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Pathophysiology > Lecture 3: Atherosclerosis > Flashcards

Lecture 3: Atherosclerosis Flashcards

1
Q

Define atherosclerosis

What size arteries does it affect?

A

Atherosclerosis is :
- disease of elastic arteries, and large and medium size muscular arteries

  • characterized by fibrous thickening of the arterial wall associated with lipid-infiltrated plaques that may calcify
  • affects mid to large size arteries
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2
Q

Explain the origin and progression of atherosclerosis

A

Progression of Atherosclerosis:

pneumonic: “Even Manny Forgets Farting Saturday’s Finnish Class”
1. Endothelial Cell Dysfunction
2. Macrophage and LDL accumulation
3. Foam Cell formation
4. Fatty streaks
5. SMC migration
6. Fibrous Plaque
7. Complex Atheroma

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3
Q

Explain the changes that happen in endothelial cells and SMCs during inflammation

A

Normally, endothelial cells are impermeable to large molecules, anti-inflammatory, resist thrombosis and promote vasodilation

When activated by inflamation endothelial cells: Increase Permeability, Increase inflamatory cytokines, Increase leukocyte adhesion, Decrease vasodilators, Decrease antithrombitic

SMCs normally: contract and contain in medial layer

Upon activation by inflamation, SMCs increase inflammatory cytokines, increase extracellular matrix synthesis and increase migration and proliferation

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4
Q

What factors cause endothelial dysfunction?

Endothelial dysfunction intitiates foam cell formation by invading _____

Lipoprotein oxidation plays a major role in ______ recruitment

A

Chemical forces and hemodynamic stress cause endothelial dysfunction

Endothelial dysfunction initiates foam cell formation by invading macrophages

Lipoprotein oxidation plays a major role in leukocyte recruitment

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5
Q

Macrophage and LDL accumulation:

The site of the lesion is determined by ________, shear stress at artery branches increase the likelihood of ______ formation, where LDLs infiltrate into the ______ region.

Endothelial cells increase their permeability due to shear stress, LDL cholesterol starts to migrate inside and gets trapped, it then binds to ______

A

The site of the lesion is determined by hemodynamic forces. Shear stress at artery branches increase the likelihood of plaque formation, where LDLs infiltrate into the sub-endothelial region.

Endothelial cells increase their permeability due to shear stress, LDL cholesterol mirgration starts to migrate inside and gets trapped, it then binds to ApoB

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6
Q

What are the following prodisease mechanisms:

_____ permeability

_____ leukocyte adhesion

_______ NO production

A

Pro-disease mechanisms:

INCREASED permeability

INCREASED leukocyte adhesion

Decreased NO production

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7
Q

Explain why LDL is “bad cholesterol” whereas HDL is “good cholesterol”

A

LDL is bad because in atherosclerosis it is the carrier of cholesterol inside the plaque

HDL, however, is acting as a positive factor, it actually binds to cholesterol and transports it outside

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8
Q

Stages of plaque development:

Foam Cells——> Fatty Streaks

How do fatty streaks (which are not necessarily pathological) become plaques?

A

Fatty streaks become fatty streaks due to foam cell recruitment

Plaque progression happens due to smooth muscle cell migration and altered matrix synthesis and degradation

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9
Q

Fatty Streaks:

  • Fatty streaks are early lesions, consist of (location) accumulation of foam cells
  • Foam cells are…..
  • Fatty streaks are found in the aorta in the ___ decade of life, in the coronary artery in the ___ decade and in the cerebral artery in ___
A

Fatty Streaks:

  • fatty streaks are early lesions, consist of sub-endothelial accumulation of foam cells

Foam cells are LDL and cholesterol engorged macrophages

  • Fatty streaks are found in the aorta in first decade of life, found in the coronaries in second decade of life and found in the cerebral arteries in 3 and 4th decades of life
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10
Q

Fatty Streaks are forecasts of _______

Fatty streaks cause _____ permeability, ______ leukocyte filtration, ______ NO, _____ vasodilation

A

Fatty streaks are forecasts of fibrous lesions

Fatty streaks cause increased permeability, increased leukocyte filtration, decreased NO, and defective vasodilation

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11
Q

SMC Migration:

Foam cells start accumulating to form a necrotic core

PDGF and FGF-Beta attract proliferation and migration of SMCS to the necrotic core

Which two molecules play a role in attraction of SMC to the lesion?

A

Antiotensin and homocystine

play a role in attraction of smooth muscle cells to the necrotic lesion

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12
Q

Fibrous legions:

Fibrous legions are characterized by accumulation of lipid rich _____ and ______.

The fibrous cap consists of ____ and ______ enclosing the necrotic core

Fibrous legions may eventually _____

A

Fibrous legions:

Fibrous legions are characterized by accumulation of lipid rich necrotic debris and SMCs

The fibrous cap consists of SMCs and extracellular matrix enclosing the necrotic core

Fibrous legions may eventually calcify

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13
Q

Explain why females are protected from atherosclerosis until after menopause:

Estrogren promotes ____ NO and ____ prostocyclins, causing ______ vasodilation

A

Females are protected from atherosclerosis until after menopause because

Estrogen promotes INCREASED NO and increased prostacyclins….. causing increased vasodilation

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14
Q

Complex atheroma and thrombosis:

Complex plaques with superimposed thrombi and THICK

Risk factor for ___ and ____ embolization

Result in vascular insufficiency, abnormal renal circulation.. aneursym… clots

“Big two” places to get clots are?

A

Complex atheroma and thrombis:
Complex plaques with superimposed thrombi and are thick

Risk factor for cerebral and peripheral embolization

Big two places to get clots: heart and brain

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15
Q

Stable vs unstable plaque

Explain stable vs unstable plaques

A

Plaques will begin to grow and obstruct blood flow

Stabilized plaques: growth of fibrous cap and decreased lipid layer/foam cells

Vunerable plaque: lipid layer/foam cell layer keeps growing, with a thin fibrous cap

Vunerable plaques are at risk for rupturing and releasing a thrombus

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16
Q

What are the pro-coagulants?

List the anti-coagulants?

tPA is _______

A

Procoagulants: tissue factor and PAI-1

Anticoagulants: thrombomodulin, protein S, protein C, heparin

tPA is pro-fibrolytic (prevents/treats blood clots)

17
Q

List the two factors that are PRO-coagulation

A

Tissue factor and PAI-1 are pro-coagulation

18
Q

Use of ______ modify the risks of complications from atherosclerosis

Example of a _____ is aspirin

Aspirin inhibits ________ (which enzyme)?

A

Use of anti-coagulants modify the risk of complications from atherosclerosis

Example of an anti-coagulant is aspirin

(other examples include thrombomodulin, protein S and C and heparin like substances)

Aspirin inhibits thromboxane

19
Q

The risk factors of Atherosclerosis (hemodynamic stress, hypertension, smoking, fatty foods, diabetes)

all lead to the _______ of LDLs

Then those altered LDLs are recognized by “______”

That then _____

A

The risk factors of atherosclerosis (hemodynamic stress, fatty foods, high cholesterol, diabetes, etc)

all lead to OXIDATION of LDLs

Then those altered LDLs are recognized by “scavenger receptors” that then bind and stimulate inflammation, further driving atherogenesis

20
Q

Explain the risk factors for atherosclerosis:

Modifiable Risk Factors

Non-modifiable risk factors

A

Modifiable Risk Factors: dyslipedemia (high LDL, low HDL), tobacco smoking, hypertension, diabetes, lack of physical activity

Non-modifiable risk factors: Age, Male gender, Heretibility/genetics

21
Q

Explain why obesity, HTN and diabetes are a bad combo for atherosclerosis

A

Obesity, HTN and diabetes all promote the same things that are PRO-atherosclerosis

Hyperlipedemia, HTN, glucose intolerance, impaired thrombolysis, inflammation, endothelial dysfunction

ALL of those things promote atherosclerosis

22
Q

Prevalence of Atherosclerosis:
- Begins early in life, Accelerated by genetics and enviornmental factors

  • Common in societies where cholesterol rich diet is prevalent
  • In the US it is the underlying cause of _____ deaths
  • Almost all patients who die of ____ (and _____ resulting from cerebral thrombosis) have atherosclerosis
A

Prevalence:

  • begins early in life, accelerated by genetic and enviornmental factors
  • Common in societies where cholesterol rich diet is prevalent
  • In the US it is the underlying cause of roughly 50% of all deaths
  • Almost all patients who die of MI’s (and strokes resulting from cerebral thrombosis) have atherosclerosis
23
Q

Explain each complication of atherosclerosis:
1. Calcification

  1. Rupture or ulceration
  2. Hemorrhage
  3. Embolization
  4. Aneursyms
A
  • Calcification: lipid core accumulates calcium, creating rigid vessels and decreasing compliance, making it more fragile
  • Rupture or ulceration of plaque causes thrombosis (clot)
  • Hemorrhage into the plaque producing a hematoma in the vessel wall further reduces lamimal diamter
  • Embolization of fragments to peripheral sites
  • Weakning of vessel wall causing aneursyms
24
Q

What is the gold standard to diagnose atherosclerosis?

What are some other methods?

A

Gold standard is catheterization (but angiograms are expensive and risky)

Other methods: look at markers like C protein, LDL, HDL HTN

25
Q

List some of the complications for atherosclerosis:

  • Heart problems/vasculature problems?
  • Cerebrovascular Diseases?
  • Kidney issues?
A

Clinical sequale for atherosclerosis:

  • Coronary Artery Disease, Peripheral Vascular Disease
  • Cerebrovascular Diseases: TIA’s, strokes
  • Renal Artery Disease: renal hypertension
26
Q

Treatment for atherosclerosis:

Explain lifestyle changes

What do the medications that you put the pt on do?

Types of surgical procedures?

A

Treatment for atherosclerosis:
- Lifestyle changes (diet and exercise, reduce blood sugar)

  • Medications: anti-hypertension meds, control LDL levels, lower blood sugar

Procedures: coronary angioplasty, bypass grafting

27
Q

Explain what coronary angioplasty is

A

Coronary angioplasty is a procedure where you basically baloon the artery around the plaque to allow more blood to flow

28
Q

Explain the following lipid modifying drugs:

Statins

Niacin

Fibric Acid Inhibitors

A

Statins inhibit HMG-CoA Reductase

Niacin is a lipase inhibitor

Fibric Acid Inhibitors (reduce LDL levels and increase HDL levels)

29
Q

Explain the mechanism of the following therapies for atherosclerosis:

  • Statins
  • Niacin
  • Aspirin
  • Beta-blockers
  • Renin-angiotensin inhibitors
A

Statins: inhibit cholesterol synthesis (inhibit HMG-CoA Reductase)

Niacin: inhibits fat breakdown and increases HDL, anti-inflammatory

Aspirin: anticoagulant (inhibts thromboxane)

Beta-blockers: antihypertensive

-Renin-angiotensin inhbitors: anti-hypertensive

30
Q

Which drug is a primary drug for atherosclerosis

A

Statins are primary prevention

31
Q

Fill in the blank for the following lipid levels:

Total Cholesterol:
Desirable level

Borderline Level

High

A

TOTAL CHOLESTEROL

Desirable is less than 200

Borderline is 200-230

High is > 240

32
Q

Fill in the blank for the following lipid levels:

LDL:

Optimal level

Borderline

High

A

LDL:
Optimal LDL is < 100

Borderline LDL is 130-159

High LDL is 160 and up

33
Q

List the following lipid levels for HDL

HDL:
Risk for heart disease

Borderline

Cardioprotective

A

HDL:
Risk for heart disease < 40

Borderline: 40-59

Cardioprotective is > 240

34
Q

What is the desirable level of total cholesterol?

What is the desirable level of LDL cholesterol?

At what level of HDL does it become cardioprotective?

A

Desirable level of total cholesterol < 200

Desirable level of LDL cholesterol < 100

At levels greater than 240 of HDL becomes cardioprotective

35
Q
A

Pathophysiology (17 decks)

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