption (B12, fat, fat soluble
vitamins, Zn, protein, fluid, electrolytes); suboptimal intake of
folate, C, E, Ca; diet induced thermogenesis and altered lipid
oxidation
Ulcerative Collitis: chronic disorder where colonic mucosa is inflamed
 Clinical presentation: chronic bloody and mucus-containing
diahrea persisting into night; andominal pain, fever, anorexia,
weight loss
 Incidence: among jewish people
 Nutritional concerns: reduced food intake due to symptoms/ belief
food is harmful; increased secretion and nutrient loss (and blood
loss); increased nutrient need( infection, inflammation, intestinal
tissue turnover)
Celiac disease: gluten induced enteropathy: autoimmune disorder caused
by sensitivity of intestinal mucosal cells to gliadin (part of gluten protein)
 Symptoms: nutrient malabsorption, diarrhea, wt. loss, anemia,
edema, hypoalbuminemia, bone weakening due to low Ca, P, Mg,
vit. D
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Treatment: life long diet to avoid gluten/gliaden (wheat, oat, rye,
barely)
o Ileostomy: Surgical removal of the entire colon so the ileum is brought
out onto the surface of the skin
 Avoid problem foods
 Add B12, fat. sol. vit
 If no IC valve, diarrhea likely
 Reduce fluid (?)
 Prevent obstruction;
 Avoid small pieces, stringy foods
 Deodorizing pills useful w/ appliance in colostomy
 Skin care important (especially w/ ileostomy)
Blackboard: You should know that PPI and H2 receptor antagonists, and antacids for that
matter (but to a lesser degree) can cause problems in the absorption of folic acid, iron,
zinc, and calcium.
Any nutrient requiring an acidic environment for optimal absorption could
become compromised if acid production/secretion is reduced (as with antacids, PPI, H2R
antagonists). Minerals compete with each other for absorption, so antacids that contain
minerals could affect absorption of essential minerals. Those meds are also used in PUD,
since acid secretion is problematic.
Diabetes – Width
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Know functions of pancreatic and counter-regulatory hormones in glucose
homeostasis
o Insulin – lowers BG
o Amylin – lowers BG
o GLP-1 – lowers BG
o Glucagon – increases BG
o Epi-/Norepinephrine – increases BG
o Glucocorticoids (cortisol) – increase BG
o Growth Hormone – increases BG
Know definitions of honeymoon period, Somoygi effect and dawn
phenomenon
o Honeymoon period – period of time shortly after diagnosis during which
there is some restoration of insulin production by the pancreas, makes
controlling BG hard because can’t predict when pancreas does this, can
last up to a year
o Somoygi effect – rebound hyperglycemia, increases BG
o Dawn phenomenon – 2-4AM increase in BG causing hyperglycemia due
to increase in GH secretion during this time
Identify diagnostic criteria for pre-diabetes and diabetes using fasting
plasma glucose test
o Pre-diabetes is 110-125 mg/dL, diabetes is 126 mg/dL or higher
Know definitions for glycemic response, index, and load
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o GR: varying response of BGL and insulin to different types of CHOs
 Affected by preparation and cooking technique
o GI: Rise in BGL following ingestion of a food as a % of the rise that
follows a control food (glucose or white bread)
 High GI means increases BG quickly, low GI takes longer
o GL: Ranking system for CHO content in food portions based on GI and
portion size
Know how to calculate glycemic load
o GL = GI X CHO content (% wt)
Know the mechanisms of action of the oral glucose-lowering medications
o Insulin secretagogues – promote insulin secretion by β-cells
 Adverse effects: wt gain, potential hypoglycemia
o Insulin sensitizers – enhance insulin action, so require presence of
exogenous or endogenous insulin
 Adverse effects: GI distress, wt gain
o α-glucosidase inhibitors – inhibit enzymes that digest carbs in SI; delay
carb absorption and lower postprandial glycemia
o Dipeptidyl-peptidase 4 – prevents breakdown of GLP-1 (short ½ time)
 Increases insulin synthesis and release
 Decreases glucagon secretion
Know what insulin-to-carbohydrate ratio and Insulin sensitivity/correction
factor are and how a patient would use them to help control blood glucose
o Insulin-to-carbohydrate ratio – amount of insulin needed to “cover” a
specified number of CHO grams
 500 divided by Total Daily Dose (all basal plus bolus insulin)
o Insulin sensitivity/correction factor – determines how much 1 unit of
insulin will decrease blood glucose levels
 1800 divided by TDD
Know definitions and differences between DKA, HHS, and lactic acidosis
o Diabetic Ketoacidosis – consists of high BG, ketosis, low blood pH,
dehydration
 Occurs in infection, missed insulin, newly diagnosed or
undiagnosed T1DM, heart attack, stroke, trauma, surgery, stress
 Treatment is immediate administration of insulin, fluids,
electrolytes
o Hyperosmolar Hyperglycemic State – similar to DKA but no ketones
present, can occur in older people with T2DM
 Mortality is higher (older patients), same cause and Tx as DKA
o Lactic acidosis – Accumulation of lactic acid in blood
 Results in low pH in muscle and blood
 Occurs most commonly in tissue hypoxia
 Other causes: Impaired liver function, respiratory failure, CVD,
metformin use
 Sx: weakness, fatigue, SOB, GI distress, abdominal pain, muscle
pain
Know definition of carbohydrate counting
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o 1 CHO choice = 15 grams of CHO
o Person with diabetes has 15 CHO choices per day
Be able to calculate number of carbohydrate choices in a given meal
o Kcal X %CHO = kcals from CHO
o Kcals from CHO ÷ 4 kcals/g CHO = g CHO
o g of CHO ÷ 15 g/CC = # of CC
Know the rule for carb counting and fiber
o If a food contains > 5 g fiber, subtract ½ the fiber g from CHO to get total
CHO
Cardiovascular Disease – Reinhard
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Identify the major lipoproteins, apolipoproteins and subclasses and identify
the associated risk
o Lipoproteins
 Chylomicron – largest, lightest
 VLDL – very low density lipoprotein
 LDL – low density lipoprotein
 HDL – (smallest, most dense) high density lipoprotein
Particle
% PRO % TG
% Chol
% PL
Chylomicron
1 –2
90
2 –7
3 -6
VLDL
5 –10
65
10 –15
15-20
LDL
25
10
45
22
HDL
50
5
20
30
IDL
varies
>
>
>
(VLDLremnant)
o Apoproteins
LipoPro:
ApoPro:
Chylo
A-I
A-IV
VLDL
B-100
E
LDL Subclass
Phenotype A
Phenotype B
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IDL
B-100
E
LDL
B-100
High
risk
HDL
A-I
A-II
Low risk
Size
Large (low CVD risk)
Small (high CVD risk)
Identify the NCEP ATP III 2004 Update Guidelines for blood lipids and risk
status
Risk
Very High
High
Moderately
Moderate
Low
Level
High
Profile CHD + DM or, 2+ RFs CHD or
2+ RFs
2 RFs
0 to 1
(HTN, HDL< 40,
DM, or
RFs
Family HxCHD, male 2+ RFs
>44, female > 54)
LDL
Goal
mg/dl
HDL
< 100
Optional: <70
> 60
Low: <40
< 100
Optiona
l: <70
> 60
Low:
<40
< 130
< 130
< 160
> 60
Low: <40
> 60
Low: <40
> 60
Low: <40
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Identify HDL, LDL goal levels for risk categories (be able to determine an
individual’s risk status for males and females
TC / HDL = Risk Ratio
Risk Status
Males
Females
Above average
6.7 –14.0
5.6 –8.3
Average
4.0 –6.6
3.7 –5.6
Below average
2.7 –3.9
2.5 –3.6

Initial treatment recommendations for hypertension
o Assess level of hypertension and presence of other risk factors
 Treat lower risk with life style changes
 Drugs for higher risk and for those with no drop after trying
lifestyle changes
o Lifestyle changes – lose weight, limit salt/sodium intake, exercise, limit
alcohol, DASH (10 fruits/veg and 2.7 dairy)

Characterize major dietary fats as to
oil/monounsaturated, coconut oil/saturated, etc.)
saturation
(eg
canola
SFA PUFA

ALA
MUFA
NCEP ATP III and American Heart Association recommendations: general
population versus high risk groups, i.e. therapeutic Lifestyle Changes (TLC)
o Step Diet
 Step 1: <10% SFA, <300 mg cholesterol (ATP III general public
recommendation)
 Step 2: <7% SFA, <200mg cholesterol
o Prehypertension and stage 1 HTN in
 Low or medium risk group
 Begin with trial of life-style modification for 6 to 12 mo.
o Prehypertension and stage 1 HTN in
 High risk group
 Begin with drug therapy and lifestyle modification
o Stage 2 all risk groups
 Begin with drug therapy and lifestyle modification
o Therapeutic Lifestyle Changes Diet (TLC) 2006
 For high risk groups, while general public continues to follow
AHA Step 1
 High LDL, other dyslipidemias
 CHD or other CVD
 DM
 Insulin resistance
 Metabolic syndrome
Components of the TLC
LDL-raising Nutrients
Therapy for LDLlowering
Total Energy
Physical Activity
SFA:
< 7%
(+ low TFA)
Dietary Cholesterol:
< 200mg/d
Plant sterols:
Soluble fiber:
2g/d
10 –25g/d
Adjust total kcals to maintain desirable wt.; prevent wt.
gain
Include moderate exercise to expend at least 200 kcal/d
Diseases of the Kidney – Width

Describe the pathophysiology, major causes, and major nutrients affected by
Renal diseases (Nephrotic and Nephritis Syndrome, AKI, Renal stones,
CKD)
A. Nephritic Syndrome (aka acute glomerulonephrities)
-Clinical Manifestations of a group of diseases
-Characterized by inflammation of capillary loops of glomerulus
-rapid onset
-Primary manifestation hematuria
-Causes:
-Streptococcal infections (postinfectious)
-IgA nephropathy and hereditary nephrities
-SLE
-Vasculitis
-Can be fatal if dialysis isn’t started quickly
-only 50 % have symptoms
-Despite the diversity of diseases that cause acute nephritis, they share
common symptoms:
-hematuria (dark, tea-colored, or cloudy)
-decreased urine volume
-swelling: facial (periorbital), later progressing to legs and feet
-joint and muscle pain
-malaise
-headache
-blurred vision
-Medical Nutrition Therapy (MNT)
-restrict protein and potassium with uremia or hyperkalemia
-mild sodium and fluid restriction of HTN is present
B. Chronic Nephritic Syndrome (chronic glomerulonephritis)
-Slow, progressive destruction of glomeruli
-normal kidney function; often asymptomatic except for
proteinuria and hematuria
-Treatment
-control hypertension
-Na restriction
-K restriction
-protein restriction
-renal failure requires dialysis or transplantation
C. Nephrotic Sundrome
-Heterogeneous group of diseases
-due to loss of glomerular barrier to protein
- >3 grams/day protein can be excreted in urine
- 25 times normal amount
- NS may occur in various conditions:
-diabetes, lupus, and amyloidosis (95% of cases)
-glomerulonephritis
-toxic drugs, esp. NSAIDs
-minimal change disease (Nil disease)- most common cause in
children
-pathophysiology of Nephrotic syndrome:
-see flow chart of pg 492 of notes
-Nephrotic Syndrome – MNT
-Replace albumin and other proteins
-supply dietary protein to:
-maintain a pos. nitrogen balance
-produce an increase in plasma albumin concentration and
disappearance of edema
-Protein: .8 to 1 gm/kg/day
-energy intake: 35 kcal/kg/day
-Na restriction: 2-3 gm/day (with edema)
-low cholesterol/saturated fat diet (chronic NS)
-Potassium usually NOT restricted
D. Tubular and Interstitial Diseases
-Kidney tubules especially susceptible to injury due to their functions:
-secretion and reabsorption
-high local concentration of toxic drugs
-High-solute concentration
1. Acute Kidney Injury (AKI)
-Characterized by:
-sudden reduction in GFR, in healthy kidney
- dec ability to excrete metabolic waste production
-Causes classified into 3 categories:
1. Inadequate renal perfusion (prerenal) 60-70%
-blood loss, loss of large amounts of Na and fluid,
heart failure, shock, liver failure
2. Diseases within renal parenchyma (intrinsic) 25-40%
-toxic substances (drugs, radiopaque dyes, poisons),
allergic reactions (antibiotics), kidney damage d/t
prolonged lack of blood supply (IATN), nephron
disorders
3. Obstruction (postrenal) 5-10%
-enlarged prostrate, stones
-Acute dialysis quality initiative: Risk, Injury, Failure, Loss, Endstage kidney disease
-Symptoms (dependent of severity, progression, and cause):
-edema (face, hands, feet, ankles_
-cola-colored urine
-oliguria, anuria (or no urine reduction)
-later…fatigue, decreased mental concentration, anorexia,
nausea, pruritis, tachycardia
-with obstruction…crampy pain in flanks, severe pelvic
pain
-clinical course and recovery rate depend on underlying cause
(mortality rate has been steady at 50 % for past 25 years
-AKI-MNT
-Nutritional care is complicated and delicate due to:
-uremia
-metabolic acidosis
-fluid and electrolyte imbalance
-underlying stress causing increased need for
protein
-early attention to nutrition (often TPN) and dialysis have a
pos. impact on patient survival
-Protein:
-TPN recommended in early stages to reduce
protein breakdown (glucose, AA, and lipids)
-specialized AA solution available
-Protein intake must balance catabolic needs of pt.
with the inability to excrete fluid, electrolytes, and
solute load
-may need continuous renal replacement therapy
(CRRT)
-recommendations: 1.5-1.8 gm/kg/day for nonCRRT pts; 1.2-2.5 gm/kg/day for CRRT pts
-Energy
-30-35 kcals/kg
-increased carbs and fat will prevent the use of
protein for energy
-Fluid
-meticulous attention is essential in early AKI
-intake should balance body output and all sources
should be monitored closely
-not as much of an issue with CRRT
-Electrolytes
-Sodium is restricted in the oliguric phase to 20-40
mEq
-Potassium restricted to 30-50 mEq and is
controlled by dialysis and IV infusions of glucose,
insulin, and bicarb
2. Fanconi’s Syndrome
-Inability to resorb enough glucose, amino acids, phosphate, and
bicarb in the proximal tubule
-Children present with polyuria, growth retardation, rickets,
vomiting
-major cause is Cystinosis
-Main form of management is dietary treatment
-large volumes of water
-dietary supplements of bicarb, potassium, phosphate,
calcium, and vitD
E. Renal Stones
-Men are 3x likely than women to develop kidney stones (age 30-50)
-stones usually formed in renal pelvis
-extreme pain due to contraction of ureter
-can cause obstruction, infection
-medical management
-prevention
-shockwave lithotripsy
-stones are crystallizations of urine components, usually calcium, uric
acid, cystine, or struvite
-Calcium Stones
-Calcium oxalate (60%)
-calcium oxalate and calcium phosphate (10%)
-calcium phosphate (10%)
-Hypercalciuria
-30-40% of those with stones are hypercalciuric
->300 mg/day in men; >250 mg/day in women
-idiopathic hypercalciuria can result from:
-exaggerated dietary calcium intake (beyond DRIs)
-increased intestinal absorption of calcium
-decreased renal tubular reabsorption of calcium
-low serum phosphorous d/t a “renal leak”
-Uric Stones
-Associated with gout, malignant disease, and some GI diseases
characterized by diarrhea
-Treatment
-Large volumes of fluid
-Potassium citrate
-Alkaline-Ash diet??
-milk, nuts, vegetables, fruit
-Acid-ash foods to limit include: meat and highprotein foods, bacon, breads and cereals, starchy
desserts
-Cystinine Stones
-Caused by a hereditary disorder of AA transport
-treatment: high intake of fluid, alkaline-ash diet may be helpful
-Struvite Stones
-No significant dietary intervention
-more common in women and form only in presence of bacteria
F. Chronic Kidney Disease
-slow, steady decline in renal function
-renal failure vs. benign course
-loss of ¾ kidney function
-kidney goes thru series of adaptations in response to a decrease in
GFG
-factors that increase glomerular pressure tend to accelerate this
process
-stages in renal function can be considered on a continuum
(impairment to failure)
-Renal Insufficiency: kidneys can’t meet extra demands of diet or
stress
-Renal failure: normal demands of the body can’t be met
-Definition of CKD
-Kidney damage for 3 or more months, with or without
decreased kidney function
-damage defined as pathologic abnormalities or
markers of damage, including abnormalities in
blood, urine test or on diagnostic imaging studies
-decreased kidney function measured by GFR<60
ml/min/1.73 m2 for 3 or more months, with or without
kidney damage
--26 million Americans affected.
-high risk groups: those with diabetes, HTN, family history
of kidney disease, African Americans, Pacifica Islanders,
Native Americans, Hispanics
-obesity and kidney disease
-Do not order “renal diet” for those with CKD
-Nutrient recommendations should be individualized
-70 gm protein, 2 gm sodium, 2 gm potassium


Know the principle nitrogenous waste products that accumulate in blood due
to kidney dysfunction
A. Blood Urea Nitrogen
-Nitrogenous waste product of protein metabolism (endogenous and exog)
-Gross index of glomerular function
-Correlates directly with protein intake, catabolism; also affected in other
situations:
-elevated: dehydration, GI bleeding, shock, CHF, steroids, burns,
fever, stress
-Decreased: liver disease, malnutrition, overhydration
7-20 mg/dl = normal
60-80 mg/dl = normal on dialysis
B. Creatine
-Waste product generated from muscle metabolism
-Not affected much by protein intake
-Most commonly used indicator of renal function, but not suitable for
detecting early stage disease
-Creatinine clearance (CrCl) is more useful
-uses creatinine’s urine concentration (Ucr), urine flow rate (V),
and plasma concentration (Pcr)
-estimating CrCl using Cockcroft and Gault equation:
= [(140-age)*mass(kg)*(.85 if female)]/72*serum
creatinine (in mg/dL)
Know the main dietary nutrients that need to be monitored in pre-dialysis
patients and major food sources of those nutrients (do not need to know
exact values of the recommendations)
Protein
-limited studies suggest that soy protein delays disease progression in the
early stages of CKD
-effect of chicken-based diet on renal function: chicken resulted in 36%
less urinary albumin (predictor of renal failure) compared to the low
protein
-Energy
-need adequate energy/kcals to spare PRO since it’s restricted
-renal diets tend to be high in fat and sugar which is a problem for ppl with
DM
-Sodium
-1000-3000 mg restriction, based on labs, BP, edema
-sodium restrictions
-no added salt (NAS)
-least restrictive
-no table salt and limit salt in cooking
-limit high-sodium smoke, cured, dried meats and cheeses;
condiments, salted snacks, canned and dried soups
-Potassium
-vital to restrict if needed, usually late in CKD
-hyperkalemia can cause cardiac arrest
-total grams allowed should be spread throughout the day, due to
rapids absorption
-Potassium level not affected by intake alone
-Dietary source of potassium
-fruits and veggies, grains, dairy products, meat
-Phosphorous
-difficult to control by diet alone, esp with dialysis
-food sources: dairy, whole grains, dried beans, peas, lentils, organ meats,
nuts and seeds, chocolate and caramels

Know pathophysiology of renal osteodystrophy and what nutrients are
involved
Renal Osteodystrophy
-Osteomalacia
-Osteitis fibrosa cystica
-as GFR increases, phosphorous is retained in plasma
-serum calcium declines for several reasons
-body secretes PTH and increases synthesis of the active vitD
-Dependence on the PTH mechanism leads to OFC
-Metastatic calcification
-serum calcium x serum phosphate
-calcium-phosphate product should remain <55 to prevent
-nutrients involved: Calcium, phosphorous, VitD
 Know definition and symptoms of uremia
Uremia – high nitrogenous wastes that accompany renal failure
o -malaise, weakness, N&V, muscle cramps, itching, metallic taste in
mouth, confusion, stupor, anorexia, edema, anemia, bleeding
 Know the three major biochemical parameters that are used to diagnose
ESKD
ESKD - Results from a variety of different diseases (chronic DM, hypertension,
glomerulonephritis)
-Uremia (see above)
-BUN > 100; creatinine 10-12 are indicative
-GFR is usually <5 ml/minute
Nutrition Support – Sanna-Gouin

Know difference between short and long term enteral access devices
a. short term
i. Nasogastric (nose)
ii. Orogastric (mouth)
b. long term
i. gastrostomy
ii. jejunostomy




1. smaller lumen, needs good flushing
2. cant check residuals in a tube in the small bowel
Know the differences in peripheral and long term parenteral access
a. peripheral:
i. easily, nonsurgical personnel can do, minimal complications
ii. difficult to maintain more than 3-4 days
iii. peripheral veins sensitive to hypertonic solutions
iv. must limit dextrose and amino acid conc. to prevent thrombophlebitis
of peripheral veins
v. need to be augmented with lipids to limit vein irritation
b. long term (3 kinds)
i. surgical catheter – single, double, triple lumen
ii. implantable device- completely under skin accessed via special needle
iii. percutaneous catheter (non surgical)
Know Details of enteral formula administration methods
a. continuous
i. set hourly rate around clock via pump
ii. use for critically ill, initiating feedings, small bowel feedings,
inadequate tolerance for bolus feeding
iii. start at 20-50 mL/hr and increase incrementally q 4 hrs to goal
b. intermittent
i. via infusion pump or gravity flow
ii. non critically ill
iii. holding for breaks around medications an during the day for transition
to PO
iv. Home TF
v. Rehab
vi. Transitioning from EN to PO
c. bolus
i. via syringe or pump, gastric access devices only, for stable pt
ii. Home TF allows mobility, ADLs
iii. Rehabilitation pt – freedom from pump/gravity hookup for therapy
Know kcal/kg provided by parenteral dextrose and aa
d. aa solutions are hypertonic and prove 4 kcal/gm (4000 kcal/kg)
e. hydrous dextrose provides 3.4 kcal/g (3400 kcal/kg) ERROR IN NOTES
First day TPN admin recommendations
f. pt should receive ½ of goal kcals day 1
g. start time is 21:00
h. admin is over 24 hours unless TPN is cycled to spare liver in long term
i. if TPN d/c, cut to ½ current rate for 2 hours before to prevent hypoglycemia