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MS2 Exam 1 > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

CVD

A

abnormal condition characterized by disorders of the heart and blood vessels

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2
Q

Common causes of CVD

A
  • HTN
  • Coronary Heart Dz
  • Stroke
  • CHF
  • Smoking
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3
Q

Atherosclerosis

A
  • 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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4
Q

Most common form of atherosclerosis

A

Arteriosclerosis

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5
Q

Build up is referred as…

A

Plaque

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6
Q

Endothelial injury Theory

A
  • 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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7
Q

Stage 1 Atherosclerosis

A

Fatty Streak Formation (Reversible)

-collateral circulation formation

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8
Q

Stage 2 Atherosclerosis

A

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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9
Q

Stage 3 Atherosclerosis

A

Complicated Lesion

-Rigidity and hardening (“Atheromas”)

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10
Q

Formed Plaque

A
  • Hemorrhage into the plaque
  • Thrombus formation on the plaque’s surface
  • Total occlusion
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11
Q

Once plaque is formed…

A
  • MI

- Stroke

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12
Q

Unmodifiable Risk Factors

A
  • Age
  • Gender
  • Genetic predisposition
  • Ethnicity
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13
Q

Modifiable Risk Factors

A
  • Elevated Serum Lipids & Cholesterol
  • HTN
  • Smoking
  • Physical inactivity
  • Obesity
  • DM
  • Stress/Behavior Patterns
  • Elevated Cholesterol
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14
Q

Lipid Synthesis

A
  • To utilize lipids: must become water soluble, done by combining with proteins
  • Provide the vehicles for fat mobilization and transport
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15
Q

Lipoproteins

A

HDL’s: High density lipoproteins

LDL’s: Low Density lipoproteins

VDL’s: very low density lipoproteins

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16
Q

HDL’s

A

“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

–

17
Q

VLDL’s

A
  • “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)
18
Q

Triglycerides

A

Made up of Fatty Acids :
– Saturated
– Unsaturated

19
Q

LDL’s

A

“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

20
Q

How do we get cholesterol?

A
  • Liver manufactures
  • Specifically food from ANIMALS

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

21
Q

Foods that do not contain cholesterol

A
  • fruits
  • veges
  • grains
  • nuts and seeds
  • Typically the body makes all the cholesterol it needs
  • We do NOT need to consume it
22
Q

Saturated Fats

A

major reason for elevating blood cholesterol

-trans fats also do this

  • AHA:
  • daily cholesterol intake = less than 300mg
23
Q

Primary Prevention

A

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
24
Q

Goals of Medication Therapy

A
  • increase lipoprotein removal
  • restrict lipoprotein production
  • decrease cholesterol absorption
25
Q

HGM CoA Reducatase Inhibitors

A

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
26
Q

The Statins

A

ATORVASTATIN (LIPITOR)

PRAVASTATIN (PRAVACHOL)

SIMVASTATIN (ZOCOR)

LOVASTATIN (MEVACOR, ALTOCOR)

FLUVASTATIN (LESCOL)

27
Q

Benefits of Statins

A

Reduction of CHD mortality

Overall reduction of coronary
events

Reduction of coronary procedures (PTCA / CABG)

Reduction of Strokes

Reduction of overall mortality

28
Q

Bile Acid Sequestrants

A

CHOLESTYRAMINE (QUESTRAN)

COLESTIPOL (COLESTID)

COLESEVELAM (WELCHOL)

  • Give before meals
  • Mix with applesauce or a beverage (Unpleasant gritty taste)
29
Q

Bile Acid Sequestrants Action

A
  • 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
30
Q

Bile Acid Sequestrants Side Effects

A
  • GI: constipation, nausea

- Interferes with absorption of other drugs (Dig, B-adrenergic blockers, coumadin and synthroid)

31
Q

Nicotinic Acid Action

A

Niacin

  • inhibits synthesis of VLDL’s and triglycerides, decreasing LDL, and cholesterol levels
  • increase HDL levels
32
Q

Nicotinic Acid Side Effects

A
  • flushing, hyperflycemia, hyperuricemia, upper GI distress, hepatoxicity
  • take with food
33
Q

Nicotinic Acid Contraindications

A

liver dz, severe gout, peptic ulcer

34
Q

Fibric Acids

A

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

35
Q

Additional Therapeutic Options to lower LDL

A
  • higher dose of a statin
  • statin and bile acid sequestrant
  • statin and nicotinic acid
  • return visit in 6 weeks
36
Q

Health Promotion (Tertiary Prevention)

A
  • initiate moderate physical activity and advance
  • begin by reducing saturated fats and cholesterol
  • weight management
  • referral to dietician
  • return for followup
37
Q

Nursing Diagnoses

A
  • not noted until client is symptomatic
  • alteration in comfort/acute pain
  • ineffective tissue perfusion
  • anxiety
  • activity intolerance
  • lack of knowledge
  • ineffective therapeutic regime management
38
Q

AHA Cholesterol Recommendation

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

MS2 Exam 1 (13 decks)

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