- HTN - Coronary Heart Dz - Stroke - CHF - Smoking

- from the greek: athere "fatty mush", skleros "hard" - process begins as soft fatty deposits and hardens with age - Hardening of the Arteries - Can occur in any artery but prefer the coronary arteries - focal deposits of cholesterol, lipids, cellular wastes, calcium, and other substances within the intimal wall of an artery

- Hemorrhage into the plaque - Thrombus formation on the plaque's surface - Total occlusion

To utilize lipids: must become water soluble, done by combining with proteins - Provide the vehicles for fat mobilization and transport

"Healthy" or Good - contain more protein by weight and less lipid - carry lipids away from arteries - increase with physical exercise - decreased with age and hx of CAD – >60 mg/dl = Negative risk – 45-59 mg/dl = Average risk – 36-44 mg/dl = Moderate risk –

Atherosclerosis Flashcards by Lindsay Paxton

CVD

abnormal condition characterized by disorders of the heart and blood vessels

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Common causes of CVD

HTN
Coronary Heart Dz
Stroke
CHF
Smoking

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Atherosclerosis

from the greek: athere “fatty mush”, skleros “hard”
process begins as soft fatty deposits and hardens with age
Hardening of the Arteries
Can occur in any artery but prefer the coronary arteries
focal deposits of cholesterol, lipids, cellular wastes, calcium, and other substances within the intimal wall of an artery

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Most common form of atherosclerosis

Arteriosclerosis

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Build up is referred as…

Plaque

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Endothelial injury Theory

Hyperlipidemia (nondenuding)
HTN (Denuding)
Chemical irritants (infections)
Factor release into sub-endothelium (CRP)
Smooth muscle cells move into intima
initiates synthesis of collage, elastic fiber protein, and proteoglycans
platelets and clotting factors accumulate (clot under the fibrous cap of the plaque)

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Stage 1 Atherosclerosis

Fatty Streak Formation (Reversible)

-collateral circulation formation

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Stage 2 Atherosclerosis

Raised Fibrous Plaque

Progressive changes (age 30 and cont’d to increase)
Chronic endothelial injury (HTN, elevated cholesterol, heredity, carbon monoxide, immune rxns, toxic substances)

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Stage 3 Atherosclerosis

Complicated Lesion

-Rigidity and hardening (“Atheromas”)

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Formed Plaque

Hemorrhage into the plaque
Thrombus formation on the plaque’s surface
Total occlusion

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Once plaque is formed…

- Stroke

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Unmodifiable Risk Factors

Age
Gender
Genetic predisposition
Ethnicity

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Modifiable Risk Factors

Elevated Serum Lipids & Cholesterol
HTN
Smoking
Physical inactivity
Obesity
DM
Stress/Behavior Patterns
Elevated Cholesterol

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Lipid Synthesis

To utilize lipids: must become water soluble, done by combining with proteins
Provide the vehicles for fat mobilization and transport

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Lipoproteins

HDL’s: High density lipoproteins

LDL’s: Low Density lipoproteins

VDL’s: very low density lipoproteins

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HDL’s

“Healthy” or Good

contain more protein by weight and less lipid
carry lipids away from arteries
increase with physical exercise
decreased with age and hx of CAD

– >60 mg/dl = Negative risk

– 45-59 mg/dl = Average risk

– 36-44 mg/dl = Moderate risk

–

VLDL’s

“LETHAL” or BAD
Contain more triglycerides
Lead to LDL’s
Elevation may increase the risk of premature atherosclerosis with other risk factors (DM, HTN, Smoking)

Triglycerides

Made up of Fatty Acids :
– Saturated
– Unsaturated

LDL’s

“LETHAL” or BAD

Contain more cholesterol

Have an affinity for arterial walls

Decreased level desirable

160 mg/dl = High risk

> 190 mg/dl = Very high risk

How do we get cholesterol?

Liver manufactures
Specifically food from ANIMALS

(egg yolds/poultry, meat, fish, seafood, whole-milk dairy products)

Foods that do not contain cholesterol

fruits
veges
grains
nuts and seeds
Typically the body makes all the cholesterol it needs
We do NOT need to consume it

Saturated Fats

major reason for elevating blood cholesterol

-trans fats also do this

AHA:
daily cholesterol intake = less than 300mg

Primary Prevention

patient education

reduce intakes of saturated fat and cholesterol
increase physical activity
control weight
smoking cessation
decrease stress or alter behavior patterns
evaluate dietary patterns

Goals of Medication Therapy

increase lipoprotein removal
restrict lipoprotein production
decrease cholesterol absorption

HGM CoA Reducatase Inhibitors

STATINS - block the synthesis of cholesterol - increase the removal of LDL's and triglycerides - increase HDL's - Admin @ bedtime - Require monitoring of "Liver Function" - S/E mild to severe, but subside as therapy continues - Generally GI - constipation, abdominal pain and cramps

The Statins

ATORVASTATIN (LIPITOR) PRAVASTATIN (PRAVACHOL) SIMVASTATIN (ZOCOR) LOVASTATIN (MEVACOR, ALTOCOR) FLUVASTATIN (LESCOL)

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

CHOLESTYRAMINE (QUESTRAN) COLESTIPOL (COLESTID) COLESEVELAM (WELCHOL) - Give before meals - Mix with applesauce or a beverage (Unpleasant gritty taste)

Bile Acid Sequestrants Action

- binds with bile acids in the intestine - forms an insoluble complex - excreted through the stool: loss of bile acids LOWERS cholesterol and LDL levels in the liver by converting them. Tends to increase triglyceride levels

Bile Acid Sequestrants Side Effects

- GI: constipation, nausea | - Interferes with absorption of other drugs (Dig, B-adrenergic blockers, coumadin and synthroid)

Nicotinic Acid Action

Niacin - inhibits synthesis of VLDL's and triglycerides, decreasing LDL, and cholesterol levels - increase HDL levels

Nicotinic Acid Side Effects

- flushing, hyperflycemia, hyperuricemia, upper GI distress, hepatoxicity - take with food

Nicotinic Acid Contraindications

liver dz, severe gout, peptic ulcer

Fibric Acids

Reduce triglycerides by decreasing VLDL’s Decreases liver synthesis of VLDL’s Increases HDL’s May enhance the effects of anticoagulants & hypoglycemia Give before meals GEMFIBROZIL (LOPID) FENOFIBRATE (TRICOR, LOFIBRA) Side Effects – dyspepsia, gallstones

Additional Therapeutic Options to lower LDL

- higher dose of a statin - statin and bile acid sequestrant - statin and nicotinic acid - return visit in 6 weeks

Health Promotion (Tertiary Prevention)

- initiate moderate physical activity and advance - begin by reducing saturated fats and cholesterol - weight management - referral to dietician - return for followup

Nursing Diagnoses

- not noted until client is symptomatic - alteration in comfort/acute pain - ineffective tissue perfusion - anxiety - activity intolerance - lack of knowledge - ineffective therapeutic regime management

AHA Cholesterol Recommendation

- less than 200 mg/dL is desirable - 200-239 is borderline high - 240+ is high