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Module 9 - Cardiovascular disorders > Dyslipidemia & Atherosclerosis > Flashcards

Dyslipidemia & Atherosclerosis Flashcards

1
Q

What is atherosclerosis?

A
  1. An inflammatory disease
  2. thickening and hardening of the arterial wall
  3. large and medium sized arteries.

‘Athere’ = fatty
‘sclerosis’ = hardening and stiffening

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2
Q

What are atheromas?

A

Fatty/fibrous plaques that develop in arterial walls

result in decreased perfusion, ischemia and infarction.

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3
Q

What are the key arteries affected by atherosclerosis (5)?

A
  1. Coronary (coronary artery disease = CAD)
  2. Carotid, vertebral, cerebral (cerebrovascular disease)
  3. Abdominal aorta (aortic aneurysm)
  4. Iliac, femoral, popliteal (peripheral artery disease = PAD)
  5. Renal (renal artery stenosis)
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4
Q

What are fatty streaks?

A

Yellow accumulation of foam cells (oxidized LDL + macrophages) and T lymphocytes

Forms on walls of arterial tunica intima

Flat, does not disturb blood flow

A non-clinical lesion and the earliest sign of atherosclerosis.
(<20 years)

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5
Q

What is a fibrous plaque?

A

The advanced lesion.

Persistent injury, inflammation and lipid infiltration = plaque grows into the artery lumen

Development is slow = 20-40 years before clinically evident.

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6
Q

Why are hypertension (3) and dyslipidemia (2) risk factors for atherosclerosis?

A

Hypertension:
- mechanical injury to endothelial cells = vascular proliferation
- increase the permeability of LDL to the intima of the blood vessel
- High angiotensin II levels = pro-inflammatory (stimulates cytokines).

Dyslipidemia:
- LDL oxidation and internalization = contribute to endothelial dysfunction
- decrease nitric oxide = vasoconstriction.

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7
Q

Which layer of the artery wall is affected by atherosclerosis?

A

The tunica intima (inner coat) which consists of the endothelial cells, connective tissue and internal elastic membrane.

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8
Q

Describe the pathogenesis of atherosclerosis (6).

A
  1. Lesion initiation (response to injury or response to retention theories).
  2. LDL deposition on injured area.
  3. FOAM cells = oxidized LDL + macrophages
  4. Fibrous plaque development and smooth muscle hypertrophy
  5. vasodi;ation capacity decreases
  6. plaque calsifies with time, fissures easily, pieces of plaque break off - travel = emoblism
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9
Q

In lesion initiation, what is the ‘response to injury’ hypothesis?

A

Endothelial injury or dysfunction (causing inflammation) is the triggering even tin the development of atherosclerosis.

Chronic endothelial injury:
- HTN
- Tobacco use
- Hyperlipidemia
- Hyperhomocysteinemia
- Diabetes
- Infections
- Toxins

Inflammation causes:
1) endothelial cell retraction allowing the infiltration of LDLs
2) recruits WBCs to the area

Supported by observations of atheromas in areas of turbulent flow (branching points, tight bends)

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10
Q

In lesion initiation, what is the ‘response to retention’ theory?

A
  • entry and retention of LDLs in susceptible areas of the arterial wall is the initiating event in atherosclerosis.
  • Trapped LDLs are oxidized by free radicals = endothelial injury and inflammation.
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11
Q

Describe how fatty streaks develop (6).

A
  1. Endothelial injury causes inflammation.
  2. LDLs infiltrate the intima layer across the leaky endothelium.
  3. trapped LDLs are oxidized by free radicals
  4. Monocytes are recruited, enter the intima, are converted to macrophages (& release free radicals)
  5. Macrophages ingest oxidized LDLs forming foam cells
  6. an accumulation of foam cells forms the fatty streak
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12
Q

What are the steps in fibrous plaque development (3)?

A
  1. Foam cells secrete factors that stimulate the migration of smooth muscle cells from the tunica media to the intima.
  2. Smooth muscle cells:
    - proliferate
    - engulf oxidized LDLs
    - migrate over the fatty streak
    - produce collagen.
  3. The fibrous plaque composed of a lipid core (foam cells, cholesterol and cell debris) and fibrous cap (smooth muscle cells and collagen) develops.
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13
Q

What is a stable atherosclerotic plaque?

A
  • thick fibrous cap and a small, fatty core
  • may slowly cause narrowing
  • obstruct blood flow, but do not tend to form thrombi

-implicated in stable angina

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14
Q

What is an unstable (vulnerable) atherosclerotic plaque?

A
  • Thin fibrous cap and a large, fatty core (soft)
  • Vulnerable to rupture, platelet aggregation, and thrombus formation
  • implicated in unstable angina and acute MI
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15
Q

In an MI, what is the difference between non-ST and ST elevation?

A

non-ST = partial blockage by thrombus

ST = full blockage by thrombus

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16
Q

What is the difference between unstable and stable angina?

A

Both involve transient ischemia.
Stable angina = fixed plaque. Is predictable with activity.
Unstable angina = Plaque disruption and platelet aggregation. Can occur while at rest

17
Q

What are non-modifiable risk factors for atherosclerosis (4)?

A
  • advanced age (all older adults have some, males > 45 and females >55)
  • biological sex (males>females until age 55) pre-menopause estrogen protects by increasing HDL levels
  • family history of CAD or stroke (for CAD, Male1st degree relative <55 and female 1st degree relative <65)
  • genetic disorders of lipid metabolism (e.g. familial hypercholesterolemia)
18
Q

What are modifiable risk factors for atherosclerosis?

A
  • HTN
  • cigarette smoking
  • dyslipidemia
  • overweight/obesity
  • insulin resistance/ diabetes
  • physical inactivity/ sedentary lifestyle
  • atherogenic diet
  • stress
19
Q

Why is smoking a modifiable risk factor for atherosclerosis?

A
  1. Nicotine (vasoconstriction)
  2. LDLs>HDLS
  3. toxins = endothelial injury
  4. free radical oxidation of LDL
    • Nicotine constricts blood vessels (via sympathetic activation) and increases BP
  • associated with increase in LDLs and decrease in HDLs
  • toxins cause endothelial injury
  • causes the generation of free radicals that may contribute to LDL oxidation
20
Q

What are lipoproteins?

A
  • Play a key role in atherosclerosis
  • Normally function to transport lipids in the aqueous environment of blood
  • outer shell of phospholipids and proteins
  • inner core of cholesterol and TGs (trigylcerides)
  • classified by their relative amounts of protein and fats
  • the more protein, the higher the density
21
Q

What are Chylomicrons?

A

Chylomicrons = largest and lease dense lipoprotein synthesized by cells lining the small intestine during a meal

Transport mostly triglycerides absorbed in the diet to adipose tissue and muscle cells

Lipids are used to make ATP or stored as triglycerides.

22
Q

What are VLDL’s?

A

Very low-density lipoprotein

Transports mainly triglycerides from the liver to tissues.

After triglycerides are removed, the remnant (IDL) is returned to the liver to be cleared or is converted by hepatic lipase to an LDL.

23
Q

What are LDL’s?

A

Low density lipoprotein

Synthesized in Liver

Transports cholesterol to tissues.

Cholesterol functions in plasma membrane durability and the synthesis of steroid hormones and Vit D.

Blood levels are regulated by hepatic LDL receptors.

High LDL levels contribute to atherosclerosis.

24
Q

What are HDL’s?

A

Synthesized in the liver.

Absorb excess cholesterol released from peripheral tissues.

Recently discovered to be able to remove excess cholesterol from arterial walls (= reverse cholesterol transport).

HDLs have a protective role in preventing atherosclerosis.

25
Q

What happens to cholesterol that is returned to the liver by HDL’s (4)?

A
  1. Stored
  2. Used in LDL synthesis
  3. Used in bile salt synthesis
  4. Removed in the bile
26
Q

What happens to HDL’s when their cholesterol is removed in the liver?

A

Return to circulation.

27
Q

List 4 consequences of atherosclerosis.

A
  1. Artery lumen narrows d/t atheroma growth.
  2. A thrombus forms on the ahteroma (partial or complete)
  3. A thromboembolus forms that blocks a distal artery
  4. Arterial wall weakening causing an aneurysm (triple A)
28
Q

What is Atherosclerotic Cardiovascular Disease (ASCVD)?

A

ASCVD = all the clinical conditions of atherosclerotic origin.
- ACS = acute coronary syndrome
- MI = myocardial infarction
- CAD = coronary artery disease
- stroke
- TIA = transient ischemic attack
- documented carotid disease
- peripheral artery disease
- AAA = abdominal aortic aneurysm

Module 9 - Cardiovascular disorders (6 decks)

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