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NURS 2500 > CLASS 20 - Central Perfusion, Atherogenesis and Intro to Ischemic Heart Disease (IHD) > Flashcards

CLASS 20 - Central Perfusion, Atherogenesis and Intro to Ischemic Heart Disease (IHD) Flashcards

1
Q

What is atherogenesis?

A

Changes in vessel walls leading to thickening + plaque formation

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2
Q

Describe the Response to Injury Theory of Atherogenesis in terms of where atherosclerotic plaques are formed.

A

States that atherosclerotic plaques tend to form wheveer arteries are most stressed (such as the bending + branching points).

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3
Q

What is the current injury of atherogenesis?

A

States that plaque formation involves an inflammatory event stimulated by a vessel wall injury.

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4
Q

What are the 2 types of stress that can cause injury to the intima of an artery ?

A

Mechanical + Oxidative

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5
Q

What are the 2 types of mechanical stress that can cause damage to the intima of an artery?

A

High blood pressure (can injure vessel wall)

Blood viscosity (thick blood from polycythemia and hyperglycemia)

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6
Q

What type of oxidative stress that causes damage to the intima of an artery?

A

High levels of ROS (reactive oxygen species such as superoxide) which damage cell structures

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7
Q

What are the 2 types of “emias” that are associated with increased production of ROS

A

Hyperlipidemia

Hyperglycemia

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8
Q

Describe the role of ROS in terms of their reactions with LDL (Low Density Lipids) and NO (nitric oxide). What effects do these reactions have on the artery wall?

A
  • ROS oxidize LDL which damages artery walls

- ROS destroys NO which eliminates its protective effect of vasodilation

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9
Q

What is the relationship between phagocytes and superoxide (ROS) during the inflammatory response ?

A

During the inflammatory response, phagocytes produce superoxide (ROS).

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10
Q

What is the role of WBCs macrophages when the arterial wall is damaged as a result of oxidative stress?

A

When the arterial wall is damaged, the inflammatory response brings WBCs to the area. Macrophages are activated and consume oxidized LDL.

Eventually, these macrophages die and become lipid filled foam cells that form a bulge in the side of the artery wall (aka a plaque).

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11
Q

What is hyperlipidemia?

Why is this problematic?

A

Hyperlipidemia is a condition of having too mnay lipids in the blood.

This is problematic because high amounts of specific lipids can cause atherosclerosis.

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12
Q

What are the 3 types of serum lipids?

A

Cholesterol

Tyiglycerides

Phospholipids

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13
Q

What is atherosclerosis?

A

hardening, occlusion, or damage to the arteries which causes the blood vessels to become narrow or blocked

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14
Q

What is cholesterol?

A

Cholesterol is a small organic molecule that is used in cell membranes and to form steroid hormones

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15
Q

What is the role of triglycerides in the body?

What is the roles of tyiglycerides when the body is in a fasting state?

A

stored in the body as an important source of energy.

bind to VDL when the body is in a fasting state

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16
Q

Are phospholipids used as a clinical indicator for hyperlipidemia in the context of atherosclerotic disease?

A

No.

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17
Q

What is the role of phospholipids?

A

Used to form plasma membranes

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18
Q

What are lipoproteins?

How do they function?

What are the 3 types of Lipoproteins?

A

Lipoproteins are lipids surrounded by a “shell” of protein.

They function to transport lipids though the blood stream.

VLDL, HDL, and LDL

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19
Q

What is the most common type of lipid in the body and a major source of energy?

A

Triglycerides.

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20
Q

What are VLDLs?

What is their function?

What do they contain?

A

= very low density lypoproteins

carry cholesterol + other lipids away from the liver to body cells

VLDLs contain high level of triglycerides

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21
Q

What will happen to the artery if we have lots of VLDLs in the blood?

A

Artery narrows due to plaque formation, therefore increases the risk of CAD.

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22
Q

identify whether these lipoprotein levels should be high or low in the blood:
VLDL
LDL
HDL

A

low
low
high

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23
Q

What are LDLs?

What do they contain? What is their function?

What risk is associated with high levels of LDL?

A

= low density lipoproteins (aka “bad cholesterol”)

Contain a high amt of cholesterol and transport cholesterol from the liver to body cells.

High levels of LDL increase the risk of plaque formation, PAD, and heart disease.

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24
Q

What is the primary risk factor for atherosclerotic disease? Why?

A

Elevated LDL.

LDLs deposit cholesterol in vessel walls for storage.

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25
Q

What is HDL?

What is its function?

What is associated with high levels of HDLs?

A

= High Density Lipoprotein

Remove cholesterol from the body and transports it to the liver for disposal.

High HDLs in the blood may lower risk of developing heart disease.

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26
Q

What is the general goal for LDL levels in mmol / L?

A

< 2.5 mmol / L

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27
Q

What is the goal for Total Cholesterol values?

A

Less than 4.0.

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28
Q

What are the optimal triglyceride levels in mmol / L

A

1.7 mmol / L

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29
Q

What is angina?

A

Ischemic pain in the heart (“chest pain”)

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30
Q

What are the 3 components of cardiac / myocardial activity?

A
  • heart rate
  • contractility
  • afterload
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31
Q

Describe the effect of the narrowing of the arteries due to arterial disease on the supply of blood/oxygen to the heart.

A

decreases it (duh)

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32
Q

What is the relationship between myocardial activity and oxygen demand?

A

activity increases, demand increases

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33
Q

What is the major cause of CAD?

A

Atherosclerosis.

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34
Q

What are the 2 major risk factors for atherosclerosis?

A

Hypertension - increased pressure can injure vessel wall and start inflammatory process

High cholesterol / Hyperlipidemia - provides material needed to develop the plawues along the insie of the vessel.

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35
Q

Identify the 3 developmental stages of atherosclerosis.

A

1) fatty streak
2) fibrous plaque
3) complicated lesion

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36
Q

Describe fatty streaks.

What drugs can we use to potentially reverse this process?

A
  • earliest atherosclerotic lesions
  • lipids accumulate and migrate into smooth muscle cells
  • may be reversed by drugs that lower LDL (Statins, bile acid resins, nicotinic acid, cholesterol absorption inhibitors, orlistat)
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37
Q

Describe fibrous plaques.

A

Collagen covers the fatty streak to form a fibrous plaque.

Vessel lumen is narrowed.

Arterial wall thickens

Blood flow is reduced.

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38
Q

Describe complicated lesions.

A

Most dangerous - results in plaque ulceration + rupture

Thrombus forms and is enlarged through a +ve feedback mechanism (platelets activated, glycoprotein IIb/IIIa receptors that bind fibrin are expressed, leads to further platelet aggregation + bigger thrombus)

Results in further narrowing or total occlusion of the vessle

39
Q

What are the 6 risk factors for a chronic endothelial injury?

A

1) Hypertension
2) Tobacco use
3) Hyperlipidemia
4) Diabetes
5) Infections
6) Toxins

40
Q

What is collateral circulation? When does it occur?

A

The body creates new circulation in the heart around a blockage.

Can form in instances of atherosclerosis.

41
Q

Identify the 2 factors that contribute to the growth and extent of collateral circulation.

A

1) angiogenesis - inherited predisposition to develop new blood vessels
2) chronic ischemia

42
Q

What happens to macrophages once they consume oxidized LDL?

A

eventually die and become lipid filled foam cells that form a bulge in the side of the artery (aka a plaque).

43
Q

What is Coronary Artery Disease?

A

Condition in which the coronary arteries (which supply the heart muscle with blood) become narrowed due to plaque in ther aery walls.

44
Q

What is a Myocardial Infarction?

What long-term effects does this have on the heart?

A

Heart attack

Blood supply to an area of the heart is interrupted due to a blockage in the coronary arteries.

Results in permament damage to the muocardium as the heart has a very limited capacity for healing and regeneration.

Depending on the extent of the damage, the heart may not be able to function normally anymore.

45
Q

What is cardiac arrest?

A

The heart stops pumping blood completely. This is a medical emergency.

46
Q

What is heart failure?

What are the 3 clinical manifestations of heart faiure?

A

The heart cannot pump blood normally anymore.

SOB
Edema in body tissues
Extreme fatigue

47
Q

What is the typical end result of coronary artery disease (CAD)?

A

MI or cardiac arrest.

48
Q

what is plaque?

A

Mixture of cholesterol + dead WBCs

49
Q

What is cardiac ischemia?

A

narrowed coronary arteries do not allow enough blood and oxygen to the heart

50
Q

What is angina?

A

Sensation of chest pain or pressure.

51
Q

What is atherosclerosis?

What is coronary artery disease?

A

Atherosclerosis is a general term that describes a condition that can affect blood vessels anywhere in the body

CAD specifically refers to atherosclerosis in the coronary arteries in the heart.

52
Q

blockage in tissues –> __________ –> infarction if untreated

A

ischemia

53
Q

Identify the 4 non-modifiable risk factors for the development of CAD.

A

1) increasing age
2) sex (men > women)
3) ethinicity (white > black)
4) genetic predisposition + family history of heart disease

54
Q

Identify the 6 Modifiable Risk Factors for the development of CAD.

A

1) Serum lipid alterations (high triglyceride + LDL, decreased HDL)
2) Blood pressure greater than 140 / 90 mmHg
3) Diabetes mellitus
4) Tobacco use
5) Physical inactivity
6) Obesity

55
Q

Identify the 3 Contributing Factors for the development of CAD.

A

1) Fasting blood glucose level > 10 mmol /L
2) Psychosocial risk factors (stress, depression, hostility + anger)
3) elevated homocysteine levels

56
Q

What is the Framingham Risk Score? What is it used for? What are the 4 components?

A

Scoring tool which provides an estimation of 10-year risk of CAD.

Step 1) add points according to patient’s age, HDL-C, total cholesterol, SBP, smoking, diabetes

Step 2) use total points from step 1 to determine the 10 year risk.

Step 3) use total points from step 1 to determine heart age

Step 4) use 10 year risk from step 2 to detemine if patient is low, moderate, or high risk

57
Q

what are the 4 determinants of myocardial oxygen demand?

A

heart rate

contractility

preload

afterload

58
Q

Once an atherosclerotic plaque has reduced the lumen size by 75%, when can ischemia occur?

90%?

A

75%: ischemia can occur during times of elevated myocardial oxygen demand (physical activity, emotional stress, hot or cold exposure, large meal, etc)

90%: ischemia can occur at rest.

59
Q

What are the 2 causes of ischemia?

A

increased demand
decreased supply

orboth

60
Q

Describe the effects of a myocardial infarction at a cellular level.

How can we reverse this process?

A

myocardium hypoxic within first 10 seconds of blockage.

w/ total occlusion, contractility stops after several minutes

anaerobic metabolism begins

lactic acid accumulates
pain fibers stimulated
referred pain in left shoulder and arm

cardiac cells begin dying in ~ 20 mins

can be reversed if blood flow returns in time.

61
Q

Describe diastolic dysfunction as a result of cardiac ischemia.

What are its effects on preload, SV, CO, and BP?

A

ischemic cardiac muscle becomes “stiff”, results in reduced muscle relaxation + filling

Can reduce preload, SV, CO, and BP

62
Q

Describe systolic dysfunction as a result of cardiac ischemia.

What are its effects on SV, CO and BP?

A

= failure of the heart to properly contract (decreased contractility)

Can reduce SV, CO, BP

63
Q

Describe electrical disturbances in heart rhythm as a result of cardiac ischemia.

A

Conduction moves around ischemic tissue or heart muscle is “irritable”

ECG changes, irregular pumping, or ineffective pumping.

Tachycardia and bradycardia can alter CO.

64
Q

Describe Angina Pectoris (chest pain or pressure) as a result of cardiac ischemia.

A

Visceral pain due to cardiac muscle ischemia.

65
Q

Describe Cardiac muscle death (necrosis) + myocardial infarction (MI) as a result of cardiac ischemia.

A

the blood supply to an area of the heart is interrupted because of blocked coronary arteries. Results in permanent damage to the myocardium as the heart has v limited capacity for healing and regeneration. Heart may not be able to function normally anymore depending on the extent of the damage.

66
Q

Where does the myocardium receive blood from?

A

The L and R main coronary arteries from the base of the aorta

67
Q

What does the left main coronary artery branch off into?

A

Immediately branches into Circumflex and Laft Anterior Descending Arteries

68
Q

Which section of the heart does the Left Anterior Descending artery supply blood to?

Circumflex artery?

A

LAD = ant left ventricle + septum

Circumflex = posterior + lateral left ventricle

69
Q

which section of the heart does the right main coronary artery supply blood to?

A

ant + post R ventricle

SA and AV nodes

70
Q

What sections of the heart does the posterior descending artery supply blood to?

A

inferior + apex of the myocardium

71
Q

Identify the 9 clinical manifestations of CAD.

A

1) Chronic Stable Angina
2) Acute Coronary Syndrome
3) Unstable angina
(UA)
4) Myocardial
infarction
5) STEMI (ST
Elevation
Myocardial
Infarction
6) Non - STEMI
7) Cardiac arrythmias
8) Heart failure
9) Sudden cardiac death

72
Q

What is the function of Antilipemic drugs?

A

Decrease lipid counts

73
Q

Describe the MOA of HMG-CoA Reductase Inhibitors (“statins”)

A
  • inhibit cholesterol synthesis in the liver by blocking HMG-CoA reductase
  • decrease LDL (30-40%) + triglyceride levels (10-30%) (causes increased LDL receptors in the liver which allows liver to remove more LDLs from blood)
  • increase HDL levels by 2-15%
  • first line drug therapy for hypocholesteremia
  • treatment of types IIa and IIb hyperlipidemias
74
Q

What are the side effects of statins?

A
  • rash
  • GI disurbances
  • insomnia
  • elevated liver enzymes
  • lens opacities
  • liver damage + myopathy (muscle pain) that can progress to rhabdomyolysis –> renal failure
75
Q

what is rhabdomyolysis?

what should we monitor for in the blood to watch for rhabdomyolysis?

A

death of muscle fibers and release of myoglobin into the blood stream

monitor for creatine kinase (ser ck) levels as a product of muscle damage somewhere (like CRP and general inflammation).

76
Q

what nursing considerations are associated w statins?

A
  • generally well tolerated
  • take drug for life or until lifestyle / diet changes permanently lower cholesterol levels
  • most cholesterol is produced at night so short-acting med should be taken at HS
  • monitor liver + eye function
  • interact w tannin (ex - grapefruit)
77
Q

provide 2 examples of statin drugs.

A
  • atorvastatin (Lipitor)

- simvastatin (Zocor)

78
Q

what is the MOA of bile acid resins? why aren’t they first line medications?

A
  • increase conversin of cholesterol to bile acids in the small bowel. Increases bowel excretion of total cholesterol and LDLs.
  • relief of pruritis associated w partial biliary obstruction
  • may be used along w statins
  • not first line due to adverse effects
79
Q

what are the 2 S/Es associated w bile acid resins?

A

unpleasant, gritty taste

GI disturbances (ex - belching, heartburn, nausea, abdominal pain, constipation)

80
Q

what are the nursing considerations associated with bile acid resins?

A 
•	Adverse effects diminish w time
•	Safe for long-term use
•	Interferes w absorption of:
o	Beta-Adrenergic blockers
o	Fat-soluble vitamins
o	Folic acid
o	Vancomycin 
•	Therefore avoid other meds / vit 1h before and 4 h after giving meds 
•	GI upset, may subside, take w lots of water
81
Q

Provide an example of a bile acid resin .

A

cholestyramine (questran)

82
Q

what is the MOA of Nicotinic Acid

A

reduces catabolism of stored triglycerides and reduces availability of free fatty acids for VLDL production by the liver

increases HDL level

83
Q

what are the S/Es associated with nicotinic acid?

A

hot flashes + pruritis in neck and chest

GI disturbances

hepatotoxicity

hyperglycemia in diabetes

84
Q

what are the nursing considerations associated with nicotinic acid?

A

most adverse effects subside w time

high doses may lead to decreased liver function + dysrhythmias

aspirin 30 mins - 1h before administering niacin may prevent flushing in face

take w food

85
Q

what are 2 other names for nicotinic acid?

A

niacin

B3

86
Q

What is the MOA of fibrates (fibric acid derivatives)?

A

decrease hepatic synthesis and secretion of VLDL therefore decreasing triglyceride levels

increase HDL

87
Q

what are the S/Es associated with fibrates ?

A

GI disturbances

Increased risk of gallstones

may increase effect of warfarin, anticoagulants, and hypoglycemic medications

88
Q

provide 2 examples of fibrates

A

gemfibrozil (Lopid)

fenofibrate (Lipidil)

89
Q

What is the MOA of cholesterol absorption inhibitors?

A

inhibits abs of cholesterol and other sterols from the SI

results in reduces total cholesterol, LDL, and triglyceride levels

increase HDL

often combined w statins

90
Q

provide an example of a cholesterol absorption inhibitor

A

ezetimibe (zetia)

91
Q

what foods are good sources of omega-3 FAs?

A

tuna, salmon, halibut, flaxseed, soybeans, walnuts, pumpkin seeds

92
Q

what is the MOA of orlistat?

A

prevent abs of triglycerides

may promote weight loss and lower LDL

93
Q

What are the S/Es associated w Orlistat?

A

oily stools + fecal spotting

flatulence

urgency

pain

NURS 2500 (22 decks)

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