CV Lecture 3 Flashcards

1
Q

What is Arteriosclerosis?

A
  • A thickening or hardening of the arterial wall

* The innermost layer undergoes a series of changes that ↓ the artery’s ability to change lumen size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is Atherosclerosis?

A
•	A type of arteriosclerosis 
•	Major Risk Factor for development of:
∗	Cardiovascular Disease – coronary artery disease (CAD) and acute coronary syndromes (ACS)
∗	Cerebrovascular Disease
∗	Peripheral Vascular Disease (PVD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the risk factors of Atherosclerosis?

A
  • Genetic predisposition and diabetes have a fairly direct effect on the development of atherosclerosis
  • Indirect risk factors – obesity, sedentary lifestyle, smoking, and stress
  • Research points to ↑ levels of C-Reactive Protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is Pathophysiology of Atherosclerosis?

A

• The exact pathophysiology is unknown but thought to occur from vascular damage R/T HTN, cholesterol levels, toxins from renal failure, or smoking.

∗ An inflammatory response triggers plaque development
∗ A stable or unstable plaque (made of collagen, cholesterol, cell debris, smooth muscle cells, and, especially in older patients, calcium) develops which partially or completely occludes the blood flow of an artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens when a plaque ruptures due to Atherosclerosis?

A

thrombosis and vasoconstriction obstruct the lumen causing inadequate perfusion to distal tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the clinical manifestations of Atherosclerosis?

A
•	Manifestations depend on 
∗	Vessel involved
∗	Site of the lesion
∗	Age of patient
∗	Genetic makeup
∗	Physiologic status of the individual
•	HTN develops if atherosclerosis ↑ systemic vascular resistance (SVR)
•	Cerebral or myocardial ischemia is a life-threatening manifestation of atherosclerosis in vessels of the brain or heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lipid levels of patients with Atherosclerosis will be?

A

Increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a desirable Total Serum cholesterol level?

A

<200 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is borderline and high risk cholesterol level?

A

▪ Borderline High Risk – 200 – 239 mg/dL

▪ High Risk – 240 mg/dL and over

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Homocysteine?

A

∗ Amino acid derived from dietary protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can an increase level of Homocysteine do?

A

∗ Positive correlation between ↑ levels and development of PVD, CAD, Stroke, and Venous Thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What level of Homocysteine is a risk factor and what happens with high levels of homocysteine?

A

∗ High levels effects cell wall elasticity and permits plaque buildup
∗ Level > 15 mmol/L is a risk factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some ways to lower homocysteine level if needed?

A

∗ Can lower by eating diet rich in B-complex vitamins, particularly folic acid
∗ 1 mg supplement of folic acid daily can improve endothelial function and lower homocysteine levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is • C-Reactive Protein (CRP)?

A

∗ One of the acute phase proteins that increases during systemic inflammation
▪ Inflammation is a common component to the development of lipid containing plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What level of C-Reactive Protein (CRP) puts someone at risk for heart disease?

A

level > 3 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How can you decrease C-Reactive Protein (CRP)?

A

∗ Can decrease with ASA, exercise, statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some ways to help manage Atherosclerosis?

A

Therapeutic Lifestyle Changes (TLC) =
- DIET : ↓ Red meats, eggs and milk products, liver, organ meats
∗ ↑ soluble fiber – fruits, vegetables, oats, and legumes (10 – 25 g/day) and plant stanols/sterols (2 g/day)
-EXERCISE: ↑ physical activity.
∗ With diet therapy the average reduction in total cholesterol is 10 – 15%
-QUIT SMOKING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

When is drug therapy usually initiated with Atherosclerosis?

A

after a 6 month trial of dietary alterations without success

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Atherosclerosis-

What is the action of HMG-CoA Reductase Inhibitors (statins) ?

A

▪ ↓ cholesterol production in the liver and ↑ clearance of LDL-C from the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Atherosclerosis-

Which medications are HMG-CoA Reductase Inhibitors (statins) ?

A

lovastatin (Mevacor), -atorvastatin (Lipitor), -pravastatin (Pravachol), -simvastatin (Zocor),
-fluvastatin (Lescol), -rosuvastatin (Crestor)

21
Q

Atherosclerosis-

What are the common side effects of HMG-CoA Reductase Inhibitors (statins)?

A

▪SE:

  • ↑ liver enzymes (ALP, AST, ALT);
  • opacities of the lenses (baseline eye exam);
  • GI effects, do not take with grapefruit juice,
  • myopathy (muscle weakness due to dysfunction of muscle fiber)
22
Q

Atherosclerosis-

What is the action of Nicotinic Acid (Niacin)?

A

▪ ↓ cholesterol synthesis in liver
▪ ↓ LDL-C and VLDL cholesterol levels, and ↑ HDL-C levels
▪ Used in conjunction with diet therapy

23
Q

Atherosclerosis-

What are examples of Nicotinic Acid (Niacin)?

A

▪ e.g. niacin, vitamin B3, Slo-Niacin – sustained release

24
Q

Atherosclerosis-

What are the side effects of Nicotinic Acid (Niacin)?

A

▪ SE: ↑ liver enzymes, severe flushing, pruritus, GI distress
• Take with food can ↓ flushing and GI distress

25
Q

Atherosclerosis-

What is the action of Fibric Acid Derivatives (fibrates)?

A

▪ ↑ HDL’s and ↓ VLDL & Triglyceride levels

26
Q

Atherosclerosis-

What are examples of Fibric Acid Derivatives (fibrates)?

A

gemfibrozil (Lopid), bezafibrate (Bezalip), fenofibrate (Tricor), – fenofibrate inhibits production LDL-C

27
Q

Atherosclerosis-
What are the side effects of
Fibric Acid Derivatives (fibrates)?

A

GI irritability, myopathy, gallstones

28
Q

Atherosclerosis-

How do Cholesterol Absorption Inhibitors work?

A

▪ Take once a day

▪ ↓ absorption of cholesterol in the small intestine

29
Q

Atherosclerosis-

What is an example of Cholesterol Absorption Inhibitors and how does it work?

A

▪ Take once a day
▪ ↓ absorption of cholesterol in the small
Example - ezetimibe (Zetia)

30
Q

Atherosclerosis-

What are the side effects of Cholesterol Absorption Inhibitors?

A

back pain and arthralgia,↑ liver enzymes when taken with statins

31
Q

What is CAD

A
  • Broad term includes Stable Angina Pectoris and Acute Coronary Syndromes
  • Single largest killer among American men and women
  • Takes many years to develop
32
Q

What happens with CAD?

A

• Causes the loss of O2 and nutrients to myocardial tissue because of poor coronary blood flow
• When patient becomes symptomatic the disease process is usually well advanced
∗ Generally no symptoms until 60% or more of the tissue’s blood supply is occluded
• Can diminish the myocardial blood supply until deprivation impairs myocardial metabolism enough to cause ischemia
∗ Persistent ischemia causes infarction

33
Q

What is the growth of Collateral Circulation attributed to?

A

∗ Inherited predisposition to develop new blood vessels
∗ Presence of chronic ischemia
• With rapid onset of CAD or coronary spasm, time is inadequate for collateral circulation to develop

34
Q

What are some Non modifiable Risk Factors for CAD?

A

∗ Age, Gender, and Ethnic Background - Blacks and Hispanic women have higher CAD risk factors.
▪ More women than men have angina
∗ Family History and Heredity-▪ Familial hyperlipoproteinemia associated with CAD occurrence at young age
▪ Individuals whose parent had CAD are more susceptible
• Modifiable Risk Factors – research shown to be definitely associated

35
Q

Modifiable Risk Factors of CAD?

A
∗	Lipid Levels
∗	Homocysteine Levels
∗	HTN
▪	Shearing stress of ↑ BP (strips endothelial lining) ↑ the rate of atherosclerotic development
▪	↑ workload of the heart
∗	Cigarette Smoking
∗	Physical Inactivity
∗	Obesity
36
Q

Why is a person with Diabetes Mellitus said to have a contributing risk factor to CAD?

A
  • Alterations in lipid metabolism

* Tend to have higher cholesterol and triglyceride levels

37
Q

Why is stress considered a risk factor for CAD?

A
  • Stimulation of SNS and its effect on the heart predisposes pt. to CAD
  • Can cause elevated lipid levels and alterations in blood coagulation
38
Q

What are some ways to identify CAD high risk individuals?

A

∗ Health History
∗ Family History of premature CAD in a first degree male relative < 55 or female relative < 65
∗ Lifestyle habits – diet, exercise, smoking
∗ Psychosocial – anxiety, depression, stress

39
Q

What are some ways to manage high risk CAD individuals?

A

∗ Risk Reduction Strategies Should Be Employed
▪ Encourage, motivate, and teach person with modifiable risk factors to make lifestyle changes.
▪ Work with patient in setting realistic goals
-Physical Fitness
∗ Health Education in Schools

40
Q

What are clinical manifestations of CAD?

A
  • Stable Angina
  • Acute Coronary Syndrome
  • Angina Pectoris
41
Q

What happening in Angina Pectoris?

A

▪ Ischemia develops when the demand for myocardial O2 exceeds the ability of the coronary arteries to supply O2
• The primary reason for insufficient blood flow is atherosclerosis

42
Q

Why is the left ventricle the most susceptible to ischemia?

A

it has a higher myocardial O2 demand, larger mass, higher wall tension, and higher systemic pressures

43
Q

What are some precipitating facors of Angina Pectoris?

A

▪ Physical Exertion
• ↑ HR, esp. with isometric exertion of the arms
▪ Strong Emotions
• Stimulate the Sympathetic Nervous System
▪ Consumption of a Heavy Meal
• Blood shunted to the GI tract during digestion, esp. if exertion after the meal
▪ Temperature Extremes
• ↑ Workload of the Heart
♥ Vasodilation (heat), Vasoconstriction (cold)
▪ Cigarette Smoking
• ↑ HR, Vasoconstriction, ↑ CO
▪ Sexual Activity
• ↑ Cardiac workload & SNS stimulation
▪ Stimulants
• ↑ HR and myocardial O2 demand
▪ Circadian Rhythm Patterns
• ↑ Incidence in the early am after waking

44
Q

What is unstable angina associated with?

A

-the deterioration of a once stable atherosclerotic plaque, which ruptures creating the risk of thrombus formation (may occlude the lumen and result in MI)

45
Q

How do you monitor a patient with Unstable Angina?

A

EKG monitoring, bed rest, ASA, and systemic anticoagulation

46
Q

What are the clinical manifestations of a patient with Angina?

A

▪ Chest Pain or Discomfort
• Description: vague sensation, strange feeling, squeezing, heaviness, choking, or suffocating
• Location: substernally; neck; between shoulder blades; radiate to jaw, shoulders, down arms
• Assessment: OLD CART or PQRST
♥ Onset, Location, Duration, Character, Aggravating factors, Relieving factors, Timing
♥ Pallative/ Provoking, Quality, Radiation/ Region, Severity, Timing
▪ Feeling of Anxiety or Impending Doom
▪ Associated Symptoms: SOB, cold sweat, weakness, paresthesias of arm(s)
▪ May be asymptomatic

47
Q

What are some complications of Angina in a patient?

A

▪ Arrhythmias

48
Q

What are some diagnostic studies that can be performed on a patient with angina?

A
▪	Chest X-ray
•	Assess for cardiac enlargement
•	Pulmonary congestion
•	Cardiac calcification
▪	Lab Tests
•	Lipid Panel
•	Cardiac Enzymes
▪	EKG
▪	Treadmill Exercise testing
▪	Nuclear Imaging
•	Assess myocardial perfusion
▪	Coronary Angiography/Angiogram
•	Contrast Dye – check allergies to shellfish?
▪	Echocardiography