Atherosclerosis Flashcards

1
Q

CAD is? and means?

A

-Coronary Artery Disease (CAD): Most common cause is atherosclerosis

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2
Q

Arteriosclerosis

A

hardening of arteries (common used term)

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3
Q

-Atheromas:

A

intimal wall plaques that consist of raised lesion with soft, yellow grumous core of lipid covered by firm, white fibrous cap.

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4
Q

Hyperlipidemia:

A

High lipid levels in the blood

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5
Q

-LDL cholesterol

A

Low Density Lipoprotein Bad cholesterol

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6
Q

HDL cholesterol

A

High Density Lipoprotein Good Cholesterol

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7
Q

etiology

A

What causes and origins of disease

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8
Q

pathophysiology

A

disturbance that a disease causes in an organ

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9
Q

Etiology of Atheroslcerosis

A

cholesterol and lipids on intimal wall of the artery

-Endothelial lining altered as a result of inflammation and injury

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10
Q

-Pathogenesis of Atheroslcerosis

List the steps

A
Injury to endothelium
Accumulation of lipoproteins
Monocyte Adhesion to the endothelium
Platelet Adhesion 
Smooth Muscle proliferation 
Lipid Accumulation
Inflamation
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11
Q

-C-reactive protein (CRP)

A

marker of inflammation

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12
Q

Where is CRP found?

A
  • Marker is found in patients with CAD

- CRP is found with unstable plaques and oxidation of LDL cholesterol

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13
Q

What is the most common heart disease?

A

-CAD is most common heart disease

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14
Q

What age groups are effected by CAD?

When are they diagnosed?

A
  • Mainly effects ages between 40-60
  • Men risk increases after 45 years old
  • Women risk increases after 55 years old (estrogen may protect), post menopausal
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15
Q

What are death rates due to CAD?

A

25% of population

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16
Q

Modifiable Risk Factor associated with development of atherosclerosis (4)

A
  • Hyperlipidemia: Can be treated, life style change
  • Hypertension: There are drugs for that
  • Cigarette Smoking: Toxins that damage Intima
  • Diabetes: Increased Risk
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17
Q

Nonmodifiable Risk Factor associated with development of atherosclerosis (4)

A
  • Genetics: Due to several conditions, hypertension, diabetes, pro-inflammatory state
  • Age: 40 – 60 is critical threshold
  • Gender: possible effect estrogen protects
  • Family History
18
Q

Additional Risk Factors associated with development of atherosclerosis (4)

A
  • Inflammation: Increases risk of plaque formation and rupture, a marker for inflammation, CPK is shown to be a risk factor for MI, stroke, PAD and cardiac death
  • Hyperhomocystinemia: Homocysteine levels correlate to increased CV disease
  • Metabolic Syndrome: central obesity, insulin resistance, HTN, high LDL and low HDL, hypercoagubility, and pro inflammatory state
  • Lipoprotein a: altered LDL, associated with CAD and CVD.
19
Q

Identify signs and symptoms of atherosclerosis

in various arteries

A
  • Coronary arteries – angina, shortness of breath, arrhythmias, MI
  • Carotid arteries – sudden weakness, paralysis, confusion, trouble speaking, problems breathing, sudden headache
  • Peripheral Arteries – numbness, pain, infections
  • Renal arteries – fatigue, loss of appetite, nausea, edema, itching
20
Q

Hyperlipidemia

  • How does it pertain to atherosclerosis?
  • What is a component of risk?
  • What causes reduced risk?
A

Major risk factor for atherosclerosis

LDL is major component associated with increased risk

Higher HDL correlates with reduced risk

21
Q

What can cause a negative affect on lipid levels

3

A

High dietary intake of cholesterol and saturated fats (egg yolks, animal fats, butter…)

Trans-unsaturated fats produced by hydrogenation of polyunsaturated oils (baked goods, margarine)

Obesity and smoking lower HDL levels

22
Q

What can cause a Positive affect on lipid levels

3

A

Diets low in cholesterol and/or higher ratios of polyunsaturated fats

Diet high in Omega-3 fatty acids (found in fish oils) appear to be beneficial

Exercise and moderated consumption of ethanol both raise HDL levels

23
Q

Pharmacotherapy for Hyperlipidemia

4

A

Statins
Fibrates
Bile acid sequestrants
PCSK9 inhibitors

24
Q

What do Statins do??

A

– HMG CoA reductase inhibitors

25
Q

What do Fibrates do?

A

– lower triglycerides and raise HDL

26
Q

What do Bile Acid Sequestrants do?

A

inhibit enterohepatic reuptake of intestinal bile salts which increase fecal loss of LDL cholesterol

27
Q

PCSK9 inhibitors

A

Proprotein converstase subtilisin kexin 9 inhibitors.

28
Q

According to the 2013 ACC/AHA Cholesterol Guidelines who should be assessed for Cardiovascular Risk?

A

For patients without atherosclerotic cardiovascular disease:

  • Assess traditional risk factors (e.g., lipids, blood pressure, diabetes) every four to six years in patients 20 to 79 years of age.2,3
  • In patients 40 to 75 years of age not receiving cholesterol-lowering therapy, and with LDL 70 to 189 mg/dL (1.8 to 4.9 mmol/L),
29
Q

According to the 2013 ACC/AHA Cholesterol Guidelines who should be treated with a Statin?

A
  • Patients with clinical atherosclerotic cardiovascular disease.
  • Patients with LDL 190 mg/dL (5 mmol/L) or higher.
  • Patients age 40 to 75 years of age with diabetes (but without clinical atherosclerotic cardiovascular disease) and LDL 70 to 189 mg/dL (1.8 to 4.9 mmol/L).
  • Patients without clinical atherosclerotic cardiovascular disease or diabetes with LDL 70 to 189 mg/dL (1.8 to 4.9 mmol/L), with an estimated 10-year risk of atherosclerotic cardiovascular disease of 7.5% or higher.
30
Q

What are 5 Key points of Statin therapy

A

Check ALT (alanine aminotransferase) at baseline. Repeat only if symptoms of hepatotoxicity

Document pre-existing muscle pain and monitor for increases in muscle pain

Check creatine kinase if symptoms of muscle pain or fatigue. Concern of rhabdomyolysis but it is rare.

Check lipid levels at 12 weeks

Monitor adherence before making dose adustments

31
Q

What are some limitation to 2013 ACC/AHA Cholesterol Guidelines?

A

Increased use of statin drugs especially in patients considered at lower risk. Overtreatment?

Risk calculator relies heavily on age and sex and not on other factors such as triglyceride levels, family history, CRP

Do not address patients younger than 40 or older than 75

No LDL targets for patients to have goals to achieve

32
Q

Who be helped by

High-dose Statin (average LDL reduction about 50% or higher):
Atorvastatin 80 mg once daily (40 mg if 80 mg not tolerated).
Rosuvastatin 20 mg to 40 mg once daily.

A

Secondary prevention in adults 75 years of age and younger.

Primary prevention in adults with LDL 190 mg/dL (5 mmol/L) or higher (VERY HIGH)

Primary prevention in adults 40 to 75 years of age with LDL 70 to 189 mg/dL

Primary prevention in diabetes patients 40 to 75 years of age with LDL 70 to 189 mg/dL (1.8 to 4.9 mmol/L)

33
Q

Who be helped by

Moderate-dose Statin (average LDL reduction about 30 to 50%)

A

Secondary prevention in adults older than 75 years.

Patients who cannot tolerate a high-dose statin.

Primary prevention in adults 40 to 75 years of age with LDL 70 to 189 mg/dL

Primary prevention in diabetes patients 40 to 75 years of age, with LDL 70 to 189 mg/dL

34
Q

Who be helped by

Low-dose Statin (average LDL reduction 30%)

A

For patients who cannot tolerate a high- or moderate-dose statin

35
Q

Who be helped by

Nonstatin

A

Patients who cannot tolerate the recommended statin dose or do not achieve the expected statin response and are high-risk

36
Q

What are other recommendations about keeping statin levels down?

A

Reinforce statin adherence and lifestyle changes, and check for secondary causes before adding a nonstatin

37
Q

What should not be added to statin therapy?

Why?

A

Fibrates

-it may cause muscle breakdown

38
Q

Adding a non statin to a statin ?

A

No proof adding a nonstatin to a statin further reduces cardiovascular risk.

39
Q

What are LDL Ranges?

A

Optimal Below 100 Near Optimal 100-129 Borderline High 130-159 High 160-189 Very High above 190

40
Q

What are total Cholesterol Ranges

A

Desirable >200
Borderline High 200-239
High >240

41
Q

What are HDL Ranges

A

Low below 40 and High above 60