atherosclerosis Flashcards
(27 cards)
pathophysiology
-an abnormal characterized by disorders of the heart and blood vessels
common causes: HTN, coronary heart disease, stroke, CHF, smoking
-process begins as soft fatty deposits and hardens with age
-can occur in any artery but prefers coronary artery
patho cont.
- focal deposits of cholesterol, lipids, cellular wastes, calcium, & other substances within the intima wall of an artery
- build up referred to as plaque
endothelial injury theory
- endothelium injury
- hyperlipidemia (nondenuding); HTN (denuding); chemical irritants(infections)
- 1) factor release into subendothelium
- 2) smooth muscle cells move into intima
- 3) initaites synthesis of collagen, lastic fiber protein, and protepglycans
- 4) platelets ad clotting factors accumulate
developmental variable
- takes many years, may start in childhood(15)
- stage 1: fatty streak formation (reversable)–collateral circulation formation
- stage 2: raised fibrous plaque–progressive changes (age 30 and up), chronic endotheial injury–HTN, elevated cholesterol, heredity, carbon monoxide, immune reactions, toxic substances
- stage 3: complicated lesion: rigidity and hardening (atheromas)
formed plaque
hemorrhage into the plaque
thrombus formation on the plaques surface
total occusion
once occurred: myocardial infarction, stroke
unmodifiable risk factors
age
gender
genetic predisposition
ethnicity
modifiable risk factors
elevated serum lipids and cholesterol correlated with : obesity, physical inactivity, high alcohol intake, intake of trans fatty acids, HDLs, LDLs, VLDLs HTN Smoking physical inactivity [decreases HDLs, decreases fibrinolytic activity, stifles collateral formation] obesity Diabetes stress/behavior patterns elevated cholesterol
lipid synthesis: to utilize lipids
must become water soluble by combining with proteins
-lipoproteins provide vehicles for fat mobilization & transport
HDLs, LDLs, VLDLs
High density lipoproteins
HDLs--healthy or good contains more protein by weight and less lipids carry lipids away from arteries increase with physical exercise decreased with age and Hx of CAD >60= negative risk 45-59=average risk 36-44=moderate risk
Very low density lipoproteins
VLDLs
lethal or bad
leads to LDL
elevation may increase the risk of premature atherosclerosis with other risk factors (DM, HTN, smoking)
triglycerides
made of fatty acids (saturated or unsaturated)
low density lipoproteins
lethal or bad -contain more cholesterol than protein --have an affinity for arterial walls -decreased level is desirable 160= high risk >190= very high risk
cholesterol
liver manufacture cholesterol directly from foods we eat
-specifically from foods we eat: egg yolks, poultry, meat, fish, seafood(shrimp and shell fish), whole-milk dairy products, organ meats (liver, gizzards, etc.)
foods that do not contain cholesterol
fruits, veggies, grains (esp whole grains), nuts and seeds(except peanuts- have lots of oil)
typically the body makes all the cholesterol it needs, people do not need to consume it
cholesterol levels
saturated fats
major reason for elevated blood cholesterol
trans fats also do this
AHA says daily cholesterol intake
primary prevention
Patient education:-reduce intake of saturated fats and cholesterol
-increase physical activity
-control weight
-smoking cessation
-decrease stress or alter behavioral patterns
evaluate dietary patterns
secondary prevention
medication therapy
goals: increase lipoprotein removal
- restrict lipoprotein production
- decrease cholesterol absorption
HGM CoA reductase inhibitors
- STATINS
- block synthesis of cholesterol
- increase removal of LDLs and triglycerides
- increase HDLs
- administered at bedtime
- require monitoring of liver function
- side effects mild-severe, but subside as therapy continues
- generally GI-constipation, abdominal pain and cramps
- statins: Atorvastatin, pravastatin, simvastatin, lovastatin, fluvastatin
benefits of statins
- reduction of CHD mortality
- overall reduction of coronary events
- reduction of coronary procedures (PTCA/CABG)
- reduction of strokes
- reduction of overall mortality
bile acid sequestrants
- binds with bile acids in the intestine
- forms an insoluble complex
- excreted through the stool: loss of bile acids lowers cholesterol & LDL levels in liver by converting them, tends to increase triglyceride levels
- side effects decreae over time: GI (consipation, nausea), interferes with absorption of other drugs: digoxin, beta-adrenergic blockers, coumadin, synthroid
bile acid sequestrants
- cholestyramine
- colestipol
- colesevelam
- give before meals
- mix with applesauce or a beverage (unpleasant gritty taste)
nicotinic acid (niacin)
- inhibits synthesis of VLDLs & triglycerides; decreasing LDL & cholesterol levels
- increase HDL levels
- Side effects: flushing, hyperglycemia, hyperuricemia, upper GI distress, hepatotoxicity( watch liver enzymes)
- take with food but do not crush or chew
- contraindications: liver disease, severe gout, peptic ulcer
fibric acids (fibrates)
reduce triglycerides by decreasing VLDLs -decreases liver synthesis of VLDLs -increases HDL -may enhance the effects of anticoagulants and hypoglycemia -give 30 mins before meals -gemfibrozil, fenofibrate side effects: dyspepsia, gallstones -avoid grapefruit juice
