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NUTR 344 > final revision > Flashcards

final revision Flashcards

1
Q

Anthropometric Data: _th and __th percentile suggest nutritional risk

A

Anthropometric Data: <5th and >95th percentile suggest nutritional risk

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2
Q

How many times should anthropometric measurments be repeated?

A

3 times

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3
Q

Ways of height measurment

A

Standing
- using a stadiometer (barefoot, heels and shoulders touching the wall, Frankfurt plane)

Knee Height
- If unable to stand (equations by age, sex and race p.50, Nelms)

Arm span-> not recommended - unable to stand straight

  • not for Asians, African Americans, spinal deformities
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4
Q

BMI for Males and Non-Pregnant Female Adults <65 years old

A

<18.5- Underweight

18.5-24.9- Healthy

25-29.9- Overweight

30-34.9- Obesity - Grade I

35-39.9- Obesity - Grade II

>40- Extreme Obesity - Grade III

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5
Q

BMI: Males and Female Adults >65 years old

A

<24.0- May be associated with health problems in some elderly

24.0-29.0- Healthy weight for most elderly

>29.0- May be associated with health problems in some elderly

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6
Q

What does skinfold thickness indicate?

How should it be carried out?

A

Indicative of subcutaneous adipose tissue

Assumes that each site is representative of total body stores

Should ideally use multiple sites:

– Triceps - most commonly used but not fully representative

– Subscapular
– Biceps
– Suprailiac

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7
Q

Describe MAC

A
  • Reflects muscle, bone, subcutaneous fat
  • Not sensitive to changes in muscle
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8
Q

Describe MAMC

A
  • Corrects for subcutaneous fat
  • Insensitive to small changes in muscle
  • Must measure MAC and TSF
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9
Q

Describe MAMA

A
  • Reflects muscle and bone
  • More sensitive to changes in muscle than MAMC
  • More adequately reflects total body muscle mass
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10
Q

describe cMAMA

A
  • Reflects only muscle without the bone
  • Not valid in elderly or obese
  • Insensitive to small changes in muscle
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11
Q

Describe MAFA

A

Mid-upper arm fat area (MAFA)
- Reflects sub-cutaneaous adipose tissue stores

  • Better indicator of total body fat than a single skinfold measurement
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12
Q

What are below and above average cut-offs for MAMA and MAFA

A

15% below average

85% above average

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13
Q

Waist circumference cut-offs

A
  • >102 cm in men; >88 cm women
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14
Q

BMI and WC measures combined as indicators of CVD and type 2 DM

A
  • High BMI Low WC - Low risk
  • High BMI High WC - High risk
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15
Q

Limitation of DXA

A

– Expensive but increasingly accessible in research settings

– Minimal exposure to radiation
– Assumes normal hydration status

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16
Q

Half-lives of serum proteins

A
  • Albumin (most abundant) - 17-21 days
  • Transferrin- 8-10 days
  • Prealbumin or transthyretin (TTR) - 2-3 days
  • Retinol Binding Protein (RBP) - 10-12 hours
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17
Q

Albumin functions

A

Maintains osmotic pressure

Transport of large insoluble molecules, drugs, calcium, zinc

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18
Q

Transferrin function

A

iron transport

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19
Q

TTR function

A

Transport of T3 and T4

Carrier for RBP

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20
Q

RBP function

A

Retinol transport from liver to periphery

Circulates with TTR

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21
Q

Name negative acute phase proteins

A

levels decrease by >25% during inflammation, illness or metabolic stress

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22
Q

CRP cut-offs tractation

A

Used to detect mild or acute inflammation:

Normal <1, mild chronic 1-5, acute >5 mg/L

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23
Q

Albumin cut-off values

A

Normal: . 35 g/l

Deficit: <35g/L

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24
Q

How to calculate nitrogen balance?

Example: Pt intake of 62.5 g protein/day and excretion of 200 mmol/L UUN in 2.0 L of urine

A

N Balance (g/day) = (pro intake g/6.25) - (UUN g + 4)]

  • Total 24-h UUN (mmol) = (UUN mmol/L)(24h-urine volume L)
  • Conversion factor: 1 mmol UUN = 0.028 g UUN

UUN (g) = (200 mmol/L x 0.028) x 2 L = 11.2 g

N balance = 62.5/6.25 - (11.2 + 4) = - 5.2 g

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25
Q

When would creatine excretion increase? Decrease?

A
  • Increase with exercise, meat intake, menstruation, infection, fever, trauma
  • Decrease with renal failure and age
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26
Q

Limitations of Creatinine Height Index

A
  • Rely on complete 24h urine collections: errors
  • Meat-free diet prior to testing
  • not sensitive
  • not possible to detect small changes
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27
Q

Laboratory Tests for Anemia: General

When woudl this marjers be increased/decreased?

What are the cut-off values?

A
  • Hemoglobin (g/L, deficit <120 women; <140 men)
    • Total amount in RBC
    • Decresed during PEM, hemorrhage and other anemias
  • Hematocrit (%, deficit <37 women; <40 men)
    • % of RBC in total blood volume
    • Increased during dehydration
    • Decreased during hemorrhage and water overload
  • RBC count
  • Mean Corpuscular Volume (MCV)
    • Size measure to differentiate between micro and macrocytic
  • Mean Corpuscular Hemoglobin (MCH)
    • Indicator of colour
  • Hematocrit
    • MCHC = Hb/Hct
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28
Q

What is the order of depletion during iron deficiency and the associated markers

A

1) Storage iron (ferritin)
2) Iron transport (Transferrin)
3) Essential iron (RBC, myoglobin, enzymes)

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29
Q

Laboratory Tests for Anemia: Iron Deficiency

When would each of these markers be affected? What does that mean?

A
  • Serum Ferritin
    • Low in early deficiency state
    • Depleted iron stores
  • Serum Iron
    • ​Low in early deficiency state
    • Reflects iron bound to transferrin
  • Total Iron Binding Capacity, TIBC
    • Measures the saturation ability for transferrin, high in deficiency
  • Transferrin Saturation
    • Progressively decreases with diminished transport iron
  • Erythrocyte Protoporphyrin
    • Increases in later deficiency state with limited Hb production
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30
Q

Graphs of how iron deficiency anemia markers change as anemia progresses

A
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31
Q

Components of TEE

A

TEF (<10%)

Physical Activity (20-30%)

REE or BMR (65-70%)

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32
Q

Protein requirements for healthy adults and elderly

A

Healthy adults: 1.0 g/kg/day Elderly adults: 1.0-1.2 g/kg/day

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33
Q

Considerations for the Elderly

A
  • Energy- Reduced due to reduced LBM and activity = low appetite
  • Protein- 1-1.2 g/kg/day, may be higher if other conditions present
  • Fat- Careful evaluation of balancing: too high vs too low
  • Calcium- Decreased Ca absorption with age (DRI=1200 mg >50 y)
  • Vitamin D- Less efficient synthesis by skin, kidney conversion, and exposure
  • Fluids- Decreased sense of thirst, presence of other diseases
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34
Q

How to differentiate types of malnutrition

A

10-40 is mild inflammation

40-100 is moderate inflammation

100-200 is marked inflammation

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35
Q

Obesity defintion

A

Progressive chronic disease characterized by excess or abnormal body fat that can impair health

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36
Q

Risk of health problems when analyzing BMI and waist circumference

A
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37
Q

BMI and waist guidelines for non-whites

A

• Asian populations
BMI: overweight ≥23, obesity ≥27 kg/m2

Waist (↑ risk): ≥90 cm in men, ≥ 80 cm in women

• African-american, hispanic, native Americans: same as for Caucasians

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38
Q

Health consequences of obesity

A

Cancer

Breathing problems: sleep apnea and asthma

Arthritis

Hepatobiliary disorders

Reproductive and obstetrical complications

Surgical risk and complications

Psychosocial and emotional consequences

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39
Q

How are BMI and all cause mortality connected?

A
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40
Q

Obesity and risk of cancer in men and women

A

Obesity increases cancer risk

Women: Endometrium, Ovary, Cervix, Breast (postmenopausal)

Men: Prostate, Pancreas, Oesophagus

Women & Men: colon, gallbladder, kidney, liver

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41
Q

Obesity and hepatobiliary disorders

A

Obesity ↑ risk of gallstones (cholelithiasis)
– More related to abdominal obesity, more in women than men

– Risk is also increased with rapid weight loss

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42
Q

Obesity and liver health

A

Abdominal obesity ↑ risk of non-alcoholic fatty liver disease (NAFLD)

– Steatosis-> steatohepatitis-> cirrhosis-> liver failure

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43
Q

Obesity and reproductive disorders in

A

• Men:
– Reduced testoterone, increased estrogens levels

– Gynecomastia

• Women:
– Polycystic ovary syndrome (PCOS) in 5-10% of women: -> irregular cycles, acne, excess body hair, infertility

– During pregnancy: ↑ risk gestational diabetes, preeclampsia (high blood pressure), labor and deliveries complications, fetal and maternal death.

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44
Q

Central regulation of food intake

A

central regulation of food intake takes place in hypothalamus, in arcuate nucleus where there are 2 main pathways of opposing functions:
has 2 pathways of opposing functions
1) NPY- with AgRP stimulates appetite
2) POMC neurones decrease appetite
the balance between the 2 dictates the regulation of appetite

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45
Q

Peripheral regulation of food intake

A

peripheral system will also regulate appetite
1) vagus nerve- lines our GI tract
distention of the stomach will signal to our brain that we ate
drinking water can thus decrease appetite -. causes distention
2) peripheral hormones and peptides will also signal the brain - stimulate or inhibit appetite

46
Q

Low. moderate and high activity levels

A

Low- 1.3

Moderate- 1.5

High- ``1.8

47
Q

What are METs?

A

• Metabolic equivalent task: energy cost of physical activities

  • 1 MET = 3.5 mL O2 uptake/kg BW/minute
  • 1 MET= 1 kcal/kgBW/hour (sitting or lying quietly)
48
Q

Which organs make up most of REE?

A

Liver-21%

Brain- 20%

Skeletal muslce- 22%

49
Q

How would lactate and pyruvta levels chnage in response to a meal?

A

they woudl increase as these are glycolysis intermediates and glycolysis increases after a meal

50
Q

What are the organs that will always be using some glucose, no matter what the time

A

Brain at a diminished rate RBCs, renal medulla

51
Q

How are ketoacids excreted?

A

via lungs (acetone) and kidneys

52
Q

Implications of ketone excretion?

A

§ When ketones are excreted via kidneys they must be “salted” out which involves the loss of either Na, K, H, or NH4
§ Ideally NH4 is excreted because it is a waste product
§ BUT K is the preferred ion to be excreted hypokalemia

53
Q

How do Urinary Nitrogen Constituents change in starvation

A

Less is excreted

Ammonia makes up a much bigger poriton, urea makes up a much smaller portion

54
Q

Physiological Changes to Severe Weight Loss: CV, renal and immune

A

Cardiovascular and Renal
• Decreased cardiac output, heart rate, BP
• Increased tachycardia (compensatory mechanism)

• Decreased stress on kidney (acid/base balance)

Immune Function
• Decreased T-cell function/lymphocytes

• Decreased cytokines

55
Q

Physiological Changes to Severe Weight Loss: GI, electrolytes

A

Gastrointestinal Function
• Decreased Lipid absorption – steatorrhea
• Decreased Gastric, pancreatic and bile secretion/production

• Decreased Villous surface area

Electrolytes
• Potassium losses (LBM and intracellular losses)

56
Q

Causes of refeeding syndrome

A
  • shift back to glucose as the main fuel
  • Rapid fluxes of insulin due to CHO load
  • Rapid shift of electrolytes and intracellular anions and cations to intracellular space (PO4, K, Mg)
  • Sodium and water retention
57
Q

Physiological changes during repletion in the refeeding syndrome

A

ECF expansion

  • Edema from increased Na intake and electrolyte imbalance

Glycogen synthesis

  • May lower serum PO4 and K concentration

Increased REE

  • Due to reversal of starvation and LBM rebuilding

Increased insulin secretion from CHO intake

  • Fed signal is now present and uptake into cells resumes
  • Stimulates N retention
  • Stimulates cell synthesis, growth, and rehydration
58
Q

Physiological changes after diet-induced weight loss that lead to increased energy storage and food intake

A

Energy storage:

  • Decreased energy expenditure
  • Decreased fat oxidation
  • Decreased thyroid hormones
  • Increased cortisol

Food intake:

  • Decreased leptin
  • Decreased PYY
  • Decreased amylin
  • Decreased insulin
  • Increased ghrelin, appetite
  • altered neural activation
59
Q

What are the effects of weight loss that improve diabetis control

A

Increased Glucose tolerance
Increased Insulin sensitivity
Decreased Need for glucose lowering medications

60
Q

Cardiovascular benefits of weight loss

A

Normalizes triglyceridelevels

Raises HDL cholesterol

Lowers LDL cholesterol

Improves CHD risk profile

Reduces need for antihyperlipidemic medication

61
Q

Benefits of weight loss on hypertension

A

Decreased Systolic blood pressure

Decreased Blood volume
Decreased Cardiac output

Decreased Sympathetic activity

Decreased Need for antihypertensive medication

62
Q

0.5 kg of fat =__ kcal

A

0.5 kg of fat =3500 kcal

63
Q

What is the best diet for maintenance

A

High protein, low GI

64
Q

Medications after a heart attack could include…

A
  • Antiplatelet agents – to prevent blood clots and keep a stent open.
  • Example: aspirin.
  • Statins – to lower cholesterol levels.
  • Beta blockers, ACE inhibitors – to treat high blood pressure
  • Nitrates – to expand the arteries and relieve chest pain. • nitroglycerin
  • Anticoagulants – to reduce the blood’s ability to clot. • Warfarin (Coumadin)
  • Medications to protect the stomach (stress + aspirin)
  • Examples: cimetidine (Tagamet), famotidine (Pepcid) and ranitidine (Zantac), or proton pump inhibitors such as pantoprazole (Pantoloc).
65
Q

Guidelines for high TGs

A

• Limit or avoid sugar, sweets, sweetened beverages

  • Avoid alcohol
  • Achieve healthy weight
  • Follow other heart healthy guidelines
66
Q

Test do determine Left-sided Heart Failure

A

Left ventricular ejection fraction (LVEF or EF) = measurement of how much blood is being pumped out of the left ventricle of the heart

67
Q

• Why does the heart enlarge in HF?

A

Less effective pump, has to pump more

Less blood flow

Kidney tries to compensate: renin + aldosterone cause vasoconstriction and try to increase blood volume

Heart has to work harder, vicious circle

With time, gets worse

68
Q

Nutritional Management in HF

A

• Sodium:2,000mg/day • Fluid:1–2L/day

  • Fluid restrictions
  • 1to2LperdayformildCHF
  • 1 to 1.5 L per day for more severe CHF or more severe hyponatremia (< 130

mmol/l Na+ in blood test)

• Texture and timing of foods should be adjusted to allow adequate energy intake without discomfort

  • Limit alcohol intake to one drink per day
  • In patients in whom alcohol is believed to be a causative factor in the heart failure, abstinence from alcohol is mandatory

EstimatedEnergyrequirement:Calculationistypicallyforcomparison purposes (to compare to intake). If edema present and low activity, then 25 kcal/kg actual weight could give a rough initial estimate. Use judgement.

Protein: 1.1 – 1.4 g/kg actual body weight as a target for comparison purposes. If edema is increasing weight, then use lower end of range. Use judgement.

Severityofdisease:Inmoreadvancedheartfailure,typicallywewantto prevent further weight loss and optimize protein and kcalorie intake since there is high risk of malnutrition and poorer prognosis with malnutrition.

69
Q

Global lifestyle modification approach to reduce CVD risk

A

weigth loss

physical activty

– Volume/intensity of exercise has greatest benefits (kcal spent)

– Resistance exercise has little effect

70
Q

What type of dietary fat has the highest effect ob blood cholesterol levels

A

saturated fat

71
Q

effect of dietary cholesterol on serum lipids

A

LDL receptor is mainly affected
Changes:
- Increased conversion of VLDL remnant to LDL

– Decreased synthesis and activity of hepatic LDL receptors

– Increased cholesterol in chylo and chylo remnantsàmore atherogenic and increased chol delivery to liver

– Increased cholesterol in VLDL and VLDL remnantsàmore atherogenic

– Interferes with ability of HDL to clear cholesterol

72
Q

What is the effect of very-low fat deit

A

may decrease HDL-c

73
Q

Effects of diets rich in SFA

A

• Reduce activity of LDL receptors by:

– Decreasing transcription of LDL receptor gene including gene transription of LDL receptor

– Altering PL composition of cell membranes to decrease binding -> decreased LDL clearign from concentration

– Altering LDL itself and delays binding to receptors

74
Q

Goal and recommendatons for intake for SFA

A

eat less than 10% of total calories

Replacing SFA with MUFAs and PUFAs -> improved lipid profile and reduced CVD risk

Replacing SFA with carbohydratesàno benefit on CVD risk

Recommendations: no limit on saturated fats, instead focus on healthy balanced diet

75
Q

Effects of Trans FA

A

Increase LDL-C, similar to saturated fats, but reduce LDL size (more atherogenic)

Reduce HDL-C

May ↑inflammatory markers and endothelial damage

76
Q

Effect of omega-6

A

Omega-6 (linoleic) increases LDL clearance: LDL lowering effect is partly passive – removes the suppressing effect of SFA (similar to oleic acid and carbohydrates)

May decrease HDL formation and/or Apo-AI especially if >10% of total

kcal. However, this level of intake is rarely found in any population.

77
Q

Goal intake for omega-6

A

5-10% of calories

78
Q

Effects of Mono-unsaturated (MUFAs) + goal intake

A
  • Goal is no more than 20% of total calories – assuming a lower saturated fat intake
  • Result in derepression of LDL-receptor synthesis that was caused by SFA
  • Compared to PUFA, oleic acid does not lower HDL-C
  • Compared to saturated fats (C:12 – C:16) oleic acid lowers LDL-C
  • But, MUFAs are often consumed with saturated fats
79
Q

Advantages of MUFAs:

A

– Do not decrease HDL as does PUFA and carbohydrates

– Less susceptible to oxidation than PUFA
– Do not increase triglycerides as carbohydrates often do

– Do not increase cancer risk as high PUFA intakes could

80
Q

Effects of omega-3

A
  • Decrease TG in hyperlipidemic and hyperTG patients
  • May reduce risk of mortality in those with CVD
  • Do not reduce the number of VLDL particles being secreted by the liver but rather decrease the TG content of these particles
  • Omega-3 PUFAs do not lower LDL-C concentrations except as their PUFA replace SFA in the diet
  • Omega-3 PUFAs interfere with platelet aggregation and thereby prevent coronary thrombosis; delay proliferation of fibroblasts
  • Reduce plaque formation and growth as they reduce adhesion molecules
81
Q

Effects of soulbe fibers on serum lipid levels

A

Soluble fibers decrease total-C and LDL-C – may be dependent on initial level of hypercholesterolemia

82
Q

Disadvantages of high CHO diet:

A
83
Q

effects of high and moderate nut intake

A

High intake (30-60 g/d) reduces risk of CHD, moderate intake reduces LDL-C and improves endothelial function

84
Q

Dietary goals for treatment of severe hyperlipidemia and hypertriglyceridemia

A
85
Q

Factors Affecting HDL Cholesterol Levels

A
86
Q

what is the first-line drug for CVD

A

statins

87
Q

ezetimibe mechanism

A

decreases intestinal absorption of cholesterol

88
Q

Lower triglyceride levels are associated with decreased __ risk

A

Lower triglyceride levels are associated with decreased CVD risk

89
Q

Are there meds that increase HDL-C?

A

no, only lifestyle modifications

90
Q

What are fibrates used for?

A

For use in highly elevated TG (familial hyperTG)

91
Q

Age and sex risk factor for atherosclerosis

A

More prevalent over the age of 65 and in men

92
Q

HDL-C cut-offs

A

low HDL-C:
<1.0 mmol/L men <1.3 mmol/L women

93
Q

Dyslipidemia Classification: primary vs secondary

Which is more prevalent?

A

Primary: single or poly-genetic abnormalities affecting lipoprotein function resulting in hyperlipidemia or hypolipidemia

Secondary: environmental causes +/- predisposition; more prevalent

94
Q

Effects of obesity on lipoprotein metabolism

A

Increased substrate flux to liver:

• Postprandial

– Due to excess calories (lipids and carbohydrates)

• Postabsorptive

– Due to high adipose tissue and hormone-sensitive lipase (HSL) activity (because of insulin resistance) resulting in increased FFA flux to liver

Hypertriglyceridemia of Obesity: overproduction of TG-rich VLDL whihc inhibit lipolytic effect-> accumulation of VLDL remnants in the circulation

95
Q

Possible mechanisms for HDL-cholesterol lowering in obesity

A

this has to do with higher production of VLDL and increased transfer of CH form HDL to VLDL; and increase TG transport from VLDL to HDL
this will result in an increased catabolism of HDL by excess adipose tissue and increased uptake by the liver-> decreased HDL levels

96
Q

Stronger association of BMI with HDL/LDL than LDL/HDL

A

Stronger association of BMI with HDL than LDL

97
Q

How to calculate MAP

MAP =
cardiac output X peripheral resistance

A

MAP = cardiac output X peripheral resistance

Cardiac Output (CO): CO = stroke volume x heart rate

Resistance:(length of vessel x viscosity of the blood) /radius^4

98
Q

Mean arterial pressure (MAP) is regulated by:

A
  • Sympathetic nervous system
  • Renin-angiotensin-aldosterone system
  • Renal function
  • Hormones involved: epinephrine, vasopressin, angiotensin II
99
Q

Classifiaction of HTN. Which is more prevalent?

A
  • *Primary/essential/ idiopathic (95% of cases)**
  • Unknown etiology
  • Interaction from environmental and genetics factors
  • Influenced by dietary and behavioral factors
  • *Secondary (5% of cases)**
  • Occurs secondary to another condition such as renal, endocrine, or neurological disorders
100
Q

Major risk factors of HTN

A

Non-modifiable
§ Age >60 y
§ Men, postmenopausal women, ethnicity (African-American, Russians, Finns)

§ Family history of CVD : women <65 y or men <55 y

Modifiable
§ Smoking
§ Sedentary lifestyle
§ Abdominal obesity, insulin resistance

§ Excess sodium intake
§ Poor diet quality
§ Stress

101
Q

Hypertension – Treatment: goals and plans

A

Goals:

  • Reduce risk of CD and renal disease
  • Lower BP to clinically appropriate level

Comprehensive plan includes :

  • Physical activity
  • Weight reduction
  • Nutrition therapy
  • Moderation in alcohol, relaxation therapy, smoking cessation
  • Pharmacological interventions: loop diuretics; thiazides; carbonic anhydrase inhibitors; potassium sparing diuretics
102
Q

Causes of HTN associated with obesity:

A

§ Insulin resistance/hyperinsulinemia

§ Overactivity of the sympathetic nervous system

§ Alterations in the RAAS

§ Leptin increases sympathetic activity; this function is preserved with leptin resistance

103
Q

__ is indicated both in treatment and prevention of HTN

A

§Weight loss is indicated both in treatment and prevention of HTN

104
Q

Recommendations for daily sodium intake

A

To decrease blood pressure, consider reducing sodium intake towards 2,000 mg (5 g of salt or 87 mmol of sodium) per day

105
Q

Potassium and blood pressure

Potential mechanisms:

A

◦ Natriuresis

◦ Suppressed renin
◦ Attenuates vascular contractionàvasodilation
◦ May reduce sympathetic activity and angiotensin II

106
Q

Are potassium supplements recommended in HTN?

A

§For normotensive people obtaining 60 mmol of dietary K daily,
K supplementation is not recommended as a means of preventing high blood pressure

§K supplementation above daily dietary intake of 60 mmol/d is not recommended as a treatment for hypertension

107
Q

The DASH diet implies:

A

increasing potassium, magnesium, calcium and fibers, while reducing saturated fatty acids and sodium.

108
Q

The DASH diet improves __

A

The DASH diet improves blood pressure, LDL, VLDL and triglycerides.

109
Q

Lung function test

A

Spirometry: Lung function test

  • Forced Expiry Volume (FEV)
  • FEV1 is the volume of air that can forcibly be blown out in one second, after full inspiration.
110
Q

Malnutrition diagnosis tests

A

Subjective Global assessment form

Acute illness and Chronic Illness form

111
Q

Nutrition Therapy when there is (or risk of) malnutrition in COPD

A
  • Small, frequent, nutrient dense, high kcal meals and snacks
  • 6 meals per day
  • Soft foods with sauces may be easier to chew and swallow
  • Nutrient dense beverages
  • Add kcalories with cream, margarine, etc
  • Limit low kcalorie or less nutrient dense foods/fluids
  • Use convenient or easy-to-prepare meals
  • Encourage healthy choices
  • May need to limit salt and fluid if fluid retention is a problem, but try not to restrict too much if malnutrition is a major concern (use clinical judgement)
112
Q

Diet for patients that use corticosteroids

A
  • Low salt/sodium
  • Long term use: High calcium/vit D (consider supplements)
  • High protein
  • May need diabetic diet (monitor glucose, TG)
  • May need heart healthy diet (monitor chol, TG)

NUTR 344 (22 decks)

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