CVD Flashcards
(25 cards)
What diseases are included within CVD
- coronary heart disease
- coronary artery disease
- Htn
- Cerebrovascular disease
- congenital heart defects
- peripheral vascular disease
- congestive heart failure
What is mortality vs. morbidity?
Mortality: death rate
Morbidity: incidence of disease
What factors can damage the arterial walls
- hypercholesterolemia
- oxidized LDL
- Htn
- Cigarette smoking
- DM
- obesity
- homocysteine
- high SFA diet
What is atherosclerosis vs. arteriosclerosis?
Atherosclerosis: form of arteriosclerosis
- development of fatty streaks in arteries which develops into
fibrous plaque, ultimately dec BF
Arteriosclerosis: thickening, loss of elasticity and calcification of
arterial walls, ultimately dec BF
What factors influence LDL
- aging
- genetics
- diet (SFA)
- dec estrogen (menopause)
- DM nephrotic syndrome
- obstructive liver disease
- obesity (inc VLDL and dec HDL)
- some Htn/steroid meds
What are the only carrier of dietary lipids in the blood?
Chylomicrons
What is familial heterozygous hypercholesterolemia?
- Cause: dec or defective LDL receptors (pts have 1/2 normal
expression of LDL receptor) - common: 1/500
- inc TC, inc LDL normal VLDL
- premature CHD (men: 30-40, women: 40-50)
Treatment: Step I or ATP III
What is familial homozygous hypercholesterolemia?
- pt receives defective LDL receptors from both parents
- LDL levels 4x greater than normal
- develop early CHD and MI, usually in childhood
What is familial combined hyperlipidemia?
- cause: hepatic overproduction of apo B-100, therefore VLDL
- inc TC, LDL, TG, VLDL
Treatment: Step 1 or ATP III (wt reduction)
What is familial dyslipidemia?
AKA type III
Cause: defective clearance of VLDL remnants
uncommon (1/5000)
inc TC and TG
Treatment: Step 1 or ATP III (wt reduction)
What is familial hypertriglyceridemia?
AKA Type IV
- very common
- excessive VLDL synthesis
- inc TG and VLDL
- Cause: dec LPL activity
What is familial Lipoprotein Lipase Deficiency?
- rare condition
- LPL activity reduced in all tissues
- no increased risk of CHD
- often develops pancreatitis unless strict avoidance of dietary fat
How do statins help manage CVD?
- HMG-CoA reductase
- Lovastatin, pravastatin, lipitor
- dec LDL (18-55%), dec TG (7-30%), inc HDL (5-15%)
- consequences: myopathy, increased liver transaminase activity
How do Bile acid sequestrants (resins) help manage CVD?
- dec LDL (15-30%), inc HDL (3-5%), no change in TG
- Cholestryamine, colestipol, colesevelam
- nutritional consequences: dec Ca absorption, fat, and fat soluble vitamins
- Side effects: N/V, belching, dyspepsia, pain, constipation
How does Nicotinic acid help manage CVD?
- most effective med at increasing HDL
- decreases FFA mobilization, therefore dec VLDL
- dec LDL (5-25%), dec TG (20-50%), inc HDL (15-35%)
- nutrition becomes component of allopathic medicine
- side effects: flushing, hyperglycemia, gout, hyperuricemia, dyspepsia/peptic ulcer, liver toxicity
How do Fibrates help manage CVD?
- increase PPAR alpha activity: a tx factor that regulates tx of genes for apolipoprotein A-1 and LPL
- Gemfibrozil, fenofibrate
- generally used to lower TG, not LDL
- dec LDL (5-20%), inc HDL (10-35%), dec TG (20-50%)
- side effects: GI symptoms, gallstones, myopathy
What are the major risk factors for CVD?
- HTN (>140 mg/dL)
- low HDL ( 45; women > 55 or premature menopause w/o ERT
- family hx of premature CHD- 1st degree relative
premature: men < 55, women < 65 - obesity (BMI > 30)
- TC >240 mg/dL OR TC > 200 mg/dL & HDL < 40 OR 2 or more
risk factors
How does SFA intake relate to CVD?
- inc TC levels because inc LDL
- inc HDL when substitute CHO or other fatty acids
- sources of SFA: animal fats, coconut, palm oil
- most hypercholesterolemic to least
-myristic acid (14:0)>palmitic acid (16:0)>lauric acid (12:0)>
stearic (18:0, neutral)
** palmitic is most prevalent (60% of all SFA consumed) - for every 1% inc in energy intake from SFA, inc TC by 2.7 mg/dL
How do MUFAs affect CVD?
- substitute MUFA for SFA: dec TC, LDL, and TG
- if total fat kcal <30%, MUFA will dec HDL
- oleic acid is most prevalent
- sources: canola, olive, peanut, rice, hazelnut, avocado
How do PUFAs affect CVD?
- replace CHO with linoleic acid: dec LDL and inc HDL
- replace SFA with PUFA in LF diet: dec LDL and HDL
- large quantities of linoleic acid inc LDL oxidation
- sources of omega 6: veg oils: corn, safflower, sunflower, soybean
- sources of omega 3: fish oils, walnuts, EB eggs
- dec TG (25-30%)
- inc LDL (5-10%)
- inc clotting times and dec BP
What are the therapeutic lifestyle changes in LDL lowering therapy?
- TLC Diet
- red intake of chol-raising nutrients: SFA and dietary chol
- other LDL-lowering options
- plant stanols/sterols
- viscous (soluble) fiber
- soy
- increased PA
- wt reduction
What are the main components of the TLC diet recommended by the NCEP ATP III? concerning: CHO, protein, total fat, SFA, PUFA, MUFA, cholesterol, fiber, plant stanols/sterols, soy
CHO: 50-60% of kcals Protein: 15% of total kcal Total fat: 25-35% of total kcal SFA: <200 mg/day fiber: 20-30 g/day plant stanols/sterols: 3-4 g/d soy: use to replace high SFA animal foods (25 g/d)
What are the fiber recommendations for CVD? For soluble and insoluble fiber?
Fiber: 20-30 g/da-y
- Soluble: 10-25 g/d
- uses chol to replace bile acid pool
- bacteria in colon ferment CHO to SCFA –> dec cholesterol synthesis
- Insoluble: no effect on TC concentrations
What are the levels of claims of fiber? What is the daily reference value used for food labels?
- High fiber: 5 g or more per serving
- Good source of fiber: 2.5-4.9 g per serving
- more or added fiber: >2.5 g/serving than reference food
- Food label:
- daily reference value:
- 25 g/2000 kcal
- 30 g/2500 kcal
- 20% daily value/serving
