- StudyBlue
- Vermont
- University of Vermont
- Nutrition, Dietetics, And Food Science
- Nutrition, Dietetics, And Food Science 254
- J.ross
- Metabolic Syndrome & Cardiovascular Disease
Metabolic Syndrome & Cardiovascular Disease
Nutrition, Dietetics, And Food Science 254 with J.ross at University of Vermont
About this deck
By: Shira Levien
Created: 2011-05-04
Size: 32 flashcards
Views: 0
Created: 2011-05-04
Size: 32 flashcards
Views: 0
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Causes of Metabolic Syndrome
Increased calorie intake, increased refined CHO, physical inactivity, abdominal obesity
Development of Metabolic Syndrome
-genetic predisposition
-central obesity
- diabetes melitus
- high fat diets
- aging
-medications
-physical inactivity
- polycystic ovary disease
-low birth weight
Criteria for Metabolic Syndrome
at least 3 of:
- abdominal obesity in men >40in waist, women >35in waist
- triglycerides = or > 150 mg/dl
- HDL cholesterol <40 in men and <50 in women
- blood pressure = or >130/85 mmHG
- fasting glucose = or >110mg/dl
Risk Factors for Metabolic Syndrome
- Atherogenic dyslipidemia
- Glucose intolerance
- Hypertension
- proinflammatory state
- prothrombotic state
Atherogenic dyslipidemia
High TGL, VLDL-C, non-HDL-C, and low HDL-C, LDL-C particle size
glucose intolerance
high fasting glucose, HBA1c, impaired glucose tolerance
Hypertension
High BP
Proinflammatory state
High WBC, hs-CRP, IL-6
Prothrombotic state
High fibrinogen, vWF, PAI-1
Management ABC's of Metabolic Syndrome
A- assessment/ aspirin
B- BP control
C- cholesterol management, LDL, non HDL, HDL
D - diabetes prevention/ diet
E- exercise
Diet considerations for Metabolic syndrome
- weight loss reduces oxidative stress
- more refined CHO lead to insulin resistance, metabolic syndrome, diabetes
- hight GI diets lead to decreased CVD especially in obese women
- low GI diets lead to high HDL, low TGL in 6 months
- omega-3 and other USFA, natural antioxidants, fiber - decrease inflammation
- mediterranean diet - lowers insulin resistance and proinflammatory cytokines
CVD prevalence
- leading cause of death in US
- US ranks 13th for women and 17th for men in world incidence
- incidence increases with age, especially in women
- african americans have highest rate, asians lowest
- death rates have declined due to prevention, behavior, and better treatment
CVD includes...
hypertension, coronary heart disease (CHD), stroke, rheumatic heart disease, congestive heart failure
Coronary heart disease pathology
results from ischemia or lack of blood flow to the heart, specifically through coronary arteries
underlying cause of decreased blood flow is atherosclerosis
complicated by hypertension
how long can atherosclerosis take to develop
decades
progression of atherosclerosis
endothelial dysfunction > less nitric oxide (vasodilator) > constriction of artery> artery permeable to LDL > LDL + macrophages = foam cells > fatty streaks > fibrous plaque (LDL, calcium, fibrin) > acute lesions > plaques imbed blood flow to heart
cause of atherosclerosis progression
LDL infiltrates intimat of arteriol wall, modified by oxidation and enzymes which cause release of leukocytes which leads to inflammatory proteins (cytokines, TNF, IL-6, C-reactive protein)
atherosclerosis treatment
reversible by diet
inflammation
response to injury/infection, nonspecific stress response, capillaries become more permeable to allow phagocytes to destroy.
Catecholamines
norepinephrine and epinephrine, increase metabolic rate, glycogen breakdown in liver and muscle, glucose production from amino acids, release of fatty acids from adipose tissue, glucagon secretion from pancreas.
Glucagon
glycogen breakdown in liver, glucose production from amino acids, release of fatty acids from adipose tissue.
Cortisol
protein degradation, enhancement of glucagons action on liver glycogen, glucose production from amino acids, release of fatty acids from adipose tissue.
Aldosterone
hormone involved in retention of stodium
antidiuretic hormone
hormone involved in retention of water
additional immune response to atherosclerosis
T cells patrol arteries for antigens, if found produce cytokines for inflammation. promote atherosclerosis in response to infection.
C-Reactive protein
acute phase protein produced by liver and increased in systemic infection. may be additional test for CVD risk. highly sensitive in increased risk of heart attack, sudden death, peripheral artery disease.
Test suggestions for CRP using global risk assessment
<10% no test
10-20% test
>20% should be treated anyway
hsCRP levels
<1mg/l - low risk
1-3mg/l - average risk
>3mg/l- high risk
factors effecting CRP levels
weight loss, exercise, diabetes, smoking cessation, BP, reducing alcohol, stress, genetics.
suggested foods to reduce CRP
fish oil, ginger, tumeric, aspirin, coenzyme Q
factors increasing release of chemicals and activation of immune cells
cigarette smoking, hypertension, atherogenic lipoproteins, hyperglycemia, all give rise to variety of noxious stimuli that cause release of chemicals and activation of cells involved in inflammatory process which can cause formation of plague and clots causing CHD.
Modifiable Risk Factors in CVD
markers in blood, lipoprotein profile, inflammatory markers, lifestyle risk factors, related diseases.
About this deck
By: Shira Levien
Created: 2011-05-04
Size: 32 flashcards
Views: 0
Created: 2011-05-04
Size: 32 flashcards
Views: 0
About StudyBlue
STUDYBLUE makes things that make you better at school.
Things like online flashcards with photos and audio.
Things like personalized quizzes and friendly reminders about when (and what) to study next.
Think of it as a digital backpack™: access to all of your study materials online and on your phone.
STUDYBLUE exists to make studying efficient and effective for every student, for free. Join us.
“I have been getting MUCH better grades on all my tests for school. Flash cards, notes, and quizzes are great on here. Thanks!”
Kathy
Kathy