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CV Block > Pathology: Vascular Injury > Flashcards

Pathology: Vascular Injury Flashcards

1
Q

What is the baseline BP for the diagnosis of HTN?

A

140/90

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2
Q

What is the most common form of HTN?

A

Essential HTN –> a combo of genetic factors, environmental causes, diet, exercise, and salt/EtOH intake.

(95% of cases)

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3
Q

The other 5% of HTN cases are cases of “secondary HTN” caused mainly by….

A

Renal disease, Renal artery stenosis, or adrenal disorders (hyperaldosteronism)

Narrowing of the renal artery causes decreased perfusion, activating the renin-angiotensin-aldosterone system, which increases stressed blood volume. Increased stressed volume (or “Filling Pressure” according to Hassid) contributes to increased MAP.

Renal disease can result in either increased or decreased BP, depending on sodium retention/excretion.

Hyperaldosteronism –> increased secretion of aldosterone due to a genetic defect

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4
Q

What are the 2 HTN-related small blood vessel diseases?

Which one is associated with benign HTN, and which with severe?

A
  1. Hyaline Arteriolosclerosis –> associated with Benign HTN

2. Hyperplastic Arteriolosclerosis –> Associated with severe HTN

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5
Q

How does Hyalin Arteriolosclerosis occur? (pathophysiology)

A

Chronic hemodynamic stress injured the endothelial cells of the intima. Plasma components are able to cross into the vessel walls, and smooth muscle starts secreting ECM.

The ECM (hyaline) secretion is what we see on histology. Homogenous and circumferential.

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6
Q

What does ARTERIOLOSCLEROSIS mean and how does it differ from ATHEROSCLEROSIS and ATHEROSCLEROSIS?

A

Arterioolosclerosis involves the ARTERIOLES, not the muscular or large arteries, and comes in 2 flavors: Hyaline and Hyperplastic Arteriosclerosis. The tunica media is the cause of these pathologies.

Atherosclerosis involves the INTIMAL thickening of medium to large arteries.

Arteriosclerosis is the OVERALL THICKENING/LOSS OF ELASTICITY of arteries. Arteriolosclerosis and Atherosclerosis are subtypes of Arteriosclerosis

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7
Q

What is the pathophysiology of Hyperplastic Arteriosclerosis?

A

Onion Skinning of an arteriole –> concentric thickening of arteriolar walls and lumenal narrowing

Smooth muscle cell hyperplasia and excess basement membrane deposition cause the onion skin layers.

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8
Q

WHat is the body’s normal response to turbulence, injury, infection, or vascular damage of any kind?

A

Intimal thickening! The healing of injured vessels involves the migration of smooth muscle cells called NEOINTIMAL smooth muscle cells into the intima. Here, they divide and secrete ECM to repair the damaged vessel.

Here’s the kicker: They CAN”T CONTRACT like medial layer smooth muscle cells.

So consistent irritation (autoimmune) or HTN causes endothelial/intimal damage, leading to physiological healing of the arteries = THICKENING

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9
Q

WHat are the 5 modifiable risk factors for atherosclerosis?

Remember: SHODDY

A 
Smoking
Hypertension
Obesity
Diabetes
DYslipidemia
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10
Q

What’s the most important (clinically indicative) constitutional (non-modifiable) risk factor for atherosclerosis?

What are the other 2 non-modifiable risk factors?

A

Family History is the most clinically significant

Age (risk increases with it)
Gender (more common in males and post-menopausal females)

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11
Q

Why are only post-menopausal women at increased risk of atherosclerosis?

A

Estrogen is protective.

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12
Q

What blood test can strongly and independanty predict the risk of MI, stoke, Peripheral arterial disease, and sudden cardiac death, even among healthy persons?

A

HIghly elevated CRP levels

Directly correlate with inflammation and activation of endothelial cells to a pro-thrombotic state.

BUT there is no direct evidence that states that lower CRP than normal reduces this chance.

Fun fact: diabetics and fat people are in a constant inflammatory state, therefore their CRP levels are always elevated, and they’re at increased risk for heart disease.

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13
Q

Describe the process of an Atherosclerotic plaque formation.

A
  1. Endothelial Injury - intact endothelium, but dysfunctional. Increaesd permeability, leukocyte adhesion, and altered gene expression (activated)
  2. Lipid Accumulation - Lipoproteins accumulate in the intima, and get oxidized by Macropahges to form Ox-LDL, which the MACs then take up with their scavenger receptors = FOAM CELLS.
    The main lipids that accumulate are Ox-LDLs and Cholesterol crystals. The crystals activate MACs and the inflammasome –> IL-1 secretion –> increased activation of endothelium/inflammation
  3. Inflammation - cytokines (IL-1) released as a result of inflammasome activation by crystalized cholesterol increase adhesion molecules on the endothelium.
    - VCAM-1 specifically targets Monocytes and T-cells.
    - T-cells secrete IFN-gamma, which activates MACs, endothelium, and smooth muscle cells.
  4. Smooth muscle cell activation by IFN-gamma (from T-cell activated MACs) causes increased proliferation and ECM deposition. This forms the fibrous cap.

The continuation of this inflammation/healing process causes FATTY STREAK FORMATION.

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14
Q

Most common causes of endothelial injury leading to atherosclerotic plaques?

A

Hemodynamic disturbance (turbulence, HTN)

Hypercholesterolemia (lipids everywhere… all the more to start a plaque with….)

-Chronic Hyperlipidemia damages the blood vessels via increase ROS production.

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15
Q

4 main vessels involved in atherosclerosis.

A

In descending order:

  1. Infrarenal Abdominal Aorta
  2. Coronary Arteries
  3. Popliteal Arteries
  4. Internal carotids

…and sometimes the circle of willis in the brain

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16
Q

What part of the plaque usually ruptures?

A

The neck (or shoulder), where the fibrous cap meets the vessel wall.

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17
Q

WHat is the point of critical arteriolar stenosis? (The point at which blood flow is so obstructed, tissue O2 demand exceeds supply.)

A

70% occlusion

18
Q

Name the structural components of an Atherosclerotic plaque.

A
  1. Fibrous cap formed of Smooth muscle cells and ECM (collagen, elastin, etc…)
  2. Shoulder/Neck - where the cap meets the artery wall (where ruptures usually occur)
  3. Necrotic Lipid Core - Cholesterol Crystals and Foam cells
  4. Neovascularization - Shitty little blood vessels that can rupture
19
Q

Strength of the fibrous plaque is proportional to __________.

A

Collagen content.

Fibrous caps are constantly remodeling via MMPs (matrix metalloproteases)secreted by MACs. They’re usually kept in check by TIMPS (tissue inhibitors of MMPs) but if this balance gets thrown off, more collagen breakdown than synthesis = VULNERABLE PLAQUE

20
Q

What 3 things can cause plaque rupture?

A
  1. Throw of the MMP/TIMP ration
  2. Inflammation –> increases collagen degradation and reduces collagen synthesis in the plaque
  3. Mechanical stress due to emotion surge: Adrenergic blast of emotion = contraction of arteries = break the plaque
21
Q

Atherosclerosis is thickening of which BV layer?

A

The INTIMA

22
Q

2 most important causes of aortic aneurysms:

A

Atherosclerosis - AAA’s

Hypertension - Thoracic Aortic aneurysms

23
Q

What type of aneurysm is caused by trauma, vasculitis, and infections?

A

Mycotic Aneurysms

Any of these processes can weaken the vessel walls: the necessary step for an aneurysm to occur.

24
Q

Aneurysms occur most frequently in the ____________ (vessel)

A

Abdominal Aorta

25
Q

What’s the typical patient profile of a person with a AAA?

A

A 60+ year old diabetic man who smokes.

26
Q

What 2 hereditary syndromes can cause an increased susceptibility to aneurysms?

A

Marfans Syndrome -> Fibrillin defect (fibrillin is the framework that elastin is connected to)

Ehlers-Danlos Syndrome –> Defective Collagen Type III synthesis

Weaker blood vessels due to lack of structural components.

27
Q

Where along the aorta do AAA’s occur?

A

In between the renal arteries and the aortic bifurcation.

28
Q

Aneurysms greater than _______ in length are surgical emergencies.

A

5 cm, because they rupture at a rate of 1% per year.

29
Q

The risk of rupture within the year for an AAA greater than 6 cm is _____.

A

25%

30
Q

Aortic dissections occur secondary to what condition? How does this weaken the walls of the artery?

A

HYPERTENSION –> must have high pressure to be able to split the layers of the vessel apart.

HTN cause the vaso vasorum to undergo hypertrophic change in response to the constant pressure. This closes them off, and the medial layer of the vessel atrophies.

31
Q

Most aortic dissections are found where on the aorta?

A

Within 10 cm of the aortic valve.

32
Q

What is Cystic Medial Degeneration?

A

Loss of bloodflow to the media by either vaso vasorum compromise or atherosclerosis. This causes medial degeneration and decrosis, and accumulation of ECM.

WALL WEAKNESS, smooth muscle atrophy!

No inflammation is present.

33
Q

The most common cause of death from an aortic dissection is……

A

Rupture of the dissection into the pericardial, pleural, or peritoneal cavity.

(First one causes cardiac tamponade, Second one suffocates you. Third one, you bleed out.)

34
Q

Where does the pain radiate with an aortic dissection?

A

Excruciating, stabbing pain begins in the anterior chest and radiates to the back between the scapulae.

35
Q

WHich is worse? A Type A aortic dissection or a Type B?

A

Type A is waaay worse. Type B have a 75% survival rate with only anti-hypertensive meds.

36
Q

According to Dr. Nichols, what is the most important cytokine in the 1st step of atherosclerosis?

A

IL-1

He put a slide in that says “canakinumab protects against IL-1”

Just remember that the Anakin (skywalker) drug defends against IL-1.

37
Q

Cholesterol crystals activate the inflammasome. Then what happens?

A

The inflammasome activates caspase-1, which cleaves Interleukin-B1 into active IL-1!

38
Q

4 benefits of taking statins for atherosclerosis:

A
  1. Decrease in the lipid contents of plaques by inhibiting cholesterol synthesis
  2. Decrease Macrophage activity in plaques (less lipid content to eat)
  3. STABILIZE EXISTING PLAQUES
  4. Anti-thrombotic, Pro-fibrinolytic, and Vasodilatory
39
Q

1/2 of all MIs are in which coronary artery?

A

LAD (left anterior descending)

1/3 are in the RCA
1/6 are in the LCx

40
Q

What are the 5 P’s of ACUTE ARTERIAL OCCLUSION?

Is this a surgical or medical emergency?

A 
Pain
Pallor
Paralysis
Paresthesia
Pulselessness

SURGICAL EMERGENCY

CV Block (13 decks)

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