final revision Flashcards
Anthropometric Data: _th and __th percentile suggest nutritional risk
Anthropometric Data: <5th and >95th percentile suggest nutritional risk
How many times should anthropometric measurments be repeated?
3 times
Ways of height measurment
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
BMI for Males and Non-Pregnant Female Adults <65 years old
<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
BMI: Males and Female Adults >65 years old
<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
What does skinfold thickness indicate?
How should it be carried out?
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
Describe MAC
- Reflects muscle, bone, subcutaneous fat
- Not sensitive to changes in muscle
Describe MAMC
- Corrects for subcutaneous fat
- Insensitive to small changes in muscle
- Must measure MAC and TSF
Describe MAMA
- Reflects muscle and bone
- More sensitive to changes in muscle than MAMC
- More adequately reflects total body muscle mass
describe cMAMA
- Reflects only muscle without the bone
- Not valid in elderly or obese
- Insensitive to small changes in muscle
Describe MAFA
Mid-upper arm fat area (MAFA)
- Reflects sub-cutaneaous adipose tissue stores
- Better indicator of total body fat than a single skinfold measurement
What are below and above average cut-offs for MAMA and MAFA
15% below average
85% above average
Waist circumference cut-offs
- >102 cm in men; >88 cm women
BMI and WC measures combined as indicators of CVD and type 2 DM
- High BMI Low WC - Low risk
- High BMI High WC - High risk
Limitation of DXA
– Expensive but increasingly accessible in research settings
– Minimal exposure to radiation
– Assumes normal hydration status
Half-lives of serum proteins
- Albumin (most abundant) - 17-21 days
- Transferrin- 8-10 days
- Prealbumin or transthyretin (TTR) - 2-3 days
- Retinol Binding Protein (RBP) - 10-12 hours
Albumin functions
Maintains osmotic pressure
Transport of large insoluble molecules, drugs, calcium, zinc
Transferrin function
iron transport
TTR function
Transport of T3 and T4
Carrier for RBP
RBP function
Retinol transport from liver to periphery
Circulates with TTR
Name negative acute phase proteins
levels decrease by >25% during inflammation, illness or metabolic stress
CRP cut-offs tractation
Used to detect mild or acute inflammation:
Normal <1, mild chronic 1-5, acute >5 mg/L
Albumin cut-off values
Normal: . 35 g/l
Deficit: <35g/L
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
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
When would creatine excretion increase? Decrease?
- Increase with exercise, meat intake, menstruation, infection, fever, trauma
- Decrease with renal failure and age
Limitations of Creatinine Height Index
- Rely on complete 24h urine collections: errors
- Meat-free diet prior to testing
- not sensitive
- not possible to detect small changes
Laboratory Tests for Anemia: General
When woudl this marjers be increased/decreased?
What are the cut-off values?
-
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
What is the order of depletion during iron deficiency and the associated markers
1) Storage iron (ferritin)
2) Iron transport (Transferrin)
3) Essential iron (RBC, myoglobin, enzymes)
Laboratory Tests for Anemia: Iron Deficiency
When would each of these markers be affected? What does that mean?
-
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
Graphs of how iron deficiency anemia markers change as anemia progresses
Components of TEE
TEF (<10%)
Physical Activity (20-30%)
REE or BMR (65-70%)
Protein requirements for healthy adults and elderly
Healthy adults: 1.0 g/kg/day Elderly adults: 1.0-1.2 g/kg/day
Considerations for the Elderly
- 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
How to differentiate types of malnutrition
10-40 is mild inflammation
40-100 is moderate inflammation
100-200 is marked inflammation
Obesity defintion
Progressive chronic disease characterized by excess or abnormal body fat that can impair health
Risk of health problems when analyzing BMI and waist circumference
BMI and waist guidelines for non-whites
• 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
Health consequences of obesity
Cancer
Breathing problems: sleep apnea and asthma
Arthritis
Hepatobiliary disorders
Reproductive and obstetrical complications
Surgical risk and complications
Psychosocial and emotional consequences
How are BMI and all cause mortality connected?
Obesity and risk of cancer in men and women
Obesity increases cancer risk
Women: Endometrium, Ovary, Cervix, Breast (postmenopausal)
Men: Prostate, Pancreas, Oesophagus
Women & Men: colon, gallbladder, kidney, liver
Obesity and hepatobiliary disorders
Obesity ↑ risk of gallstones (cholelithiasis)
– More related to abdominal obesity, more in women than men
– Risk is also increased with rapid weight loss
Obesity and liver health
Abdominal obesity ↑ risk of non-alcoholic fatty liver disease (NAFLD)
– Steatosis-> steatohepatitis-> cirrhosis-> liver failure
Obesity and reproductive disorders in
• 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.
Central regulation of food intake
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
Peripheral regulation of food intake
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
Low. moderate and high activity levels
Low- 1.3
Moderate- 1.5
High- ``1.8
What are METs?
• 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)
Which organs make up most of REE?
Liver-21%
Brain- 20%
Skeletal muslce- 22%
How would lactate and pyruvta levels chnage in response to a meal?
they woudl increase as these are glycolysis intermediates and glycolysis increases after a meal
What are the organs that will always be using some glucose, no matter what the time
Brain at a diminished rate RBCs, renal medulla
How are ketoacids excreted?
via lungs (acetone) and kidneys
Implications of ketone excretion?
§ 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
How do Urinary Nitrogen Constituents change in starvation
Less is excreted
Ammonia makes up a much bigger poriton, urea makes up a much smaller portion
Physiological Changes to Severe Weight Loss: CV, renal and immune
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
Physiological Changes to Severe Weight Loss: GI, electrolytes
Gastrointestinal Function
• Decreased Lipid absorption – steatorrhea
• Decreased Gastric, pancreatic and bile secretion/production
• Decreased Villous surface area
Electrolytes
• Potassium losses (LBM and intracellular losses)
Causes of refeeding syndrome
- 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
Physiological changes during repletion in the refeeding syndrome
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
Physiological changes after diet-induced weight loss that lead to increased energy storage and food intake
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
What are the effects of weight loss that improve diabetis control
Increased Glucose tolerance
Increased Insulin sensitivity
Decreased Need for glucose lowering medications
Cardiovascular benefits of weight loss
Normalizes triglyceridelevels
Raises HDL cholesterol
Lowers LDL cholesterol
Improves CHD risk profile
Reduces need for antihyperlipidemic medication
Benefits of weight loss on hypertension
Decreased Systolic blood pressure
Decreased Blood volume
Decreased Cardiac output
Decreased Sympathetic activity
Decreased Need for antihypertensive medication
0.5 kg of fat =__ kcal
0.5 kg of fat =3500 kcal
What is the best diet for maintenance
High protein, low GI
Medications after a heart attack could include…
- 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).
Guidelines for high TGs
• Limit or avoid sugar, sweets, sweetened beverages
- Avoid alcohol
- Achieve healthy weight
- Follow other heart healthy guidelines
Test do determine Left-sided Heart Failure
Left ventricular ejection fraction (LVEF or EF) = measurement of how much blood is being pumped out of the left ventricle of the heart
• Why does the heart enlarge in HF?
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
Nutritional Management in HF
• 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.
Global lifestyle modification approach to reduce CVD risk
weigth loss
physical activty
– Volume/intensity of exercise has greatest benefits (kcal spent)
– Resistance exercise has little effect
What type of dietary fat has the highest effect ob blood cholesterol levels
saturated fat
effect of dietary cholesterol on serum lipids
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
What is the effect of very-low fat deit
may decrease HDL-c
Effects of diets rich in SFA
• 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
Goal and recommendatons for intake for SFA
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
Effects of Trans FA
Increase LDL-C, similar to saturated fats, but reduce LDL size (more atherogenic)
Reduce HDL-C
May ↑inflammatory markers and endothelial damage
Effect of omega-6
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.
Goal intake for omega-6
5-10% of calories
Effects of Mono-unsaturated (MUFAs) + goal intake
- 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
Advantages of MUFAs:
– 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
Effects of omega-3
- 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
Effects of soulbe fibers on serum lipid levels
Soluble fibers decrease total-C and LDL-C – may be dependent on initial level of hypercholesterolemia
Disadvantages of high CHO diet:
effects of high and moderate nut intake
High intake (30-60 g/d) reduces risk of CHD, moderate intake reduces LDL-C and improves endothelial function
Dietary goals for treatment of severe hyperlipidemia and hypertriglyceridemia
Factors Affecting HDL Cholesterol Levels
what is the first-line drug for CVD
statins
ezetimibe mechanism
decreases intestinal absorption of cholesterol
Lower triglyceride levels are associated with decreased __ risk
Lower triglyceride levels are associated with decreased CVD risk
Are there meds that increase HDL-C?
no, only lifestyle modifications
What are fibrates used for?
For use in highly elevated TG (familial hyperTG)
Age and sex risk factor for atherosclerosis
More prevalent over the age of 65 and in men
HDL-C cut-offs
low HDL-C:
<1.0 mmol/L men <1.3 mmol/L women
Dyslipidemia Classification: primary vs secondary
Which is more prevalent?
Primary: single or poly-genetic abnormalities affecting lipoprotein function resulting in hyperlipidemia or hypolipidemia
Secondary: environmental causes +/- predisposition; more prevalent
Effects of obesity on lipoprotein metabolism
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
Possible mechanisms for HDL-cholesterol lowering in obesity
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
Stronger association of BMI with HDL/LDL than LDL/HDL
Stronger association of BMI with HDL than LDL
How to calculate MAP
MAP =
cardiac output X peripheral resistance
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
Mean arterial pressure (MAP) is regulated by:
- Sympathetic nervous system
- Renin-angiotensin-aldosterone system
- Renal function
- Hormones involved: epinephrine, vasopressin, angiotensin II
Classifiaction of HTN. Which is more prevalent?
- *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
Major risk factors of HTN
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
Hypertension – Treatment: goals and plans
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
Causes of HTN associated with obesity:
§ Insulin resistance/hyperinsulinemia
§ Overactivity of the sympathetic nervous system
§ Alterations in the RAAS
§ Leptin increases sympathetic activity; this function is preserved with leptin resistance
__ is indicated both in treatment and prevention of HTN
§Weight loss is indicated both in treatment and prevention of HTN
Recommendations for daily sodium intake
To decrease blood pressure, consider reducing sodium intake towards 2,000 mg (5 g of salt or 87 mmol of sodium) per day
Potassium and blood pressure
Potential mechanisms:
◦ Natriuresis
◦ Suppressed renin
◦ Attenuates vascular contractionàvasodilation
◦ May reduce sympathetic activity and angiotensin II
Are potassium supplements recommended in HTN?
§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
The DASH diet implies:
increasing potassium, magnesium, calcium and fibers, while reducing saturated fatty acids and sodium.
The DASH diet improves __
The DASH diet improves blood pressure, LDL, VLDL and triglycerides.
Lung function test
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.
Malnutrition diagnosis tests
Subjective Global assessment form
Acute illness and Chronic Illness form
Nutrition Therapy when there is (or risk of) malnutrition in COPD
- 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)
Diet for patients that use corticosteroids
- 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)
